NEUROBIOLOGY

LABORATORY PRACTICAL MANUAL

III SEMESTER PAPER -II (302)

M.SC. Final
ZOOLOGY

Dr.V.SAILAJA
M.Sc.B.Ed.,Ph.D.,
ASSITANT PROFESSOR,

DR.C.V.NARASIMHA MURTHY
M.Sc.,Ph.D.,M.Ed.,
P.G.DIP IN HIGHER EDUCATION,
P.G.DIPLOMA IN JOURNALISM
P.G.DIPLOMA IN PUBLICRELATIONS AND ADVERTISING
PROFICIENCY IN GENETIC ENGENEERING
ASSOCIATE PROFESSOR (CONTRACT)

DEPARTMENT OF ZOOLOGY

V.S.U.P.G.CENTRE

KAVALI

2018
1 Page

Dr.V.SAILAJA & Dr C.V.N.M. ,DEPT ZOOLOGY, VSUPGC , KAVALI, -302- NeuroBiology -LAB MANUAL 2018
 INDEX

S.No. Name of the experiment Page No.

ESTIMATION OF ACETYL CHOLINE IN THE

1 GIVEN TISSUE SAMPLE OF CHICK 3-5

ACETYL CHOLINESTERASE ACTIVITY IN

2 DIFFERENT REGIONS OF SHEEP BRAIN 6-8

EFFECT OF PHYSOSTIGMINE ON ACETYL

9-11
CHOLINESTERASE ACTIVITYIN DIFFERENT
REGIONS OF SHEEP BRAIN
3

ESTIMATION OF ATPase ACTIVITY

4 12-15

5 NERVOUS SYSTEM
REGIONS OF OF
SHEEP PRAWN
BRAIN 16-20
6 SPOTTERS 21-61
7
8

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ESTIMATION OF ACETYL CHOLINE IN THE GIVEN TISSUE SAMPLE OF CHICK

Aim: To estimate the acetyl choline content in the given tissue sample of chick.

Introduction:

Acetylcholine (ACh) was first identified in 1915 by Henry Hallett Dale for its actions on
heart tissue. It was confirmed as a neurotransmitter by Otto Loewi, who initially gave it the name
Vagusstoff because it was released from the vagus nerve. Both received the 1936 Nobel Prize in
Physiology or Medicine for their work. Acetylcholine was also the first neurotransmitter to be
identified.

Acetyl choline is s a neurotransmitter—a chemical messenger released by nerve cells to

send signals to other cells [neurons, muscle cells, and gland cells]. Its name is derived from its
chemical structure: it is an ester of acetic acid and choline. Parts in the body that use or are
affected by acetylcholine are referred to as cholinergic. Substances that interfere with
acetylcholine activity are called anticholinergics. Acetylcholine is the neurotransmitter used at
the neuromuscular junction—in other words, it is the chemical that motor neurons of the nervous
system release in order to activate muscles. This property means that drugs that affect
cholinergic systems can have very dangerous effects ranging from paralysis to convulsions.
Acetylcholine is also used as a neurotransmitter in the autonomic nervous system, both as an
internal transmitter for the sympathetic nervous system and as the final product released by the
parasympathetic nervous system.

In the brain, acetylcholine functions as a neurotransmitter and as a neuromodulator. The

brain contains a number of cholinergic areas, each with distinct functions; such as playing an
important role in arousal, attention, memory and motivation.

Partly because of its muscle-activating function, but also because of its functions in the
autonomic nervous system and brain, a large number of important drugs exert their effects by
altering cholinergic transmission. Numerous venoms and toxins produced by plants, animals, and
bacteria, as well as chemical nerve agents such as Sarin, cause harm by inactivating or
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hyperactivating muscles via their influences on the neuromuscular junction. Drugs that act on
muscarinic acetylcholine receptors, such as atropine, can be poisonous in large quantities, but in
smaller doses they are commonly used to treat certain heart conditions and eye problems.
Scopolamine, which acts mainly on muscarinic receptors in the brain, can cause delirium and
amnesia. The addictive qualities of nicotine are derived from its effects on nicotinic
acetylcholine receptors in the brain.

Reagents:
1. Ferric chloride solution: Dissolved oneG ml of concentrated Hydrochloric acid in 120 of
water. For that 800 mg of Ferric chloride was added.
2. Alkaline Hydroxylamine hydrochloride solution: Dissolved 18.9 grams of hydroxylamine
hydrochloride in 100 ml water. In another beaker for 14 grams of sodium hydroxide is
dissolved in 100 ml water. Mix both of them.
3. 0.1 N Hydrochloric acid: one ml of hydrochloric acid was made up to 120 ml with water.

Procedure:
Tissue preparation: one gram of tissue was boiled in 10 ml water for deactivation AchE
activity. It was homogenized in 10 ml distilled water. The reaction mixture was prepared as
shown in the table and color developed was read at 540 nm against blank in spectrophotometer.
S.No Tissue Tissue Fe Distilled Alkaline 0.1 Optical Ach
Name homogenate Cl3 water hydroxylamine N density content
volume solution Hydrochloride HCl
solution
1 Chick 2 ml 1ml Nil 2 ml 1
brain ml
2 muscle 2 ml 1ml Nil 2ml 1
ml
3 Blank Nil 1ml 2 ml 2ml 1
ml
4 Standard Nil 1ml 2 ml 2ml 1 1.000 10
ml

Calculations
Ach content = O.D.of sample x amount in Standard x1000X2
O.D of standard weight of the tissue taken
mill moles of catalase for gram weight of tissue.
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Conclusions:
From the experimental results it can be concluded that brain tissue of chick contained …. milli
moles of catalase for gram weight of tissue.

Acetylcholine is an organic cation that acts as a neurotransmitter in many organisms, including

humans. Acetylcholine is also the principal neurotransmitter in all autonomic ganglia. In cardiac
tissue, acetylcholine neurotransmission has an inhibitory effect, which lowers heart rate.
However, acetylcholine also behaves as an excitatory neurotransmitter at neuromuscular
junctions in skeletal muscle.

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ACETYL CHOLINESTERASE ACTIVITY IN DIFFERENT REGIONS OF
SHEEP BRAIN

AIM: To estimate the acetyl cholinesterase activity in different regions of sheep brain

INTRODUCTION:

Acetylcholinesteras
es (AChEs) are enzymes
that hydrolyze the
neurotransmitter
acetylcholine (ACh) to
acetate and chorine. AChE
is located at the synaptic
cleft and functions to
terminate synaptic
transmission by catalyzing
the breakdown of ACh allowing cholinergic neurons to return to a resting state after activation.
Changes in AChE activity may result from exposure to certain insecticides, which act as
cholinesterase inhibitors. Inhibitors of AChE are also used to treat certain conditions such as
dementia.

PRINCIPLE:

This assay is an optimized version of the Ellman method in which thiocholine, produced
by AChE, reacts with 5,5′-dithiobis(2-nitrobenzoic acid) to form an colorimetric (412 nm)
product, proportional to the AChE activity present. One unit of AChE is the amount of enzyme

6|Page
that catalyzes the production of 1.0 μ mole of thiocholine per minute at room temperature at pH
7.5.
The assay is based on measurement of the change in absorbance at 405 nm. The method
is described in detail by Ellman, G. L., et al, Biochem. Pharmacol., 7, 88-95, 1961. The assay
uses the thiol ester acetylthiocholine instead of the oxy ester acetylcholine.

