Chapter 2 _How does the nervous System Function?

The size of the human brain is the biggest
among all vertebrates, in comparison to body
weight. Our brains can conduct very complex
tasks. The brain is plastic because neural
tissues change to adapt to changing
environment. Simple “learning” is based
changes of connections between neurons.
Epigenetic factors affect the rate of expression
of genes but don’t change genes.
CNS- Brain and Spinal cord. Can function
independently but connected in order to
establish e.g our planning and voluntary
actions.
PNS- Composed of neurons outside brain and
spinal cord. ANS and SNS are part of it.
There are different functions carried out by
each system.
Afferent information is sensory information
that enters CNS. Efferent is the reversed.
Dimensions For study: Dorsal, anterior,sagtial
et.c
Protection of Brain
Three layers of protection:
 Skull
 Meninges:
o Dura mater- Outer dense
tissue of fiber.
o Arachoid membrane: Thin
delicate tissue, like spiderw.
-Space between has
Cerebrospinal fluid between
A and P , a cushion of salt
solutions.
o Pia mater delicate layer
closest to neocortex.
Cerebral cortex
Nerve tissue that is folded. Divided into lobes.
Gray matter: Areas with mainly cell bodies,
gather info of facilitates transport of it.
White matter: Area with mainly axons, lots of
fat.
 Ventricles: 4 Cavities in brain have
cerebrospinal fluid. Cushioning and
maintain brain metabolism.
o (bi)Lateral ventricles. Third
and fourth ventricles-> Drains
in to cerebral aqueduct ,
entire spinal cord.
Corpus callosum: Dense composition of axons
(white matter) making way for hemisphere
intercommunication.
Cells and fibers:
Two types of cells in brain: Neurons: info.
transmitor. Glia cell : Nourish and
protect(myelin),support neurons
Connection between cells by: Axons. A
gathering of them = tract, CNS.
Clusters of similar cells: Nuclei
Stages in Brain evolution and development
First stage consisted of
Prosencephalon(forebrain) -> Tele-&Dienc.
Mesencephalon(midbrain) and
Rhombencephalon(hindbrain).
Connected to Spinal cord. New tissues
developed as the vertebrate organism
develops and is exposed to new
environments. Result is then several nervous
system that make complex behaviours.
Natural selection did the rest. Non vertebrate
complex NS can still learn in similar
ways.#Octopus.
Fully developed human brain with Central
nervous system
CNS has three major components. Each
“higher” level replicates the work of lower
ones and enable complexity and refinement
of behaviour.
1) Spinal cord: Made of tracts, and different
segments receive and send information to
different parts of body.
2)Brain stem: From spinal cord entry in skull
until lower ----. Receiver of afferent nerves
and sender of efferent nerves. Master
controller. Hind- and midbrain developed first
in brain. Sensory structures dorsally and
motor ventrally
 Romb. Hindbrain:
o Cerebellum: Controls complex
movement coordination &
balance. Has a cortex and
gray, white matters.
o Reticular formation:
Stimulates forebrain. Eg.
Waking from sleep
o Pons: A bridge that channels
info from cerebellum to
forebrain. Vital movements
o Medula: Breathing rhythm
 Mes. Mid brain:
o Tectum: Sensory component.
Dorsal location. Info from
optic nerves and auditory
paths to its superior
respective inferior colliculus.
Orienting movement, eg see
source of noise.
o Tegmentum: Motor structure
with many “nuclei” Ex red
nucleus, Substantia niagra
m.m- initiator of movements.
Parkinsons.
 Diencephalon (between brain):
Gathers sensory and motor info going
to cortex
o Thalamus: Large. All sensory
info different systems gather
here and then forwarded to
cortex. “Relay place”
o Hypothalamus: Links NS with
Pituitary gland/hypofys to
control Hormon production
that manages sex, sleep,
movement, basically
everything.
3) Forebrain:
 Neocortex: The folded thin tissue we
see from outside. Last developed.
Divided in Lobes. What happens if
damaged.
o Frontal lobe: Planning,
problem solving ,execution…
o Temporal : Auditory and
language, music
o Parietal: Directs movement
toward a task. Pick a coin.
Sensory too: touch,temp.taste
o Occipital: Vision process
centre.
Motor cortex in Frontal lob. och
Somatosensory cortex in parietal lob: --
Gyri (vindling) , sulci(fåror,spricka), major
ones separating lobes, increase brain area.
Berg och dal.
Fissures(djupare fåror cracks) on cortex
separate lobes and hemispheres.
Lack of blood or bleeding = stroke
 Basala Ganglia: Together with
thalamus and other systems, primarily
involved in control of voluntary
movements. Parkinsons.
Tourettes(Tics).
o caudate nucleus. C shape
o the putamen,
o The globus pallidus,
o (Nucleus accumbens :
Reward, addic. Motivat.
Control.)
o Subthalamic nucleus: Slow
down signals from B.G. even
decisions->correct ones.
o Substantia niagra is related
to it.
 Limbic system: A system with many
functions: memory, motivation and
 emotions… Hippocampus(info via
fornix=, Amygdala and
Some principals to keep in mind about NS
Cingulate/Limbic cortex. Behind
rewarding properties of drugs and 1) Brain creates world and moves in that
addiction. world.
 Olfactory System: Part of forebrain. 2) Neuroplasticity: +Learning and
Small compared to other animals. survival. -Addictions.
Inputs takes a detour to a pyrifom 3) For every higher level in the NS comes
cortex before going to thalamus. refined and complex elaboration of
tasks.
Peripheral nervous System
4) Hierarchy in NS
Somatic Nervous System(SNS) 5) Sensory and Motor divisions.
6) Sensory input is divided for object
Controlled by Brain and Spinal cord segments. recognition and motor control. T.ex
LEARN MORE ABOUT SNS occipital lobe.
 Cranial Nerves : Nerves between 7) Excite and inhibit
brain and many parts of face , neck 8) Functions local and distributed.
and internal organs. Sensory and Compensable to a certain extent
motor functions. Eg. Feel face and during injuries.
move face. Ipsilateral. . Receive in
and command parts that they
control*
 Spinal Nerves : Classified in 5
independent segments : Cervical,
thoracic,lumbar,sacral and coccygeal.
Bilateral. Ipsilateral... Each spinal cord
segment controls body
segment(dermatome) adjacent to it,
when viewed from a crawling
position. *

Connections of SNS

Collection of fibres known as axons = roots.

Dorsal roots in connected to spinal cord
receive info(sensory) and ventral (motor)
sends out info. Law of BELL AND Magendie for
the nervous system.

Autonomic Nervous System (ANS)

Keeps us alive without our conscious effort.
Uses SNS. Two divisions :

Parasympathetic: Relax, rest and digest, uses

mostly cranial nerves.