AChE hydrolyses the acetylthiocholine to produce thiocholine and acetate. The

thiocholine in turn reduces the Dithiobis-Nitrobenzoic Acid liberating nitrobenzoate, which is
yellow in color that absorbs at 405 nm. The intensity of yellow color is directly proportional to
enzyme activity.

Reagents:
1. 0.25 M Sucrose solution: 8.155 grams of sucrose is dissolved in 90 distilled water and
made up to 100 ml.
2. Phosphate Buffer: 600 mg of monobasic sodium phosphate and 2.82 grams of dibasic
sodium phosphate was dissolved in 200 ml distilled water.
3. 0.1M Acetyl thio choline iodide soloution: 290 mg of Acetyl thio choline iodide was
dissolved in 100 ml distilled water.
4. 0.01 M DTNB solution: Dissolved 40 mg of 5,5'-Dithiobis(2-nitrobenzoic Acid) and
15 mg of sodium bicarbonate in 10 ml of Phosphate Buffer.
5. 1% Homogenate preparation: Dissolved one Gram of Brain tissue in 100 ml of 0.25M
sucrose solution.

Procedure:
The reaction mixture was prepared as follows and incubated at room Temperature for 30
minutes and colour developed was read at 412 µ in colorimeter against blank.
Protein content was estimated by using Lowry et al method.

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s . N o . Name of the Phosphate buffer Homogenate solution Acetyl choline 0.01M DTNB Protein content Optical density Ach activity
S a m p l e Chloride solution mg/gram Mg/protein /hr.
tissue
1 Hippocampus 3 m l 0.1 ml 0.2 ml 0.1 ml 37.76
2 C o r t e x 3 m l 0.1 ml 0.2 ml 0.1 ml 36.52
3 Cerebellum 3 m l 0.1 ml 0.2 ml 0.1 ml 34.38
4 Medulla oblongata 3 m l 0.1 ml 0.2 ml 0.1 ml 32.14
5 Diencephalon 3 m l 0.1 ml 0.2 ml 0.1 ml 35.96
6 B l a n k 3ml N i l 0.2 ml 0.1 ml N i l
7 Standard 3 m l N i l 0.2ml o.1 ml 1 1.0415

Method of calculation:

Ach E Enzyme activity = OD of unknown X vol of sample x duration X 1000

-----------------------------------------------------------------
OD of standard X incubation time X protein content

mg protein/hour

Results:

1. Ach E activity in Hippocampus =

2. Ach E activity in cerebrum =
3. Ach E activity in medulla oblongata =
4. Ach E activity in diencephalon =
5. Ach E activity in cortex =

Discussion:

Acetyl cholinesterase is an enzyme that catalyzes the breakdown of acetylcholine and of some
other choline esters that function as neurotransmitters. AChE is found at mainly neuromuscular
junctions and in chemical synapses of the cholinergic type, where its activity serves to terminate
synaptic transmission. It belongs to carboxyl esterase family of enzymes. It is the primary target
of inhibition by organophosphorus compounds such as nerve agents and pesticides

8|Page
EFFECT OF PHYSOSTIGMINE ON ACETYL CHOLINESTERASE
ACTIVITY IN DIFFERENT REGIONS OF SHEEP BRAIN
Aim: To know the effect of Physiostigmine on the acetyl cholinesterase activity in different
Regions of sheep brain

Introduction:
Physiostigmine is a cholinesterase inhibitor that is rapidly absorbed through membranes.
It can be applied topically to the conjunctiva. It also can cross
the blood-brain barrier and is used when central nervous
system effects are desired, as in the treatment of severe
anticholinergic toxicity.Physostigmine is a Cholinergic
Agonist (Indirect acting/ Anti-cholinesterase agent Reversible), used as miotic agent to treat
glaucoma.

The chemical was synthesized for the first time in 1935 by Percy Lavon Julian and Josef
Pikl. It is available in the U.S. under the trade names Antilirium and Isopto Eserine, and as
eserine salicylate and eserine sulfate. Today, physostigmine is most commonly used for its
medicinal value. However, before its discovery by Sir Robert Christison in 1846, it was more
prevalent as a poison. The positive medical applications of the drug were first suggested in the
gold medal winning final thesis of Thomas Richard Fraser at the University of Edinburgh in
1862.

Principle:

Acetyl cholin enzymatically broken down into thiocholine and acetate. Physiostigmin
inhibits the AchE activity by competitively binding with active sites of AchE enzyme. This
prevents the formation of enzyme substrate complex by forming the Ach E Physiostigmin
complex. AchE estimation is a an optimized version of the Ellman method in which thiocholine,
produced by AChE, reacts with 5,5′-dithiobis(2-nitrobenzoic acid) to form an colorimetric (412
nm) product, proportional to the AChE activity present. One unit of AChE is the amount of

9|Page
enzyme that catalyzes the production of 1.0 μ mole of thiocholine per minute at room
temperature at pH 7.5.
The assay is based on measurement of the change in absorbance at 405 nm. The method
is described in detail by Ellman, G. L., et al, Biochem. Pharmacol., 7, 88-95, 1961. The assay
uses the thiol ester acetylthiocholine instead of the oxy ester acetylcholine.
AChE hydrolyses the acetylthiocholine to produce thiocholine and acetate. The
thiocholine in turn reduces the Dithiobis-Nitrobenzoic Acid liberating nitrobenzoate, which is
yellow in color that absorbs at 405 nm. The intensity of yellow color is directly proportional to
enzyme activity.

Reagents:
1. 0.25 M Sucrose solution: 8.155 grams of sucrose is dissolved in 90 distilled water and
made up to 100 ml.

2. Phosphate Buffer: 600 mg of monobasic sodium phosphate and 2.82 grams of dibasic
sodium phosphate was dissolved in 200 ml distilled water.
3. 0.1M Acetyl thio choline iodide soloution: 290 mg of Acetyl thio choline iodide was
dissolved in 100 ml distilled water.
4. Physiostigmin inj: Antilirium injection was purchased from local Medical shop
5. 0.01 M DTNB solution: Dissolved 40 mg of 5,5'-Dithiobis(2-nitrobenzoic Acid) and
15 mg of sodium bicarbonate in 10 ml of Phosphate Buffer.
6. 1% Homogenate preparation: Dissolved one Gram of Brain tissue in 100 ml of 0.25M
sucrose solution.
Procedure:

The reaction mixture was prepared as follows and incubated at room Temperature for 30 minutes
and colour developed was read at 412 µ in colorimeter against blank. Protein content was
estimated by using Lowery et al method.

10 | P a g e
s.n Name of the Phos Homogen Acetyl Physi 0.01 Protei Optic Ach
o. Sample phat ate cholin o- M n al activity
e Solution e stigm DTN conten densi Mg/prot
buffe Chlori in B t ty ein /hr.
r de ml mg/gr
solutio am
n tissue
1 Hippocampu 3 ml 0.1 ml 0.2 ml 0.1 0.1 37.76
s ml ml
2 Cortex 3 ml 0.1 ml 0.2 ml 0.1 0.1 36.52
ml ml
3 Cerebellum 3ml 0.1 ml 0.2 ml 0.1 0.1 34.38
ml ml
4 Medulla 3ml 0.1 ml 0.2 ml 0.1 0.1 32.14
oblongata ml ml
5 Diencephalo 3ml 0.1 ml 0.2 ml 0.1 0.1 35.96
n ml ml
6 Blank 3ml Nil 0.2 ml 0.1 0.1 Nil
ml ml
7 Standard 3ml Nil 0.2ml o.1 1 1.041
ml 5

Method of calculation:

Ach Enzyme activity = OD of unknown X vol of sample x duration X 1000

------------------------------------------------------------
OD of standard X incubation timeX protein content

mg protein/hour

Results:
Ach activity in Hippocampus =
Ach activity in cerebrum =
Ach activity in medulla oblongata =
Ach activity in diencephalon =
Ach activity in cortex =

Discussion:

Acetyl cholinesterase is an enzyme that catalyzes the breakdown of acetylcholine and of some
other choline esters that function as neurotransmitters. AChE is found at mainly neuromuscular
11 | P a g e
junctions and in chemical synapses of the cholinergic type, where its activity serves to terminate
synaptic transmission. It belongs to carboxyl esterase family of enzymes. It is the primary target
of inhibition by organophosphorus compounds such as nerve agents and pesticides

ESTIMATION OF ATPase ACTIVITY

Aim: To estimate the ATPase ACTIVITY in different regions of chick brain

Introduction:

Active transport is the movement of molecules across a membrane from a region of their lower
concentration to a region of their higher concentration—in the direction against the concentration
gradient. Active transport requires cellular energy to achieve this movement. There are two types
of active transport – primary active transport that uses ATP, and secondary active transport
that uses an electrochemical gradient. An example of active transport in human physiology is the
uptake of glucose in the intestines.

Primary active transport, also called direct active

transport, directly uses metabolic energy to transport
molecules across a membrane.[12] Substances that are
transported across the cell membrane by primary active
transport include metal ions, such as Na+, K+, Mg2+, and Ca2+. These charged particles require
ion pumps or ion channels to cross membranes and distribute through the body.

Most of the enzymes that perform this type of transport are transmembrane ATPases. A
primary ATPase universal to all animal life is the sodium-potassium pump, which helps to
maintain the cell potential. The sodium-potassium pump maintains the membrane potential by
moving three Na+ ions out of the cell for every two K+ ions moved into the cell. Other sources
of energy for Primary active transport are redox energy and photon energy (light). An example of
primary active transport using Redox energy is the mitochondrial electron transport chain that
uses the reduction energy of NADH to move protons across the inner mitochondrial membrane
against their concentration gradient. An example of primary active transport using light energy
are the proteins involved in photosynthesis that use the energy of photons to create a proton

12 | P a g e
gradient across the thylakoid membrane and also to create reduction power in the form of
NADPH.

Principle:

ATPase will hydrolase the ATP into ADP + Pi in the presence of calcium or potassium or
sodium ions. The amount of freeinorganic phosphate released is directly proportional to the level
of ATPase activity. The released ionorganic phosphate is released by the method of Fisk and
subbarao.S Proteins hydrolyze ATP in a reaction that results in inorganic phosphate release, and
the amount of phosphate liberated is then quantitated using a colorimetric assay. This highly
adaptable protocol can be adjusted to measure ATPase activity in kinetic or endpoint assays.

Reagents:

1. 0.05 M Mangnesium Chloride: Dissolved 1.065 grams of 1000ml of distilled water.

2. 0.05M Sodium chloride: 292 mgof sodium chloride was dissolved in 1000 ml of distilled
3. 0.05M Potassium chloride: Dissolved 372.75 grams of Potassium chloride in 1000 ml
distilled water.
4. Tris buffer: 165.52 mg of Tris was dissolved in 1000 ml distilled water.
5. 0.01M Adenosine Tri phosphate : 275 mg of adenosine triphosphate was dissolved
in1000 ml distilled water.
6. 10 N. Sulphuric acid: 28 ml of sulphuric acid was made up to 100 ml with distilled water.
7. 10% Trichloroacetic acid : 10 grams of TCA was dissolved in 100 ml of distilled water.
8. Ammonium molybdate solution: 2.5 grams of ammonium molybdate was dissolved in 20
ml of distilled water. For that 30 ml of 10 N sulphuric acid was added.
9. 15% Sodium bisulphate : 15 grams of sodium bisulphate was dissolved 1in 100 ml of
distilled Water.
10. 20% Sodium sulphate : 20 grams of sodium sulphate was dissolved in 100 ml distilled
warter.
11. ANSA( 1 amino 2 naphta 4 sulphonic acid). 20 mg of ANSA was dissolved in 90 ml of
15 % sodium bisulphate solution. For that 2.5 ml of 20% sodium bisulphate solution is
added.
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 12. 0.25 M sucrose solution: 8.6 grams of sucrose was dissolved in 100 ml distilled water.
Homogenate preparation : 500 mg of tissue was homogenized in 50 ml of ice cold 0.25 M
sucrose solution.centreguged it for five minuts at 1500 rpm. Collected the supernatant and used it
as enzyme source.

Experimental procedure:

The reaction mixture were prepared as shown in the table.It was incubated at 37 0C for 15
minutes and reaction was stopped it by adding 1.5 ml of 10% trichloro acetic acid solution. Then
the contents were centrifuged at 2000 rpm for 3 minutes and supernatant was collected and
inorganic phosphate content was estimated as detailed below.
For one ml of supernntant one ml of ammonium molybdate solution anfd 0.5ml of ANSA
solution and colour was developed was read at 660 nm inspectrophotometer.
Bi sulphate

370C for 15
Tris buffer

Incubate at

and collect
supernatan
Homogena

Centrifuge

OPTICAL
molybdate

DENSITY

ACTIVIT
Ammoniu
Na Cl(ml)
Paramter

Kcl (ml)

minutes

ATPase
ANSA
Mgcl2

t (ml)
TCA
s.No.

ATP
(ml)

(ml)
(ml)

(ml)

(ml)

(ml)

(ml)
(ml)
m
te

Y
1 Mg Nil 0. 0. 0.5 Nil Nil 1ml Incu 1.5 1 ml 1ml 0.5
ATPas 5 5 bate ml ml
e at
370C
for
15
minu
tes
2 Total 0.5 - 0. - 0.5 0.5 1 Incu 1.5 1 ml 1ml 0.5
ATPas 5 ml bate ml ml
e at
370C
for
15
minu
tes
14 | P a g e
3 Blank 0.5 - 0. - 1.5 0.5 Nil Incu 1.5 1 ml 1ml 0.5
5 bate ml ml
at
370C
for
15
minu
tes
4 Standa Nil N Ni nil Nil Nil Nil Nil
rd il l

Method of calculation:

ATPase activity = OD of unknown X vol of sample x duration X 1000

-------------------------------------------------------------
OD of standard X incubation time X protein content

mg protein/hour

Results:
1. Mg ion dependent ATPase activity in Medulla oblongata =
2. Mg ion dependent ATPase activity in cerebrum =
3. Total ATPase activity in medulla cerebrum =
4. Total ATPase activity in medulla cerebrum =

Discussion:

In the present experiment Total ATPase and Mg ion dependent activity levels were
estimated in the different regeions of brain. The cerebral cortex recorded highest level of Total
ATP enzyme activity level over other tissue.

15 | P a g e
 Nervous system Of Prawn

The nervous system of Palaemon consists of:

1. Central nervous system

16 | P a g e
2. Peripheral nervous system

3. Sympathetic nervous system

I. Central Nervous System:

Central nervous system consists of:

1. Brain or a pair of supra-oesophageal ganglia,

2. A pair of circumoesophageal commissures,

3. Ventral thoracic ganglionic mass, and

4. A ventral nerve cord.

. Brain or Supra – Oesophageal Ganglia:

The brain or supra-oesophageal ganglion is a bilobed structure which lies at the base of rostrum,
anterior to the oesophagus.

It is embedded in a thick mass of fat. It is formed by the fusion of several ganglia as it appears
from the fact that several nerves arise from it to innervate the eyes, antennules, antennae and
labrum etc. However, from segmentation point of view it is supposed to be formed of
protocerebrum, paired optic ganglia, mesocerebrum and metacerebrum.

The following nerves originate from the brain:

(i) Antennulary nerves:

A pair of antennulary nerves arise from below the origin of optic nerves. Each nerve enters the
antennule of its side into which it sends a statocystic branch to statocyst.

(ii) Optic nerves:

A pair of stout optic nerves arise from the dorsal surface of the brain, one on each side, to supply
the compound eye of its side.

(iii) Ophthalmic nerves:

A pair of ophthalmic nerves arise from the brain, one on each side, and supply the ocular
muscles in the eye-stalks.

(iv) Antennary nerves:

17 | P a g e
A pair of stout antennary nerves originate from the ventral surface of the brain. Each nerve
divides into two branches, the outer innervating the squama and the inner innervating the feeler
of antenna.

(v) Tegumental nerves:

A pair of slender tegumental nerves arise just behind the origin of antennary nerves. These
nerves innervate the labrum.

2. Circumoesophageal Commissure:

These are two stout nerves, which arise from the posterior end of brain and run backwards and
downwards around the oesophagus. It unites ventrally with the sub-oesophageal ganglia which
form the indistinguishable anterior part of the ventral thoracic ganglionic mass.

Each commissure bears a small commissural ganglion near its anterior end, and gives off small
nerve to the mandible of its side. The two circumoesophageal commissures are connected with
each other by a slender transverse commissure near the posterior end.

3. Ventral Thoracic Ganglionic Mass:

The ventral thoracic ganglionic mass is an elongated oval structure situated immediately above
the thoracic sternal plates in the mid-ventral line. It is a composite mass which is formed as a
result of fusion of the eleven pairs of ganglia. It gives off eleven pairs of nerves on the lateral
sides. The first three pairs are of cephalic nerves, supplying the mandibles, maxillulae and the
maxillae respectively.

The last eight pairs are of the thoracic nerves, of which the first three pairs give off branches to
the three pairs of maxillipedes respectively and the remaining five pairs supply the five pairs of
walking legs. Each nerve to a leg becomes bifurcated before entering the leg.

4. Ventral Nerve Cord:

The ventral thoracic ganglionic mass is continued posteriorly into the ventral or abdominal nerve
cord. It runs posteriorly along the mid-ventral line of the abdomen up to the last segment. In each
abdominal segment there is an abdominal ganglion. The ventral nerve cord and the abdominal
ganglia are double.

Each of the first five abdominal ganglia gives off three pairs of nerves in its segment:

(i) A pair of pedal nerves supplying the pleopods,

(ii) A pair of nerves to the extensor muscles of its segment, and

(iii) A pair of nerves to the flexor muscles of the succeeding segment.

18 | P a g e
The last or sixth abdominal ganglion or stellate ganglion is comparatively large and is formed by
the fusion of paired ganglion of the sixth segment with a number of post-abdominal ganglia. This
ganglion supplies two pairs of nerves to the flexor muscles of the sixth segment, two pairs of
nerves to the uropods, two pairs of nerves to the telson, and a single median nerve to the rectum
and hindgut.

II. Peripheral Nervous System:

The various nerves originating from the central nervous system to innervate the different parts of
the body constitute the peripheral nervous system.

III. Sympathetic Nervous System:

The sympathetic or visceral nervous system is represented by a few small ganglia and nerves. A
small nerve arising from the posterior part of the brain, runs on the roof of the cardiac stomach
and bears two visceral or oesophageal ganglia, one anterior and another posterior.

The anterior visceral ganglion is joined with the two commissural ganglia by a pair of
connectives. The posterior visceral ganglion is free and gives off two pair of nerves to the
muscles of the wall of oesophagus and the cardiac stomach.

19 | P a g e
 SPOTTERS

1. Typical neuron
2. Types of neurons
3. Different types of neurons
4. Classification of neurons basing on function
5. Types of neurons
6. Brain structure
7. Brain stem
8. CS of spinal cord
9. CNS
10. PNS
11. Sympathetic nervous system
12. Parasympathetic vs sympathetic
13. Synapse
14. Sodium potassium pump
15. Action potential
16. Nerve impulse propagation
17. Nerve conduction at myelinated neuron
18. Ligand binding
19. Ligand gated ion channel
20. Calcium Chanel
21. Voltage gated Chanel
22. G protein linked Chanel
23. Calmodulin linked Chanel
24. Tyrosine kinases lined Chanel
25. Oxytocin
26. Vasopressin
27. Alcoholism
28. Smoking
29. Cocaine
30. Marjuana
31. Depression
32. Schizophrenia
33. Parkinsonism
34. Alzheimer’s disease

20 | P a g e
TYPICAL NEURON

1. The neural system of all animals is composed of highly specialized cells called neurons.
2. Neurons are the structural and functional unit of nervous system.
3. Neurons are formed of mainly 3 parts – cell body, dendrites and axon.
4. The cell body contains cytoplasm with typical cell organelles.
5. Nissal granules are the granular bodies present in the cytoplasm of neurons.
6. Dendrites are short fibers which branch repeatedly and project out of the cell
body are known as dendrites.
7. Axon is the long fiber in the neuron.
8. Schwann cells are special type of cells which cover the axon.
9. Synaptic knob is bulb like structure present at the end of dendrites. These knobs
contain synaptic vesicles, which contains neurotransmitters.

21 | P a g e
 TYPES OF NEURONS

Based on the number of axon and dendrites, the neurons are classified into 3 types.

1. Multipolar neurons
a. These are neurons with one axon and two or more dendrites.
i. Eg . Neurons in the cerebral cortex.
2. Bipolar neurons
a. Neurons with one axon and one dendrite e.g. Neurons in the retina of eye.

3. Unipolar neurons
a. Cell body with one axon only. These types of neurons are found only in the
embryonic stage.

4. Psudo unipolar neuron ;

A pseudounipolar neuron (pseudo – false, uni – one) is a kind of sensory neuron in

22 | P a g e
 the peripheral nervous system. This neuron contains an axon that has split into two
branches; one branch runs to the periphery and the other to the spinal cord

Different types of neurons

Sensory neurons

Sensory neurons are the nerve cells that are activated by sensory input from the environment -
for example, when you touch a hot surface. Most sensory neurons are pseudounipolar, which
means they only have one axon which is split into two branches.

Motor neurons

Motor neurons of the spinal cord are part of the central nervous system (CNS) and connect to
muscles, glands and organs throughout the body. These neurons transmit impulses from
23 | P a g e
the spinal cord to skeletal and smooth muscles (such as those in your stomach), and so directly
control all of our muscle movements motor neurons have the most common type of ‘body plan’
for a nerve cell - they are multipolar, each with one axon and several dendrites.

Interneurons

As the name suggests, interneurons are the ones in between - they connect spinal motor and
sensory neurons. As well as transferring signals between sensory and motor neurons,
interneurons can also communicate with each other, forming circuits of various complexity.
They are multipolar, just like motor neurons.

TYPES OF NERVE CELLS

1. Dendrites are Short fibers which branch repeatedly and project out of the cell body are
known as dendrites they receive information from surroundings

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2. Axon is the long fiber in the neuron. They conduct nerve impulse

3. Schwann cells are the special type of cells which cover the axon.
4. Glial cells: They are thus known as the "supporting cells" of the nervous system. The four
main functions of glial cells are: to surround neurons and hold them in place, to supply
nutrients and oxygen to neurons, to insulate one neuron from another, and to destroy and
remove the carcasses of dead neurons
5. Astrocytes: they are star like structure in the nervous system. Hey regulate the
transmission of electrical impulses within the brain. ... Metabolic support: They provide
neurons with nutrients such as lactate.