Sympathetic: Arousal, fight or flight, uses

mainly spinal nerves
Chapter 3- Cells and Genes
Neurons are the basic units of work in the
brain. Acquire info from sensory receptors
and transfer info from brain to create
movement. Groupwork. Neuroplasticity. CNS
neurons exception.
Parts of a neuron
Dendrites, Cell body Axon, Axon hillock,
myelin (speed,-short circuiting)
Three types of Neurons:
1. Sensory neurons: Collects info from
sensory receptors in eg skin. Sends to
CNS. A cell body, long dendrites.
2. Interneurons: Collects information
from many places and link up sensory
and motor neurons. Pyramidal cell.
3. Motor neurons: With many dendrites
for info gathering and long axons to
command muscles.
Neurons receive many signals and acts
depending on if sum of yes (excitatory) signals
are greater than no(inhibitory) signals.
Five types of Glia cells
1. Ependymal cells: Produces
celebrospinal fluid in venticles , Spinal
cord…
2. Astrocyte: Supports neurons and their
axons. Taps nutrition even oxygen
from blood give to neurons. Stops
things..
3. Microglial cell: Defends against
infections and helps repair damages
4. Oligodendroglia cell: Wrap their flat
branches =the myelin on axons in CNS
5. Schwann cell: Same here but on
axons in PNS
Internal structure of a cell
Cell membrane: a barrier, even around
dendrites, impermeable. Fosfolipider,
Channels, pumps.
Intra/extracellular fluid: Different
concentrations between them. Extracellular
fluid =CFS in CNS.
Organelles; Nuclear membrane
Endoplasmic reticulum(ER): Protein factory
Golgi bodies: Protein post office
Tubules, microtubules : Cell structure
maintenance and Protein road, flimmer hår
Mitochondria ; Lysosomes.
Protein synthesis
 Transcription: RNA
polymerase(enzyme) opens gene in
DNA strand in Chromosome with
needed info. Lose nucleotides attach
to the open DNA strand. Nucleotides
(k-base + socker) join together to
form mRNA. The sequences of bases
state the order of genetic code.
Nucleotide bases: Pair of bases in DNA.
Always A-T, C-G.
 Translation: mRNA goes to Ribosome
in Er. Ribosome catalyst the following.
It reads 3 bases(a codon) at a time.
Then a tRNA with corresponding
codon comes carrying a specific
amino acid. Then attaches to codon
on mRNA. Same process for next
tRNA. Amino acids attach to each
other by a peptide bond. A chain of
amino acids= polypeptide. Packed:-
sheet, helix, 3D structure.
All 20 Aminoacids have same similar
structure with amino group and carboxyl
group. Making peptide bonds possible.
 Golgi bodies: Proteins are packed,
and destination is marked. The
“mark” , attachment can also change
structure of protein. Proteins loaded
on motor molecules= microtubules.
Put in vesicles if kick outside.
These protein affects process in other cells,
tissues and organs. Affecting behaviour.
Membrane: Channels-size and specific ions let
through. Pumps-shape shifts to carry ion
through M. and Gates (open and close)
Genes, Cells and Behaviour
Genotype. Phenotype.
Chromosomes: Sex chromosomes and
autosomes (behaviour and appearance). 23
pairs , except in sperm and ovary. Each pair
carry “similar” genetic codes
Alleles: A variant form of a gene in
chromosomes. Homozygous: If both
4- Communication between Neurons
Tools for measuring neurons activity: EEG,
microelectrodes to the axon,
oscilloscope(screen)
Movement of ions creates electrical charges.
Diffusion: A concentration of ions spread out
to places with lower concentration. To same
amount everywhere. Requires no energy. As
they diffuse, a concentration gradient is
formed due to different concentrations
among areas of solution/container.
Voltage gradient: Negative ions are drawn to
positive ions. Same charges repel. Diffusion
spreads cations and anions in a solution.
Creating a difference in charges between
areas of solution. Yet ions want to move from
area of higher charge to area of lower charge-
> V. gradient.
Barrier in solution: A hole in it. Diffusion. Then
ions will move to places with lower charge so
create an equilibrium. If hindered, a potential
is created.
Electrical activity of a membrane.
Cations : Na, K ; Anions : Protein Cl.
chromosomes carry same alleles for same
trait. Heterozygous: Both Ch. Different alleles
for same trait.
Dominant Alleles: Expressed independently. If
gene of sickness here, it happens.
Recessive Alleles: Needs to be homozygous,
to be expressed. Gene for sickness needed
from mamma and papa.
Mutation: A change in genetic code eg, a
single nucleotide base is removed or added.
Deadly consequences of beneficial-> on the
long wrong natural selection.
Extra copy of chromosome->Downs
syndrome. Affecting genotype and phenotype.
Membrane is a barrier regulating equilibrium
both in voltage and concentration of ions.
Ions don’t diffuse nor balance out charges
freely. Difference in charges between intra-
and extracellular fluid takes place, (electrical)
Membrane potential. Meaning: The energy to
flow is stored waiting to flow, which would
create electrical activity.
Resting potential: The relative difference in
charge /electrical charge between cell
membrane while resting. -70mV.
Maintenance: K+ (Cl-)freely diffuse throw
channels; Na+ channels closed; Na+/K+ Pump
out “3Na” (and in “2K”) that eventually
diffuse through membrane or in action
potential.
Inside: Anions (proteins) can’t leave cell. Yet
K+ not allowed to balance /neutralise inner
charge by their quantity. Secondly, there are
more K+ inside and open channel leading to
diffusion to outside. Inside is negatively
charged, diffusion makes charge on
membrane positive.
Outside: Few K+ that stay outside maintain
negative charge inside. Na+ gates are closed
so they can’t diffuse in neutralise/(depolarise)
the charge inside. If Na+ eventually leaks, it is
pumped out. Many and more Na+ outside
cell making it relatively positively charged.
Cl-: Diffuse through channels. At resting
potential, they are at equilibrium,
voltage=concentration gradient. Little
contribution to resting potential.
Graded potentials: Conditions that change
voltage across membrane. Stimulations or
neurotransmitters can create these
conditions. It can lead to:
Depolarization: Voltage levels moves closer to
threshold. Less electrical charge.
Hyperpolarization. -80-90Voltage levels
moving lower than from resting p. More
electrical charge.
Threshold potential: -55 The voltage level if
reached triggers action potential
Action Potential: -55<+30Huge reverse of
charge that progagates through axon->Signal.
Summation of excitatory signals or simply
stimulation of receptors that so intense that a
receptor lets in great amount of Na+.
(Absolutely refractory= no response to new
stimulus) Na+ gate is opened leading to
depolarisation in that area of membrane. It
passes threshold and action potential takes
place. Moreover, adjacent Na+ Voltage
sensitive channels (-50mV) open to
propagating it along the axon. Na+ gates open
faster and close fast, at +30mV
(Ab. Fractory) K+ voltage sensitive channels
open slower. Yet flushing out many K+ to
outside. To reverse depolarization- to
repolarise- caused by Na+ influx.
K+ continuous efflux leads to
hyperpolarization.
Relatively refractory period would require
very intense simulation greater than former
to create another action potential.
Pumps help restore resting potential and put
ions on “right side”
When action potential spreads through axon
it is called a nerve impulse. Unidirectional due
to repolarisation by K+ gates that follow each
action potential.
Saltatory Conduction: Action potential jumps
between nodes of Ranvier, because of myelin
sheaths. Action potential doesn’t happen
inside myelin areas and nodes have many
voltage sensitive gates, that can trigger
opening of gates on next node.
Excitatory and inhibitory postsynaptic
potentials.
EPSP produce local depolarisation. IPSP->
(receptors of K+/Cl- open)