6. Ependymal cells: Ependymal cell, type of neuronal support cell (neuroglia) that forms the
epithelial lining of the ventricles (cavities) in the brain and the central canal of the spinal
cord.
7. Secretary cells: Specialized neuron clusters called neurosecretory cells in the
hypothalamus produce the hormones Antidiuretic Hormone (ADH) and Oxytocin (OXT),
and transport them to the pituitary, where they're stored for later release
8. Nissil’s granules: These are the granular bodies present in the cytoplasm of neurons.

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Brain structure

The brain can be divided into three major parts-

1. Forebrain 2. Midbrain 3.hindbrain

Forebrain
The forebrain consists of cerebrum, thalamus and hypothalamus
Cerebrum
Cerebrum is the major part of the brain .cerebrum is divided longitudinally into two
halves, termed as the left and right cerebral hemispheres
Corpus collosum
The group of nerve fibers which connect the two cerebral hemispheres are called corpus
collosum.
Cerebral cortex
The layers of cells which cover cerebrum externally are called cerebral cortex.
The neuron cell bodies are concentrated in the cortex and it has grey in colour, so called
greymatter.
Cerebral medulla
The inner layer of cerebrum is medulla .medulla contains nerve tracts which are covered
with myelin sheath, which give an opaque white appearance to the layer and hence, called

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 white matter.
Areas of cerebrum
Sensory area are concerned with perception and identification of impulses from sense
Organs .motor area gives out motor information to effects organs.
3 . Association area responsible for complex functions like intercessory associations,
memory and communication.

Thalamus
Thalamus is the major coordinating centre for sensory and motor signalling
It functions as the relay centre of impulses to and from the cerebrum.

Hypothalamus
Hypothalamus lies at the base of thalamus .it controls body temperature, urge for eating
and drinking etc.the neurosecretory cells of hypothalamus secrete Oxytocin and
vasopressin.
Limbic system
The inner parts of cerebral hemisphere and a group of associated deep structures like
amygdala, hippocampus etc. Form a complex structure called the limbic lobe or limbic
system .it is involved in the regulation of sexual behaviour, expression of emotional
reactions like excitement, pleasure, fear, motivation etc.

Midbrain
Midbrain is located between the forebrain and hindbrain.
Cerebral aqueduct is the canal which passes through the midbrain.
Dorsal portion of the midbrain consists four round swelling called corporaquadrigemina

Hindbrain
The hindbrain consists of Pons, cerebellum and medulla
Pons consists of nerve tracts that interconnect different regions of the brain.
Medulla is connected to the spinal cord .medulla oblongata controls respiration, cardiovascular
reflexes and gastric secretions
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 Brain stem

1. The brainstem is the region of the brain that connects the cerebrum with the spinal cord. It
consists of the midbrain, medulla oblongata, and the Pons.
2. Motor and sensory neurons travel through the brainstem allowing for the relay of signals
between the brain and the spinal cord. Most cranial nerves are found in the brainstem.
3. The brainstem coordinates motor control signals sent from the brain to the body. This
brain region also controls life supporting autonomic functions of the peripheral nervous
system. The fourth cerebral ventricle is located in the brainstem, posterior to the Pons and
medulla oblongata. This cerebrospinal fluid-filled ventricle is continuous with the cerebral
aqueduct and the central canal of the spinal cord
4. The brainstem controls several important functions of the body including: alertness,
arousal, breathing, blood pressure control, digestion, heart rate etc.
5. The cerebellum is important for regulating functions such as movement coordination,
balance, equilibrium, and muscle tone.

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C.S. OF SPINAL CORD

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 CENTRAL NERVOUS SYSTEM

1. The central nervous system consists of the brain and spinal cord. It is referred to as
"central" because it combines information from the entire body and coordinates activity
across the whole organism.
2. The brain can be divided into four main lobes: temporal, parietal, occipital and frontal.
3. In total, around 100 billion neurons and 1,000 billion glial (support) cells make up the
human brain. Our brain uses around 20 percent of our body's total energy.
4. The spinal cord, running almost the full length of the back, carries information between
the brain and body, but also carries out other tasks.
5. From the brainstem, where the spinal cord meets the brain, 31 spinal nerves enter the
cord.
6. Along its length, it connects with the nerves of the peripheral nervous system (PNS)
that run in from the skin, muscles, and joints.

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 7. Motor commands from the brain travel from the spine to the muscles and sensory
information travels from the sensory tissues — such as the skin — toward the spinal
cord and finally up to the brain.
8. The spinal cord contains circuits that control certain reflexive responses, such as the
involuntary movement your arm might make if your finger was to touch a flame.

PERIPHERAL NERVOUS SYSTEM

1. The PNS consists of the nerves and ganglia outside the brain and spinal cord.
2. The main function of the PNS is to connect the to the limbs and organs, essentially
serving as a relay between the brain and spinal cord and the rest of the body.
3. Unlike the, the PNS is not protected by the vertebral column and skull, or by the blood–
brain barrier, which leaves it exposed to toxins and mechanical injuries.
4. The peripheral nervous system is divided into the somatic nervous system and the
autonomic nervous system.
5. In the somatic nervous system, the cranial nerves are part of the PNS with the exception
of the optic nerve (cranial nerve ii), along with the retina.
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 6. The second cranial nerve is not a true peripheral nerve but a tract of the diencephalon.[3]
Cranial nerve ganglia originated in the.
7. However, the remaining ten cranial nerve axons extend beyond the brain and are
therefore considered part of the PNS. The autonomic nervous system is an involuntary
control of smooth muscle and glands.
8. The connection between and organs allow the system to be in two different functional
states: sympathetic and parasympathetic.

SYMPATHETIC NERVOUS SYSTEM

Sympathetic nerves arise from near the middle of the spinal cord in the intermediolateral nucleus
of the lateral grey column, beginning at the first thoracic vertebra of the vertebral column and are
thought to extend to the second or third lumbar vertebra.

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The sympathetic division consists of two paired chains of collections of nerve cell bodies called
ganglia. These ganglia lie just to the left and right of the spinal cord in the centrally located
thoracic and lumbar regions.

Axons extend from the ganglion to the body's organs. Because the ganglia of the sympathetic
division are linked, they tend to work as a group; or "in sympathy" with each other.

The sweat glands, adrenal glands, muscles that constrict blood vessels and muscles that erect
skin hairs are under control of the sympathetic division only.

Most of the final synapses of the sympathetic division use the neurotransmitter nor epinephrine,

Parasympathetic nervous system

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1. Para- means beside or related to; and indeed the functions of the parasympathetic division
work in conjunction with the sympathetic division by opposing its effects.
2. Although the two divisions of the ANS work in opposition to one another, they are
normally both active simultaneously.
3. The parasympathetic division is sometimes known as the craniosacral system because its
nerves derive from the cranial nerves at the base of the brain and the sacral spinal cord.
4. Unlike the sympathetic division, the nerve cell collections or ganglia of the
parasympathetic division are located close to the organ and not along the spinal cord. In
addition, the parasympathetic ganglia are not connected like those of the sympathetic
division. They are, therefore, capable of acting independently on the organs they control.
5. The final synapses of the parasympathetic division use the neurotransmitter acetylcholine.
This difference in neurochemical activity makes selective stimulation of each division
possible with certain drugs.

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 Synapse

1. The function of the synapse is to transfer electric activity (information) from one cell to
another.
2. The transfer can be from nerve to nerve (neuro-neuro), or nerve to muscle (neuro-myo).
The region between the pre- and postsynaptic membrane is very narrow, only 30-50 nm. It
is called the synaptic cleft (or synaptic gap).
3. Direct electric communication between pre- and postjunctional cells does not take place;
instead, a chemical mediator is utilized. The sequence of events is as follows:
4. An action pulse reaches the terminal endings of the presynaptic cell.
5. A neurotransmitter is released, which diffuses across the synaptic gap to bind to receptors
in specialized membranes of the postsynaptic cell.
6. The transmitter acts to open channels of one or several ion species, resulting in a change
in the transmembrane potential. If depolarizing, it is an excitatory postsynaptic potential
(EPSP); if hyperpolarizing, an inhibitory postsynaptic potential (IPSP).

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SODIUM POTASSIUM PUMP

1. When a stimulus is applied to a neuron at resting potential , the polarity

of the cell membrane changes.
2. The sodium – potassium pump upsets for a moment, and the cell membrane
becomes highly permeable to Na+ ions.

3. The heavy influx of Na+ i on s into the membrane leads to the reversal of
polarity and outside of the membrane become negatively charged and inside
positively charged.
4. This change in polarity is called depolarization.
Repolarisation
5. The change in polarity due to nerve impulse extremely short lived.
6. The sodium – potassium pump quickly regains its activity and pumps out Na+
ions and K+ ions accumulate inside and resting potential is regained.
7. This recovery is called repolarisation.

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ACTION POTENTIAL

1. The momentary depolarization and repolarization of the axonal membrane is called

action potential.
2. The action potential can be called as the nerve impulse.
3. The propagation of the nerve impulse is due to the alternate depolarization
and repolarisation of the membrane or the conduction of the action potential .
4. Resting membrane potential is -90 mv and after depolarization it reaches + 35 m
5. After repolarization it comes back to -65 mv

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NERVE IMPULSE PROPOGATION

1. In a resting neuron, the axonal membrane bears an electrical charge .Normally, the external
surface of the membrane is positively charged and the inner surface is negatively charged.
2. The positive charge of external membrane is due to the high concentration of Na+ ions .The
inner axoplasm contains K+ ions and negatively charged organic proteins.
3. The organic proteins are greater than K+ ions , hence inside of the axonal membrane has
negative charge.
4. At this resting stage, neurons posses an electrical potential known as resting potential.

5. The normal resting potential is -70mv.

6. The outside of the axonal membrane contains more Na+ ions and inside has more K+ ions.
The cell membrane is more permeable to K+ ions and nearly permeable to Na+ ions.
7. However , some Na+ ions enter into the axoplasm and these ions are pumped out actively
by a mechanism known as sodium – potassium pump
8. This pump maintains the resting potential by pumping out three Na+ ions and pumping in
two K+ ions at a time .
Depolarization
When a stimulus is applied to a neuron at resting potential , the polarity of the
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 cell membrane changes.
1. The sodium – potassium pump upsets for a moment, and the cell membrane becomes
highly permeable to Na+ ions.

2. The heavy influx of Na+ i o ns into the membrane leads to the reversal of polarity and
outside of the membrane become negatively charged and inside positively charged.
3. This change in polarity is called depolarization.

NERVE CONDUCTION AT MYLINATED NEURON

1. Myelinated axons only allow action potentials to occur at the unmyelinated nodes of Ranvier
that occur between the myelinated internodes.
2.
It is by this restriction that salutatory conduction propagates an action potential along the
axon of a neuron at rates significantly higher than would be possible without the myelination
of the axon (150 m/s compared to 0.5 to 10 m/s).
3. As sodium rushes into the node it creates an electrical force which pushes on the ions already
inside the axon. This rapid conduction of electrical signal reaches the next node and creates
another action potential, thus refreshing the signal.
4. In this manner, salutatory conduction allows electrical nerve signals to be propagated long
distances at high rates without any degradation of the signal.

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5. Although the action potential appears to jump along the axon, this phenomenon is actually
just the rapid, almost instantaneous, conduction of the signal inside the myelinated portion of
the axon.

LIGAND BINDING

1. Ligand is a substance that forms a complex with a biomolecule to serve a biological

purpose.
2. In protein-Ligand binding, the Ligand is usually a molecule which produces a signal by
binding to a site on a target protein.
3. The binding typically results in a change of conformational isomerism (conformation) of
the target protein.
4. Binding occurs by intermolecular forces, such as ionic bonds, hydrogen bonds and Van
der Waals forces. The association of docking is actually reversible through dissociation.
Measurably irreversible covalent bonding between a Ligand and target molecule is
atypical in biological systems.
5. The interaction of most ligands with their binding sites can be characterized in terms of a
binding affinity. In general, high-affinity Ligand binding results from greater

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 intermolecular force between the Ligand and its receptor while low-affinity Ligand
binding involves less intermolecular force between the Ligand and its receptor.
6. In general, high-affinity binding results in a higher degree of occupancy for the Ligand at
its receptor binding site than is the case for low-affinity binding;

1. Ligand-gated ion channels ( LGIC), also commonly referred as ionotropic receptors, are a
group of transmembrane ion-channel proteins which open to allow ions such as Na+, K+,
Ca2+, and/or Cl− to pass through the membrane in response to the binding of a chemical
messenger (i.e. A Ligand), such as a neurotransmitter

2. 5-HT receptors, also known as the serotonin receptors, or 5-hydroxytryptamine receptors,

are Ligand-gated ion channels. They activate an intracellular second messenger cascade
to produce an excitatory/inhibitory response.
3. They are found in mammals, both central nervous systems (CNS) and peripheral nervous
system (PNS), as well as other animals.
4. Its natural Ligand is Serotonin, and it modulates the release of multiple neurotransmitters,
such as dopamine, epinephrine/nor epinephrine, glutamate, and GABA

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CALCIUM CHANNELS

1. A calcium channel is an ion channel which shows selective permeability to calcium ions. It is
sometimes synonymous as voltage-gated calcium channel, [1] although there are also Ligand-
gated calcium channels.
2. Upon activation by membrane depolarization allows calcium to flow into the cell.
3. Calcium channels contribute to membrane depolarization during action potentials and
stimulate the contraction of cardiac and skeletal muscle and the secretion of
neurotransmitters.
4. At the cellular level, calcium channels are a major link between electrical signalling and
intracellular biochemical signalling. Calcium channel function is modulated strongly by a
variety of intracellular enzymes and signalling pathways.
5. Many genes encode calcium channels. Different subtypes often carry out distinct
physiological functions, via distinct cellular locations and biophysical properties.
6. Calcium channels govern physiological functions including neurotransmitter and hormone
release, muscle contraction and the regulation of gene expression.

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7. Calcium channel dysfunction contributes to diseases including cardiac arrhythmia,
hypertension, chronic pain, epilepsy and migraine. They are under investigation for their role
in diseases including autism, schizophrenia and bipolar spectrum disorder.

VOLTAGE GATED CHANNEL

1. Voltage-gated ion channel any ion channel that opens and closes in response to changes in
electrical potential across the cell membrane in which the channel is situated.
2. There are several types of voltage-gated channel, each allowing the selective passage of a
particular ion.