repolarization/hyper... They cancel out each
other if at they occur at same time and place;
temporal and spatial. Vice versa
Summation: Potentials of same kind can add
to increase depolarisation or to hyperpolarise
more. Generally, no A.P in n-cell body, lack of
voltage sensitive channels. EPSP must reach
axon hillock that has v.s.channels.
Depolarization here that reaches threshold =
action potential.
Sensory stimuli lead to action potentials
Hair moves, light in eye, air movement ear…
stimulate corresponding channels on
dendrites-> summate in axon hillock. Eg.
Stretch-sensitive channels. They open up and
let in Na+ , depolarise , threshold->action
potential. Nerve impulse sent to brain. You
feel, see and hear.
On muscles: Transmitter sensitive channels
have receptors opened by chemical
transmitters. Na+ influx. Summation or very
intense to create action potential. Voltage
sensitive channels of muscle membrane open
and action potential propagates among them-
Chapter 5
Neurotransmitters consist of chemicals such
as acetylcholine (excite or inhibit) ,
norepinephrine. When they circulate in blood
streams, they are called hormones, affecting
autonomic system. Slower.
Influence voltage on next postsynaptic
membrane, also message back to presynaptic
membrane-receptors to enable endocytos.
Structure of synapse:
Microtubule. Axon terminal, presynaptic
membrane, storage granule, synaptic cleft,
mitochondrion. Postsynaptic membrane,
Postsynaptic receptor.
Neurotransmission:
1) Transmitters are synthesised in DNA
or in axon terminals with chemicals
from blood(food). Microtubule
transport the first to presynaptic
terminal wrapped in versicles made
by golgi bodies. Other versicles are in
storage granules
2) Action potential reaches axon.
Calcium voltage sensitive channels
open and Ca2+ influx. They bind to a
protein that release versicles on
presynaptic membrane->exocytosis.
ATP is used as energy supply for Na/K pumps depolarise from “hyperpolarisation” back to resting
potential. How much focus on this? What info about it is included in 5 th edition book? Which chapter
then? If not use youtube 😉
Autonomous System and the Endocrine System
Parasympathetic- Connected to cranial and
sacral spinal nerves. Long axons that send info
to ganglia close to organs. Ach through first
neuron and Ach also released by ganglia.
>muscle contracts.
Also release versicles on
microtubules.
3) Diffusion across synaptic cleft and
land on specific receptors. They either
cause depolisation or hyperpolisation.
One versicle’s release of contents
produce the smallest postsynaptic
potential. Amount of ca2+ and
number of versicle important.
4) Neurotransmitters detach from
receptors and Diffuse away,
consumed by enzymes or reuptake by
presynaptic membrane. Endocytosis.
*ATP: Energy molecule created in
mitochondria used on pumps, versicle
transport and exocytosis… P breaks
and energy produced. ADP goes back
gets new P
Many types of synapse yet same message.
Excitatory or inhibitory. Summation or
“cancelation” affects action potential.
Inhibitory synapses tend to be on cell body to
say “excitatory potential you shall not pass”
Dendritic spines: Increases in size to match
changes of size of axon terminal. More
transport versicles=more space in cleft. Bigger
area of axon = more area for more versicle in
exocytos.
Effect: Rest and Digest. Relaxing organs,
reducing heartbeat, glucose production,
reduce stress.
Sympathetic : Nerves from Thoractic-lumbar
spinal region. Info sent to ganglia. Ganglia : A
group of neuron bodies forming a parallel
chain to the spinal cord; a relay station for
impulses from spine. An impulse from Spine
can affect many organs simultaneously due to
ganglia. Ach(acetlykolin) enters ganglia but
Norepinephrine released in final synaptic
cleft.
NE and Ach synapses excite or inhibit organs
depending on organ receptors. Most are
excited by NE but a few are
inhibited ,stopping digestion. Same for ACH
that can excite stomach but inhibit heart.
Homoestas: Kroppen strävan att behålla
förhållanden och miljön inuti stabila. Three
components of a homestatic system :
Receptor, control organ(brain,pituitary g) and
effector(hormons).
Hormones and hierarchy
Chemical substance sent through the blood to
signal organs in the body. Could be same as
neurotransmitters. Hormone’s speed is
slower.
Hypothalamus controls pituitary gland which
in turn releases hormones. Sensory or
cognitive activity->
1) Hormones from Hypothalamus
produced.
2) Enter through blood Anterior P. lob
uses blood vessels while
3) Entering posterior P. lob “by”
axons ,uses nervous systems
neurotransmitters.
4) Endocrine glands (bukspott,
binjuren,testiklar…) are signalled and
they also produce hormones targeting
organs, even brain.
Classes of Hormones
Steroid hormones : Synthesized from
cholesterol in glands (gonads, adrenal,
thyroid) that can diffuse through
lipids(membranes). Enters nucleus and affects
specific genes->More or less proteins
produced.
Peptide hormones: Consists of aminoacids,
therefore a result of transcription. Ex: insulin,
endorphins. They bind to receptors on cell
membrane-> chain of reactions that affect
stress, use of energy, growth…. Signalkaskad.
Functions of Hormones
Homeostatic hormones : A stable and
constant state in the body’s systems, “pro-
survival” homoestas. They control
concentrations ions in/out cells. Balancing
level of nutrients and water anywhere these
are used in body. Överallt. Insulin from
Bukspottskörtel counteracting glucose from
Njuren. High levels of sugar damage
organs :nerves, heart, brain…
Gonadal (sex) hormones: Control
reproductive aspects. Testosterone (enter
brain cells) or Oestrogen-> tell body to
become man or woman Sperm production,
fertlization, mens, birth, milk… Y-
chromosome has SRY gene, determines if
testis or ovary will be developed in embryo.
Sertoli (build AMH peptide hormons -> stop
female organs development )and Leydig cells-
create testerosterone->more male organs.
-Anabolic-androgenic steroids: Less
testosterone produced but more muscle.
Fertility reduces.
Problems with receptors of testerone in body-
> yes testicles but female organs developed in
other parts of body. No mens.
Glucocorticoids (ex: cortisol- steroid) :
Produced in times of stress. Affect sugar levels
and it’s absorption.
Stress : A stimulus/event/stressor that
requires rapid adaptation of the body, affects
homoestasis, triggers arousal. Body response
is same not depending on situation. +/- Stress
response:
  Fast stress system: neurotransmitters *Ephinerine effects subside, then CRH from
from hypothalamus through Hypothalamus, activates ACTH in P.gland
p.pituitary lob, (Ach->NE neurons) which tells A.gland to pump cortisol in body.
gets to medulla(middle) of adrenal High alert maintained until threat gone. OR
gland, peptide hormones. ELSE:
Epinephrine/adrenalin released in
Prolonged Stress and effects: Hippocampus
blood arousing /activating cells,
glucocorticoid receptors detect high level of
organs brain.
cortisol in blood and tells hypothalamus to
 Slow Stress system: Hypo-> CRH
reduce it. If not , they damage hippocampu s
Signal to Anterior pituitary gland,
neurons if levels high for long time. In turn
ACTH hormone to blood-> affects
less H.neurons to regulate cortisol levels by
cortex of A.gland->glucocorticoids
telling hyppthalums. Vicious circle. Memory
=cortisol->Out in blood->Eg high sugar
affected: PTSD remembering the stressor and
level. Improves conditions for Fast S=
body mobilises as if it is real. Injuries to
icke livs nödvändiga funktioner
Hippocampus can cause same vicious circle.
stängs.
-Sperm production decrease, immune system
Short stress: Resources mobilised to face fight
suppressed, growth stopped, digestion and
or flee and parasympathetic system used to
uptake too.
turn of arousals. When stressor is taken care
off.