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3. Two types are especially important in transmitting action potentials along axons: voltage-
gated sodium channels and voltage-gated potassium channels. The sodium channels open
rapidly in response to initial depolarization of the axon plasma membrane, allowing sodium
ions (Na+) to flood in.
4. Depolarization also triggers less rapid opening of the potassium channels, which permits
outflow of potassium ions (K+), thus acting to restore the membrane potential to its resting
state.
5. Voltage-dependent calcium channels also carry some of the depolarizing current in some
cells. The sodium channel protein has positively charged voltage-sensing regions, which
move towards negative charges on the outer surface of the membrane when the latter
becomes depolarized.

G PRITEIN LINKED CHANNEL

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 1. G protein-coupled receptors (gpcrs) are a large family of cell surface receptors that share
a common structure and method of signalling.

2. The members of the GPCR family all have seven different protein segments that cross the
membrane, and they transmit signals inside the cell through a type of protein called a G
protein (more details below).

3. Gpcrs are diverse and bind many different types of ligands. One particularly interesting
class of gpcrs is the odorant (scent) receptors. There are about 800800800800 of them in
humans, and each binds its own “scent molecule” – such as a particular chemical in
perfume, or a certain compound released by rotting fish – and causes a signal to be sent to
the brain, making us smell a smell!3^33start superscript, 3, end superscript

4. When its Ligand is not present, a G protein-coupled receptor waits at the plasma
membrane in an inactive state. For at least some types of gpcrs, the inactive receptor is
already docked to its signalling target, a G protein4^44start superscript, 4, end
superscript.

5. G proteins come in different types, but they all bind the nucleotide guanosine
triphosphate (GTP), which they can break down (hydrolyze) to form GDP. A G protein
attached to GTP is active, or “on,” while a G protein that’s bound to GDP is inactive, or
“off.” The G proteins that associate with gpcrs are a type made up of three subunits,
known as heterotrimeric G proteins. When they’re attached to an inactive receptor,
they’re in the “off” form (bound to GDP

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CALMODULIN LINKED CHANNEL

1. Calmodulin (cam) (an abbreviation for calcium-modulated protein) is a multifunctional

intermediate calcium-binding messenger protein expressed in all eukaryotic cells.
2. It is an intracellular target of the secondary messenger Ca2+, and the binding of Ca2+ is
required for the activation of Calmodulin.
3. Once bound to Ca2+, Calmodulin acts as part of a calcium signal transduction pathway by
modifying its interactions with various target proteins such as kinases or phosphatases.
4.
Calmodulin is a small, highly conserved protein that is 148 amino acids long (16.7 kda).
The protein has two approximately symmetrical globular domains each containing a pair
of EF-hand motifs (the N- and C-domain) separated by a flexible linker region for a total
of four Ca2+ binding sites.
5. Each EF-hand motif allows Calmodulin to sense intracellular calcium levels by binding
one Ca2+ ion.

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 6. Calcium ion binding regions are found in the following positions in the sequence of
amino acids: 21-32, 57-68, 94-105 and 130-141; each region that calcium binds to is
exactly 12 amino acids long.

TYROSINE KINASE LINKED CHANNEL

1. Receptor tyrosine kinases (rtks) are the high-affinity cell surface receptors for many
polypeptide growth factors, cytokines, and hormones.

2. Kinases is a type of enzyme that transfers phosphate groups from high-energy donor
molecules, such as ATP (see below) to specific target molecules (substrates); the process
is termed phosphorylation

3. This allows a tyrosine in the cytoplasmic portion of each receptor monomer to be trans-
phosphorylated by its partner receptor, propagating a signal through the plasma
membrane.

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OXYTOCIN

1. Oxytocin is a hormone that acts on organs in the body (including the breast and uterus)
and as a chemical messenger in the brain, controlling key aspects of the reproductive
system, including childbirth and lactation, and aspects of human behaviour

2. Oxytocin is produced in the hypothalamus and is secreted into the bloodstream by the
posterior pituitary gland.
3. Secretion depends on electrical activity of neurons in the hypothalamus – it is released
into the blood when these cells are excited.
4. The two main actions of Oxytocin in the body are contraction of the womb (uterus)
during childbirth and lactation. Oxytocin stimulates the uterine muscles to contract and
also increases production of prostaglandins, which increase the contractions further.

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 5. Manufactured Oxytocin is sometimes given to induce labour if it has not started naturally
or it can be used to strengthen contractions to aid childbirth. In addition, manufactured
Oxytocin is often given to speed up delivery of the placenta and reduce the risk of heavy
bleeding by contracting the uterus.
6. During breastfeeding, Oxytocin promotes the movement of milk into the breast, allowing
it to be excreted by the nipple. Oxytocin is also present in men, playing a role in sperm
movement and production of testosterone by the testes.

VASOPRESSIN

1. Vasopressin (arginine vasopressin, AVP; Antidiuretic hormone, ADH) is a peptide

hormone formed in the hypothalamus, then transported via axons to the posterior
pituitary, which releases it into the blood.
2. AVP has two principle sites of action: the kidney and blood vessels.
3. The primary function of AVP in the body is to regulate extracellular fluid volume by
regulating renal handling of water, although it is also a vasoconstrictor and presser agent
(hence, the name "vasopressin"). AVP acts on renal collecting ducts via V2 receptors to
increase water permeability (camp-dependent mechanism), which leads to decreased
urine formation (hence, the Antidiuretic action of "Antidiuretic hormone"). This increases
blood volume, cardiac output and arterial pressure.

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4. A secondary function of AVP is vasoconstriction. AVP binds to V1 receptors on vascular
smooth muscle to cause vasoconstriction through the IP3 signal transduction pathway and
Rho-kinases pathway, which increases arterial pressure; however, the normal
physiological concentrations of AVP are below its vasoactive range. Studies have shown,
nevertheless, that in severe hypovolemic shock, when AVP release is very high, AVP
does contribute to the compensatory increase in systemic vascular resistance.
5. There are several mechanisms regulating the release of AVP, the most important of
which are the following:
6. Hypovolemia, as occurs during haemorrhage and dehydration, results in a decrease in
atrial pressure. Specialized stretch receptors within the atrial walls and large veins
(cardiopulmonary bar receptors) entering the atria decrease their firing rate when there is
a fall in atrial pressure. Afferent nerve fibers from these receptors synapse within the
nucleus tractus solitarius of the medulla, which sends fibers to the hypothalamus, a region
of the brain that controls AVP release by the pituitary. Atrial receptor firing normally
inhibits the release of AVP by the posterior pituitary. With Hypovolemiaa or decreased
central venous pressure, the decreased firing of atrial stretch receptors leads to an
increase in AVP release.
7. Hypotension, which decreases arterial baroreceptor firing, leads to enhanced sympathetic
activity that increases AVP release.

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ALCOHOLISM

Drinking too much – on a single occasion or over time – can take a serious toll on your health.
Here’s how alcohol can affect your body:

Brain:
Alcohol interferes with the brain’s communication pathways, and can affect the way the brain
looks and works. These disruptions can change mood and behaviour, and make it harder to think
clearly and move with coordination.

Heart:
Drinking a lot over a long time or too much on a single occasion can damage the heart, causing
problems including: Cardiomyopathy – Stretching and drooping of heart muscle; Arrhythmias –
Irregular heart beat; Stroke and High blood pressure

Research also shows that drinking moderate amounts of alcohol may protect healthy adults from
developing coronary heart disease.

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Liver:
Heavy drinking takes a toll on the liver, and can lead to a variety of problems and liver
inflammations including: Steatosis, or fatty liver, Alcoholic hepatitis, Fibrosis Cirrhosis

Pancreas:
Alcohol causes the pancreas to produce toxic substances that can eventually lead to pancreatitis,
a dangerous inflammation and swelling of the blood vessels in the pancreas that prevents proper
digestion.