Regelbunda område av förtätningar i luften.

Outer hair cells : Receives info from brain ,efferent axons. Change form, thickness, changing
resonance In liquid, we can hear weak noises.

Inner hair cells : Send to brain, afferent axons. Actions potential, connect axons on x ganglia

The Auditory system

Anatomy and functions of parts of ear. How
info goes from cochlea nucleus to auditory
cortex. What happens in auditory cortex.
That’s it!
Tiplink connected to ion channels on cillias
Deporalisation when Basilar membrane
swings upward, cilias move to one direction ,
A specific frequency will create (maximum)
movement enough movement of BM at a
specific area of BM. The movement will the be
enough to also move the cilia on hair cells in
that specific area of basilar Membrane. Then
hair cells will register that frequency and tell
brain.
Tonotopic representation: Parts of Primary
cortex correspond to apex and base of
cochlea.
Periodicitets teori : When 20-200hz, Area
exactly ON THE apex swings. ALL the cells in
the area of 20-200hz respond to any frek
between 20-200hz, not just specific groups
for specific frequencies as in other areas.
Compensation for it: Hjärnan känner av
frekvensen av aktionspotentialen här när det
i normala fallet räcker att med känna av
vilket område som svänger för att identifiera
ljud och dess frekvens.
Område på Basilar M nära apex svänger
samtidigt för tonhöjder mella 20-200hz. Ger
aktionspotential som avgör hur vi uppfattar
tonhöjden. Meaning that not just one area of
BM moves but a bigger area allowing us to
perceive frequencies 20-200hz.
Sound localization:
Superior Olivary complex: Info from ventral
nucleus.: Medial SOC: Measures differences
in Time that waves/Sound arrive to each ear
Lateral part : Measures Differences in sound
amplitude(volume/ljudstyrka) arriving to
each ear. Co-worker Trapetzoid bodies. *SOC
simple measures and forwards data, not
making decisions.
Hög frek: svagare dör dem, mer fokus på
styrka skillnad. Låg frekvens: Amp är viktigt
håller sig längre i distans.
Lateral Lemniscus i brainstem: Tract of axons
used by auditory system
Inferior Colliculus: Process changes in pitch
and mediate movement of neck in response
to loud noises
Primary Audio-cortex: Ljudstyrka och
Tonhöjd
Medial geniculate nucleus – relay place
APASIA- språknedsättning
Volume: Bigger area of basliar membrane
swings due to high amplitude. Not only more
frekvent AP from the particular hair cells but
even more AP to brain due to adjacent hair
cells that react. The close adjacent reacting to
frekvens not precisely their own.
The secondary auditory pathway is essential
for sound ID & localization. Identification and
language comprehension = analysis of
complex sounds
Outer hair cells- info from brain, change
form och hårdhet. Ändrar resonans i
vätskan. Vi uppfattar väldigt svaga ljud.
.
9- Visual system
Perception is the subjective interpretation
we give to what we sense: A car, music. Not
objective as sensation, an object, a
soundwave, or noise. Receptor density: The
more receptors the more sensitive a sensory
system is. Different sensations, due to
different cortex for processing. Tonopographic
map.
Electromagnetic radiation is light. We see
“Blue” 400-700nm “Red”.
Frequency =” colour” high frek=
shorter wave length and amplitude
“intensity of light/”colour”.
Receptive field: The area that a (ganglion)
neurons can receive information. Parvo cells
have smaller receptive field. are
hierarchic :100 photoreceptors->25 RGN->6
LGN-> 1 Primary cortex cell.
Parts of the eye:
Sclera(ögonvita): White area.
Cornea(hornhinna): transparent outer layer.
Iris: Light regulating muscle. Pupil. Lens: Light
bender, upside down image. Glaskropp:
Transparent lösning mellan retina och lins.
Retina: Light falls on it. Macula (Gula
fläcken): The area with most cones, aligned
with lens. Fovea(Centralgrop) : pit with ,no
rodes . Nasal retina & temporal retina. Optic
disc(blinda fläcken) with Optic nerves: Eye
visual field overlap->B.spot not seen using
both eyes
The layers of the retina
Retina ganglion cells: Transparent, receive
synaptic info. Also called P and M cells in
retina, receive info from cones and others
from rodes.
Support cells: Converging info from
photoreceptors
Photoreceptors
 Rodes(stavar): Registers difference in
light intensity, low light
sensitive ,night vision without details
and “colours”, Larger and scattered in
periphery area of retina frequency.
(Prefers a certain wavelength). M.
cells.
 Cones(tappar): Registers difference in
wave lengths(colour) and details.
Smaller, packed in central area,
mostly in macula. 3 “types” of cones
for S(blue), M(green) and L(red)
wavelengths. More reds than blues.
Connect to P cells going to P. layers in
thalamus
Light absorbing visual pigments: On the outer
layer face towards brain of rods and cones.
Different pigments absorb different light
frequencies/wavelengths->three types of
cones and one type of rode.
Visual pathway:
Cornea->lens->
->Nasal and Temporal retina: Info from
photoreceptors on nasal retina cross to
opposite hemisphere at optical chiasm.
Temporals are ipsilateral. Info from visual field
to both hemi.
->Photoreceptors: Light through Retina
ganglion cells. Reaches light absorbing
pigments on cone and rode that absorb light
and release chemical substances through
synaptic end. Dendrites of RGC receive info,
summation of excitatory/inhibitory may lead
to more action potential or not. Brighter light,
bigger amplitude, stronger colour-> frequent
action potentials. Enters neuron and out
through axons.
->Optic nerve to Optical chiasm: ipsilateral
and contralateral afferent nerves from T/N
retina
->Lateral geniculate nucleus in Thalamus with
six layers: Parvocellular (4) and
Magnocellular. Then relay to other nerve
cells. OBS: Info from each eye is segregated all
the way to cortex
->Primary visual/striate cortex V1 in occipital
lob and transmit info to Dorsal and Ventral
streams. V1 Receives info from LGN.
Secondary visual cortex the other areas of
cortex
Colour, form, and motion are put together in
these streams to create a unified vision of the
world. Ventral stream, “what” ->Temporal
lob: Functions that identify object; Dorsal
stream ”how”&(where) ->Parietal lob: guiding
action with vision.
Left hemisphere receives input from right
side of the visual field. R-hemi-left V.field.
We not necessary talking about entire eyes
but about visual field, based of nasal/temp.
retina.
(Tectopulvinar pathway, info to superior
colliculus from LGN -> orientating
movements)
Evolution of eyes: Photoreceptors on flat area
to depressing into a pit. Limiting sensitivity,
then pinhole to increase focus, membranes
for protection and soon lens and iris.
Visual field: The world I see with eyes focuses
on single point, steady head. 4 quadrants. Info
from each quadrant goes to opposite brain
hemisphere. Light from different directions hit
opposite locations on retina. Up ->down on
retina->inverted image. Topographic
organization of Primary visual cortex: Left V.F
is projected on right primary visual cortex.
Colour vision:
Evolved from competition for fruits.
Different wavelengths simulate cone
receptors in different ways. Receptors, in
general in 1/3 of cones are more sensitive to
the same wavelengths. This particular waves
length is interpreted by brain to be blue(400),
green(500) or red(600).
Trichromatic theory =we see colour because
of the relative difference in response among
these 3 types of cones. Per say: S cones
responds more to 400 nm so we “see” blue,
M cones to 500 we see green , red Equal
response->white colour.
More light in mixture creates colour,
white ,less light creates black , dark.
Colour- deficient vision: Missing one or more
cones can distinguish some colours but not all.
Only rodes= one colour type literally black and
white.
Opponent process: Opposing pairs of colours
are important, red-green and blue-yellow.
Inbihit vs excit ganglion cell->colour
perception 4 colours.
(Outer part of the receptive field of a retina
ganglia cell is more sensitive to green while
the centre responds best to red. Same for
blue in middle and yellow in outer region.)
Only wave length for “green” light-> reaches
“green absorbing cone”->then to green/red
ganglion cell, which is excited by red light and
inhibited by green light-> ganglion cell sends
an inhibitory postsynaptic potential
interpreted as green by brain.
(wave length 600”red” leads to excitation->
red) Put yellow/blue above. Blue light
absorbed by blue cone and inhibits ganglion
leading to “blue” signal. Yellow light enters
green and red cones, excit and inbhit
red/green ganglion= cancelation. Response
from red and green cones to excite
yellow/blue ganglion cell-> yellow signal.
Applicable to blue light too. OBS: Colours are
only in our brain. Light don’t have colours.
Vision defects
Hemispatial neglect: Most frequent after
stroke. Information on/from one side of visual
field and space is ignored by brain. Seeing or
acting on that side is an inexistent mental
process. On sided attention. Contralateral: left
eye due to damage of right hemi.
Agnosia (Visual): Damaged ventral stream
“What” region = lack of recognition. But can
still grab object and use it.
Then using feeling and memory to recognise.
If no Tactical agnosia. Some could still process
face because the separate fusiform area, if
not damaged.
Prosopagnosia: Fusiform face area, No face
recognition, can still see faces but don’t
remember them.
9-Olfactory and Gustatory Senses and “Kemiska hudsinnet”
Olfactory system
Identification difficulties in
 -Finding the precis name for what we
smell. “Tip of the nose” Tasty-
>Eatable->Fruity->”Apple”.
 Hints help
 Discovering difference in intensity
levels.
Origin of good/bad smell classification
1. -/+Experiences from childhood and
rest of life. Survival!!
2. Environment congruent memory :
Abusive, stressful place->bad smell
3. Familiarity: Well-known smells ->
experienced as good smell.
4. Information from others: affect how
we perceive a smell of something.
5. Taste and colour too.
Smell and memory: Smells registered from
childhood(senses central) are well stored in
brain. Memory connected to smell is
Myopia: Mer avlångad ögonkropp. Light
focuses infront retina instead on the retina.
Hypermyopia- Kortare avstånd, plattare lens
refract errors.
Anopia: Blindness of eye due to damage of
optic nerve, LGN or V1. Hemi -, quadrant-
part of visual damaged. scotoma(blind spot)
but compensated by brain.
Visuell avsökning: Brain creates hypothesis in
order to see and find what we seek. Uses
semantic memory and Expectations. Eyes
finds the horse before you consciously realise
it. Guided search tasks. An attribute of the
item stands out , uteslutar platser att söka.
Experts use same basic ability but more
effectively. Not a new ability though.
unconsciously and suddenly Triggered if
exposed to smell in future. Even for words
and pictures. Not so useful for studying for
exams though…
Functions of Olfactory System:
 Preserve life by identifying hazards :
Food safety, stranger(amygdala
activates) or family
 Communication?
o Pheromones, biochemical
odorant from one animal
affect the other. Humans lack
this abililty
o Role in social behaviour-
förmedla känslor
 Bonding with Mother as a baby.
Enjoy food: with taste too.
Habituation(habituering): Get used to smells,
nerves stop firing if same smell constant. But
recovers. Also detects new smell fast
Smell sensitivity changes: Age->Younger
more sensitive, genetic?, environment=
medicine, habituation. Attention
From receptors to Olfactory Cortex:
#Ipisilateral!!!
To smell it, it must be airborne, or retronasal
from mouth particles = chemicals of it must
reach your:
Olfactory Epithelium= Surface in nose with
receptor cells/Olfa-rec-neuron. (and support
cells). Cilia (end of receptor cells) sticker ut in
olfactory mucosa. Chemicals dissolved in
mucosa reach receptors on cilia. A certain
group of chemicals stimulates a specific group
of receptors. If they react, Na+ channels open,
depolarisation->(AP).
->Presynaptic membrane of receptor cells +
post synaptic membrane of mitral cells. Meet
at glomeruli(axons of recep-cells of same
odorant ->same glomeruli, förfina)
->Mitral cells forward info to Primary
olfactory cortex = Pyriform + entorhinal
cortex + amydala ID smell. Without going
through thalamus.
Other Axons ->thalamus -> relays signals to
Secondary Olf-cortex: Orbitofrontal cortex.
Position : In Prefrontal cortex behind
eye =Social behaviours such as eating.
Gene encode these 400+ receptor cell-The
summation of activity of receptors lead to us
perceiving a type of odour. All receptors
combined and we can discriminate trillion
smells. Many chemicals>”one” smell
Liknande ämne inte likande lukter. Lukt är en
blandning av olika kemikalier.
400 receptors BUT 1 trillion odours.
Kombination av olika intryck från olika
receptorer leder till 1 trillion lukter. INTE en
receptor- 1 lukt.
Gustatory System
Differences in taste sensitivity: Age,
environment, gender, Gene:
Genotype: An allele in gene ->codes taste
receptors sensitive to very small bitter tastes..
Proved by PROP experiment. Supertasters
and nontasters. Advantage is that bitter
mostly=poisonous. Non tasters, recessive, may
eat more veggie and fruits.
Phenotype: No. of Papillae (bumps on
tongue) correlate with amount of taste buds.
More= better detect bitterness.
Types of Papillae : From Tip of tongue
Svampform-> bladformad-
vallgravpapilae (close to svalg)
Receptors for taste
Taste buds (smaklökar) are on Papillae. They
contain taste receptors cells.
5 types of taste receptor cells each
corresponding to one these:
o Salt, Sugar, sweet,
o Sour and Umami (reacts to
glutamate=a neurotransmitter and
protein)
From tongue to afferent nerves
Tip of taste receptors = Microvilli. Food
component touches “appropriate” microvilli
and they open->
->Ion influx->Depolarisation->exocytos ->
Afferent nerves receive a signal. Ipsilateral
They are cranial nerves:
Ansiktsnerven : info from Posterior of
tongue; Tungnerven: Medial ;
Vagusnerven: Anterior.
From afferent nerves to Gustatory cortex,
insula
Those cranial nerves gather as a nerve ->
medulla next is-> pons. There are ipisilateral?
Route 1: Medulla-> (ventroposterior medial
nucleus) Thalamus->
a) Primary gustatory cortex =insula.
Taste.
Also gathers info from Orbitalfrontal cortex
(2nd Olf-cortex) Input from Gustatory and
olfactory into the orbitafrontal cortex affect-
> flavour.
->b) Primary somatosensory cortex.
Food texture.
Route 2: Hypothalamus and amygdala.
Feeding behaviour, connecting feeling to
food, good or bad
Det kemiska hudsinnet
En del av vår känsel som reagerar på samma
kemikalier som (smak) och luktsinnet MEN
vid höga koncentrationer.
Conveys info together with smell and taste
(stickande,bränande, kyla..) about chemicals
in our environment.
Funktion: Varningssystem som inte?
Habitueras inte till simulus utan signalerna
ökar med tid.
11-Sensation, Somatosensory System
Somatosensory system is unique because it