Cancer:
Drinking too much alcohol can increase your risk of developing certain cancers, including
cancers of the Mouth, Oesophagus, Throat, Liver and Breast

Immune System:
Drinking too much can weaken your immune system, making your body a much easier target for
disease. Chronic drinkers are more liable to contract diseases like pneumonia and tuberculosis
than people who do not drink too much. Drinking a lot on a single occasion slows your body’s
ability to ward off infections – even up to 24 hours after getting drunk.

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SMOKING

1. Cigarette smoking harms nearly every organ of the body, causes many diseases, and
reduces the health of smokers
2. Smoking causes stroke and coronary heart disease, which are among the leading causes
of death in the United States.1,3
3. Even people who smoke fewer than five cigarettes a day can have early signs of
cardiovascular disease.1
4. Smoking damages blood vessels and can make them thicken and grow narrower. This
makes your heart beat faster and your blood pressure go up. Clots can also form.1,2
5. A stroke occurs when:
1. A clot blocks the blood flow to part of your brain;
2. A blood vessel in or around your brain bursts.1,2
6. Blockages caused by smoking can also reduce blood flow to your legs and skin.
7. Lung diseases caused by smoking include COPD, which includes emphysema and
chronic bronchitis.
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COCINE

Cocaine’s effects appear almost immediately after a single dose and disappear within a few
minutes to an hour. Small amounts of cocaine usually make the user feel euphoric, energetic,
talkative, mentally alert, and hypersensitive to sight, sound, and touch.

The drug can also temporarily decrease the need for food and sleep. Some users find that
cocaine helps them perform simple physical and intellectual tasks more quickly, although others
experience the opposite effect.

The duration of cocaine’s euphoric effects depend upon the route of administration. The faster
the drug is absorbed, the more intense the resulting high, but also the shorter its duration.
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Snorting cocaine produces a relatively slow onset of the high, but it may last from 15 to 30
minutes.

Side effects of use include: Tremors, Muscle twitches or tics. Paranoia, Vertigo, Constricted
blood vessels, Dilated pupils, Increased heart rate, Increased blood pressure, Increased body
temperature and decreased sexual function.

Overdose from cocaine can result in: Cardiac arrest, Stroke, Respiratory arrest and Sudden death.

The risk of overdose is compounded when it is used with another dangerous substance like
alcohol or other drugs.

MARJUANA

1. When marijuana is smoked, THC and other chemicals in the plant pass from the lungs
into the bloodstream, which rapidly carries them throughout the body to the brain.

2. Many people experience a pleasant euphoria and sense of relaxation. Other common
effects, which may vary dramatically among different people, include heightened sensory
perception (e.g., brighter colors), laughter, altered perception of time, and increased
appetite.

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3. If marijuana is consumed in foods or beverages, these effects are somewhat delayed—
usually appearing after 30 minutes to 1 hour—because the drug must first pass through
the digestive system. Eating or drinking marijuana delivers significantly less THC into
the bloodstream than smoking an equivalent amount of the plant. Because of the delayed
effects, people may inadvertently consume more THC than they intend to.
4. Some people experience anxiety, fear, distrust, or panic. These effects are more common
when a person takes too much, the marijuana has an unexpectedly high potency, or the
person is inexperienced.

5. People who have taken large doses of marijuana may experience an acute psychosis,
which includes hallucinations, delusions, and a loss of the sense of personal identity.
These unpleasant but temporary reactions are distinct from longer-lasting psychotic
disorders, such as schizophrenia

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DEPRESSION

1. Depression is a mood disorder characterized by low mood, a feeling of sadness, and a

general loss of interest in things
2. Symptoms include lack of joy and reduced interest in things that used to bring a person
happiness.
3. Life events, such as bereavement, produce mood changes that can usually be
distinguished from the features of depression.
4. The causes of depression are not fully understood but are likely to be a complex
combination of genetic, biological, environmental, and psychosocial factors.
5. A number of lines of evidence indicative of decreased adrenergic activity in depression
have been reported. Findings include decreased activity of tyrosine hydroxylase,
decreased size of the locus coeruleus, increased alpha 2 adrenergic receptor density, and
decreased alpha 1 receptor density.Furthermore, nor epinephrine transporter knockout in
mice models increase their tolerance to stress, implicating nor epinephrine in depression.

SCHIZOPHRINIA

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1. Schizophrenia is a mental disorder that usually appears in late adolescence or early
adulthood. Characterized by delusions, hallucinations, and other cognitive difficulties,
schizophrenia can often be a lifelong struggle.
2. A sizable proportion of people with schizophrenia have to rely on others because they are
unable to hold a job or care for themselves.
3. Many may also resist treatment, arguing that there is nothing wrong with them.
4. Some patients may present clear symptoms, but on other occasions, they may seem fine
until they start explaining what they are truly thinking.
5. Delusions - the patient displays false beliefs, which can take many forms, such as
delusions of persecution, or delusions of grandeur. They may feel others are attempting to
control them remotely. Or, they may think they have extraordinary powers and abilities.
6. Hallucinations - hearing voices is much more common than seeing, feeling, tasting, or
smelling things which are not there; however, people with schizophrenia may experience
a wide range of hallucinations.
7. Thought disorder - the person may jump from one subject to another for no logical
reason. The speaker may be hard to follow or erratic.
8. Other symptoms may include:
9. Lack of motivation (avolition) - the patient loses their drive. Everyday actions, such as
washing and cooking, are neglected.
10. Poor expression of emotions - responses to happy or sad occasions may be lacking, or
inappropriate.

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 11. Social withdrawal - when a patient with schizophrenia withdraws socially, it is often
because they believe somebody is going to harm them.
12. Unawareness of illness - as the hallucinations and delusions seem so real for patients,
many of them may not believe they are ill. They may refuse to take medication for fear of
side effects, or for fear that the medication may be poison, for example.
13. Cognitive difficulties - the patient's ability to concentrate, recall things, plan ahead, and
to organize their life are affected. Communication becomes more difficult

PARKINSONISM

1. Parkinson's disease is a progressive nervous system disorder that affects how the person
moves, including how they speak and write.
2. People with Parkinson's disease also experience stiffness and find they cannot carry out
movements as rapidly as before - this is called bradykinesia. The muscles of a person
with Parkinson's become weaker and the individual may assume an unusual posture.
3. Parkinson's disease can cause varying and progressive symptoms throughout its course.
Some of the most common symptoms associated with the disease include:
4. Difficulty showing facial expressions
5. Muscle stiffness
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 6. Slowed, affected movements
7. Speech changes
8. Tremor, especially of one hand
9. A person with Parkinsonism may have some, but not all, of the symptoms listed above.
This is because they also have an additional disorder that affects the brain's functioning.
10. For example, people with Parkinsonism often do not have the hand tremor that affects
many people with Parkinson's disease.
11. Other symptoms associated with Parkinsonism include , dementia ,issues with the
autonomic nervous system, such as problems with controlled movements or spasms, early
problems with balance. Rapid onset and progression of symptoms

ALZHIMERS DISEASE

1. Alzheimer’s disease is an irreversible, progressive brain disorder that slowly destroys

memory and thinking skills, and eventually the ability to carry out the simplest tasks. In
most people with Alzheimer’s, symptoms first appear in their mid-60s.

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2. Taking poor judgments and decisions a lot of
the time
3. Problems taking care of monthly bills
4. Losing track of the date or time of year
5. Trouble having a conversation
6. Misplacing things often and being unable to
find them

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