located, mostly outside the brain and
connected to all parts of the body.
Somatosensory receptors
Receptor cells sit at the end of dendrites
underneath the skin. Not part of neurons but
connected to them.Some dendrites without
these cells are called free nerves. Eg.
Connected to hair root.
Sensitivity and receptive fields
Sensory receptors: Free dendrites(nerves),
Density of these receptors affect sensitivity
levels of different parts of the body. Palms,
feet and lips are glabrous skin that most
Använder:
Kemoreceptorer sk TRP- kanaler. Olika typer
dessa receptorer finns.
Trp- reagerar på värme/kyla och
aktiveras också av kemikalier som
capsaicin in chillipeppar och vi
upplever heta. Mentol ->kyla.
Andra Kemorecep- regerar på
Smärtaintryckt från e.x wasabi
Info via Kranialnerv V, Trigeminus
Dessa receptorer är kopplade till
kranialnerver. De ta med signaler från tre
olika zoner i hela ansiktet: panna, ögat; runt
näsa, övre munhål; nedre munhål).
Oftalmiska, Maxillära och Mandibulär
förgreningen, motsvarar områden ovan.
Vidare till pons -> thalamus-> till
Somatosensory cortex, orbitofrontalcortex
and to Limbic system, insula m.
Flavour= ett samlad intryckt from smell+ taste
and Kemiska hudsinnet. Dessa tre bidrar till
totala smakupplevelsen.
dense in sensory receptors->Respond to a
huge range of stimulus.
Receptive fields: The area their dendrites
cover/receive info. E.g., Two point
sensitivity= Area of skin=> Non converged
receptive field with few S.neurons synapse
on secondary S. neurons" send two or more
signals to brain. We feel two fingers.
Converged R.fields, overlap and many
S.neurons relay info on one 2nd S.neuron or
less than number stimulus ->we fail in
recognising num.. Hands "better" than thighs.
 Group and types of Somatosensory
(mechano)Receptors
Drag I nervcell, ett rör med håll , då skickar
den massor AP! .The deeper in skin the bigger
their receptive field, comparing 1 receptor vs
another 1. Ju mindre receptive fält desto
större upplösning.
1. Nociception (pain,temperature, itch)
 Free nerves pain: Slow
 Free nervtrådar Temperature: Slow.
-Hit hand, body cell layer close to F-nerves
break. F-nerves signal pain
2. Hapsis (fine touch and pressure)- with
tissue capsules
 Meissner’s corpuscle (Stryker
huden,lätt tryck)- Rapid
 Merkel's receptor -Slow (steady skin
pressure and texture) Fin känsliga och
mest känsliga. Upptäcker sandkorn.
o *M + M Upper skin layer vs
P+R
 Pacinian corpuscle (Vibration)- Rapid
 Ruffini corpuscle (Skin stretch) Slow
 Free nerve on hair (vid drag eller
rörelse av håret. upper layer
De samarbetar vid rörelser
3. Proprioception (Body awareness)
- Muscle spindles
- Golgi tendon organs (tendon stretch) rapid
- Joint receptors(joint movement" -rapid
Adaption to constant stimuli = rapid(stops
with AP) or slow(continues send AP!).
Dorsal-Root Ganglion Neurons
Only tip of (long) dendrite is sensitive in
S.neurons.
Dorsal root ganglion: (Secondary?)
Somatosensory neurons, long, that
“synapse” at spinal cord. Cell body closer to
spinal cord. Carry Info about fine touch and
pressure. Each type responding to particular
sort of info. Eg. Temp. if connected to nocio.
From Spine to Brain
1) Dorsal ganglion neurons carry info to
spinal cord.
2) a- Dorsal column-medial
lemniscal pathway: Haptic-
proprioceptivee info. Ipsilateral->At
Medulla, cross side then ->Medial
lemniscus->(Ventrolateral)Thalamus-
>Primary S. cortex.
b- Spinothalamic tract:
Nociooeptive sensations are
contralateral at spine and ipsilateral
all the way to S. Cortex.
*obviously connects to subcortical organs.
Damage: Haptic ipsilerarll and nocio
kontralaterally.
Spinal Reflexes:
Hit patella->Quadriceps stretched activation
"muscle spindle" tells somatosenstory
.neuron-> Info to spinal cord. Divides 1-input
direct to motor neuron goes back to frontal
quadricep to contract it. 2-Input to
interneuron, back to dorsal quadricep-
>relaxes(streches). you kick. #Monosynaptic
flex.
Same principle for Inner reflex: Golgi tendon
tells s.neuron, I can't bear weight for too long
and damage bone, tendons-> afferent nerve
to spines interneuron-> efferent nerves to
inbhit the contracted side-> you drop load.
Pain
Origin: Stimulate nocio- receptors or Frontal
lob’s failure to inhibit pain
Different pain fibers in body. Explain pinching
someone. There pathways connect eg.
Amygdala, reticular formation -arousal…
Lateral inhibition.
A stimulus affects a receptive field of primary
sensory neuron A (that may have receptors
cells at the tips) that is directly beneath
stimulus. It sends more action potentials than
the lateral B, C, Primary neurons. At their
synapse with secondary neurons, Secondary
neuron A inhibits the lateral neurons=B,C.
Result only signal from "A"s pathway go to
brain.
Gate way theory:
Hapsis and nocio connect to a common
interneuron while going to brain.
No pain: Interneurons inbhits pain and temp
C-fiber’s pathway och låter signaler från
beröring Från Alfa--fiber att passera.
Pain time: Signaler från nocio route hämmar
interneuron. Connects to next neuron and
goes to brain.
Pain relief :Vi blåser på såret ->signal via fine
touch and pressure/ mechanoreceptors-
axons->Aktiverar
interneuron->hämmar/minskar smärta
signalernas omkoppling på spinal neuron.
Interneuron hämmas och exiteras samtidigt
spinal neuron hämmas lite grann= mindre
smärta.
The somatosensory Cortex , Homunuculus
Primary S.S. cortex: Info from body.
Secondary S.S cortex: info from primary SS.
Cortex.
The Primary somatosensory cortex is
organised as a homunculus. The bigger areas
correspond to most sensitive parts of body.
Legs smaller but lips bigger. These areas
represent the sensitivity of skin,muscle and
joints of each part body.
Homunculus: What we would look like with
consideration to sensitivity of different body
parts.
Vestibular System and Balance
11- Motor System
Afferent (bigger region in s. cortex)
somatosensory info and efferent (Bigger in
Motor cortex) motor system. Nerves and
tracts. Different types of movements, even
internal=visceral
1) Cerebrum (cortex, conscious
control of movements)
2) Brainstem
-Beteende som är specifika för arter.
Stå upp, simma, rita . Hållning
Part of Somatosensory system, for balance.
Anatomy:
 3 Semicircular canals: Endolymph-
>Hair cells in cupula of Ampulla.
Canals together tells of Heads motion
in 3D.
 Otolithic organs: Utricle & Saccule:
Egg shape with hair cells and gelatine
substance. For/backward movement,
gravity
Receptors cells = hair cells’ function:
1) Tell brain Position of body
referenced from gravity.
2) Signal brain about head's
movement direction and
acceleration/deacceleration
3) Head orientation
As result we don't fall when we stand. Mr
compensation. We maintain posture and
balance
How?
Ex: Head movement to right = movement of
cillia to right->Depolarisation->A.P!->Increase
of AP! In s. neuron. OR hyperpolarization-
>decrease Neuron resting avfiring. Also, if
Hair cells one side fires more the opposite side
fires less- when we tilt head
- Photoreceptors and balance hair cells
receptors out of sync= dizziness, nausea.-
>Vertigo = contradictory signals in ampula due
to calcium substances in endolymph, that
supposed to be there. You a not actually
moving.
- Vi reagerar på olika sätt beroende på
situationen.
-Skador ->Cerebral Pares: not moving
bodies parts voluntary. Locked-in
Syndrome- Medveten, rör bara ögat.
3) Spinal cord:
-Reflexer, rytmik. Bebis sparkar när
de hålls upp.
Skador: Quadriplegia: Paralysis from
neck to toe. Paraplegia: Paralysis of
legs to toe.

Hierarchy and parallel order in Movement
control
Sensory system ex: Eyes see target. Informs
sensory system good for location. Frontal lobe
plans and executes. Sensory info back to
sensory cortex and B.G and cerebellum
engage to correct movement.
(Sensory receptors->sensory cortex->)
Prefrontal->Premotor->Primary Motor
cortex-> Brain stem Spinal cord. Parallel
connection too.
Initiating a motor sequence:
Complex movements involve complex
decisions. There is a sequence/order behind
movements. Motor sequence
Prefrontal cortex: Plans and sets goals. Right
or wrong->decision. Involves some
consciousness.
Premotor cortex: Organises and coordinates
goals to apropiate order of
movements/Behaviour. Mental imagery
Imagines, imitates others with eg Mirror
neurons. Damage: Lack of co.
Primary Motor cortex: Does the action, with
help of liljhärnan adjust movements to goals.
The Motor cortex Organization
Motor cortex is on each hemisphere controls
the contralateral side of body. Except for
reflexes, all command from P. M.cortex.
Homunculus in M-Cortex. Bigger body parts
show complex and precis movements of those
parts.
Behaviour not just movements:
Topographic map: A representation of each
sensory body parts on the motor cortex.
 Pre och Primära motor cortex visar
olika typer av rörelser som ett djur
kan göra, modifierarbar med övning.
Ett lexikon av rörelser- Oflexibla
rörelsekategorier.
- Inte bara enskilda
muskler.
A specific area ,t.ex hand area doesn't just
make muscles hand to twitch. Rather it
creates a behaviour. Hand moves to mouth.
Continue stimulating area hand stays in
mouth. Stimulate "drop hand area" instead.
Motor cortex visar olika typer av rörelser som
ett djur kan göra, modifierarbar med övning.
Position-point teory: En rumslig
representation av rörelsekategorier i cortex.
En punkt i cortex står för handen som rör sig
upp. En annan punkt rör den åt sida. Olika
rikttningar 1i rummet
Motor cortex before and during movements.
Motor cortex is active (more AP!) b4 you pick
the plastic cup. It is planning. Still active
during execution.
Same for heavy cup but activity increases as
you lift it. Increment due to Motor cortex
adjusting to force and duration of
movement.
Flexibility: Motorcortex can plan, withhold,
and imagine movements that might not be
able to produce yet.
Plasticity:
Damage on e.g., hand cortical representation
-> Using that hand less-> hand cortical region
becomes smaller, less mobility of hand -
>Elbow and shoulder bigger.
Rehab-> Same size of hand c-region over
time.
-Some parts of hand worked a bit because of
new connections in Hand-shoulder cortical
region. Even though specific region for
"finger" is gone.
Constraint induced therapy.
Corticospinal tracts- From Motor cortex to
muscles
Axons from: Pyramidal celler i lager V in
Motor cortex, Premotor - and sensory cortex.
--> to Brain stem and divide in medulla at
Pyramidal decussation:
Lateral Kortikala bana(Tract) : 90% Korsar till
andra sidan. Synapse with interneurons that
forward info to motor neurons that then
reach limb, fingers, and toes.
Anterior/Ventrala kortikala bana: Ipisilateral-
>interneurons in spinal cord-> Motor
neurons-> Styr muskler kroppens mitt. Bålen
-Ryggmärgen också som Homunculus.
Kortikobulära banan:
Cortex->Pons ->motorneurons->Kranial
nerver(ansikte, tunga, mun). Rörelse av
huvud, hals, ansikte.med
Control of muscles
Lateral inbitions at spinal cord. Interneurons
inhibit extensors and flexors one at a time.
Teamwork .You can't flex tri and bicep same
time. Extensor Motor neurons- limb away
from body. Flexor motor neurons: opp. ACHL
neurotransmitter for contraction
Basal Ganglia_
Regulator of force of movements, emo,
motiv-. Input from Limbic, sensor-, motor
systems
Damage of caudate putamen: Hyperkinetic:
Unwanted movements, Huntingtons
Hypokinetic: Can't produce movement, loss of
dopamine from S.nigra. Parkinsons.
Basal Ganglia Pathways for regulation:
Yes movement. Direct pathway;
 Motor Cortex-> X Caudate Putamen->
Hämma GP i-> exciteras Thalamus- ok
> M.cortex- Brainstem-> Spine...
*S.nigra: Dopa-> “Putamen->Gp i” Neurons =
More Inbition Gp i
*Subthalamic X s-nigra
Stop unwanted movements. Indirect pathway
 Same as above but Striatum inbites
Gp extern>Sub thalamic nucleus then
excite Gp i ->Hämmar ännu mer
Thalamus
Thalamus vill alltid sätta igång rörelse. Gp i
vill stoppa honom och rörelser. Aktiverad Gp-i
stoppar thalamus=stop movement. Vice versa.
Cerebellum
Anatomy: Two hemi. Ipsilateral control.
Homunculus organization two on each.
Topographically. Imagine a little doll lying
down:
 Ventral part
o Flocculus: a small lobe -
>Balans, ögonrörelser.
 Medial region:
o Vermis: (Lilhjärnsmasken),
input from spinal cord,
connect both hemi.
Movement kroppens mitt.
Balans.
 Intermediary region
o Input och export of info
från/till nucleusruber. Jämnar
ut rörelsen
 Lateral region
o Input från somatosensoriska
och motoriska cortex (primära
och sekundära)
o Complex muscle coo.
Cerebellum functions
Timing: Rörelsen sker när du vill det.
Justera rörelserna: Jämför det rörelsen som vi
gjort med den tilltänkta. Då justerar den nästa
rörelse för att matcha tilltänka bättre. *-
>Inlärning av nya rörelser mönster. Shoot ball.
Hur: Får en kopie av planen innan och
feedback efter första exekution. Korrigerar så
de matchar bättre->Skickar till Motor cortex.
Gör om.
*Även om du har prismglasögon.
*Skador: Tänk på saker som cerebellum kan
göra.
3 Cerebrala pedunklerna (nervbanor):
Vägen för cerebellums kopplingar still resten
av CNS
• Superior cerebrala -> efferent banor till
superior colliculus
•
Mediala afferent bana med input från Pons
•
Inferiora efferent och afferent banor från
ryggmärg och hjärnstam
8- Earlier development of Brain
From Zygote till Newborn
Fertilization-ZYGOT >Cell division->Embryonic
disc(groddblad) #15th day.
Origin of body organs and issues in the 3
layers of E. disc: Endoderm: Digestive system,
lever, lungs. Mesoderm: Muscles, blood
vessels and bones. Ektoderm (groddblad):
Skin, nervous system, neck, and head.
Ektoderm, 3 weeks-> 4th week
 Neural plate: Tät område på yttersta
lager Bildas. Viks blir en neural grop
 Neural tube: Resultatet när Neural
plate viks och stängds ännu mer ->
cylinder form. A very sensitive period
for embryo development. Errors-
>termination of fetus formation. The
upper region in it matures to become
canal for spinal cord and brain
vesticles.
After 4th week- 9th month Neural tube with
structures called >¤Pros-(later ->Tele &
Dience-). ¤Mese-, ¤Rhombechephalon (later-
>Mete & Mye) and ¤end of tube spinal cord.
Soon forebrain wraps it all in. Sex
differentiation due to testosterone or
oestrogen appearance.
TH
9 month: Fetus brain has general
appearance of adult brain, different on
cellular structure.
Stages of Brain development
1) Cell birth _Neurogenesis , 250 000
cells/min created before birth. Rapid
formation of Stam as N.tube closes.
Prenatal Brain weight increases as fast
as prenatal body weight
2) Cell migration_ Progenitor cells travel
to their locations shortly after genesis
of 1st neurons. Up to week 25.
Subventricular zone: A Line of stem cells
around ventricles or neural tube walls in
embryo. But in Fetus they have map of
destination for migrating neurons going to
cortex.
Radial glia cells: Create a fibre that Is road
from sub.ventrical zone to predetermined
destination for neurons on cortex.
Transportation: Passive-New cells push old
ones further out-> inner structures like
thalamus. Active-Young cells pass through old
ones->Building cortex
3) Cell origin and differentiation
Neural Stem cells: Forms in neural tube but at
subventricular zone around lateral vesicles
and spinal cords in adults ( S.cells exist but
quite restricted; blood cell, neuron. Self-
renewal= 1->2->1 dies+ 1 lives. Multipotent
DNA can become any cell it e.g:
Progenitor cells : Precursor cell from Stem
cells migrates to become N&G at destination:
Neuroblasts and Glioblasts that don’t divide->
Mature and become :
Different types of specialised neurons and
Glia cells. Diff. complete after birth.
4) Maturation of neurons
Dendrites grow and branch, specialise and
more functional as they create surfaces for
synapses. Gradually become more complex
until child reaches 2yrs. Important so as to
become systems and not just “parts”.
Importance: Språkutveckling, synutveckling
pga koppplingar, Myelinasering-Motorik.
Neurons connect
Axons are extended to appropriate target
cells and makes contact b4 dendrites in cell is
fully formed. Important in dendritic
differentiation. “Growth cones” : like a hand
with fingers seeking target cells. With
filopodia=tip of extensions responds to
different come or reject chemical signals from
target cells.
5) Synaptic Development,
Axons and dendrites meet guided by signals to
right place-> Creation of lots of Synapses.
1st Simple contacts. 2ndMore Complex
contacts -> more development in cortical
neurons in deeper brain region. Multi-
connectivity among diff. skill regions
After birth: Massive increment 1st years of life
Gives us all opportunities. Reaches a Plato and
starts reduces during life->death.
6) Cell death and Elimination/pruning
of Synapses
Rise and fall of synaptic density->Behaviour
changes eg. Mood changes in kids and youth.
Elimination according to 1) Neural Darwinism:
Neurons leading to survival traits= fitness
stay, The rest weeded out. 2) Apoptosis: Får
av tillväxtfaktorer= död Failure in step 4 or
Certain genes not expressed in that neuron ->
Programmed cell death. Throughout life +/-
More space
Gene controlled initially but enviro after
birth decides which synapses stays
Synapses enter adulthood only if part of a
functional neural network<- Experience and
rate of use.
Leads to environmental adaptions: E.g two
cultures meet, language
7) Myelination
 Proximal axons nära mttlinjen b4
Distant.
 Sensory nerves then Motor nerves.
 Projection(sending) routes b4
Association (back and forth) routes.
An Index for maturation. E.g Frontal
lobe last myelinated, control high
mental functions. SPEED
Starts I Brainstem vk 29 until adulthood
GENE->Potential AND ENVIROMENT affects
all this.
Behaviour and Nervous-System
Development
Motor behaviour- Lie,crawl, walk; Grasping
response 2-4-10mths+ In babies : Random
hand movements->Hand towards goal->
Entire hand holds object->Thumbs and fingers
hold a pebble. Simple to sophisticated
movement. Due to myelinated motor
neurons in/from motor cortex developing:
More dendritic branching, axons from motor
cortex myenalite.
Language development
Vocabulary starts by 12 months. Language
skills + motor skills develop parallelly to
Coordinate speech. Yet vocabulary grows
gradually. Increase of neuronal connectivity
and speech zones myelinate-> Language
acquisition complete. 12 years.
Problem solving ability:
Piagé development stages. Comes with age as
brain makes complex connections
Brain development and Environment
Not just appearance of structures -
>development<- Environment changes and
experiences within and without. Eg.
Hormones, mutation, medicine, uppfostran
Stimulating or Poor enviroment-> Growth of
Relative Intelligence (Farmer vs Psychologist).
Adaptability may be greater intelligence.
Touch your children => stimulates brain
development. OBS: Multiple variables.
Richness of environment->More neurons even
in adults
  Critical periods: 6-7 year. Eg. Visual synapses. Neuroplasticity in adult slower than
development depends on stimuli from in kids.
environment. Right time must eye be
OBS! Correlation of events with neural
used. Might not regrow later. If
changes doesn’t always mean causation!!
problem as embryo=permanent. Use
Remember third variable, directionality
it or lose it. Language RRRR-
problem and selection bias.
Different Experiences (may)change Neuron
Abonormal experience creates defects on
structures differently-> Still leads to
development.
Bigger/smaller size and quantity more/less

*Att kunna: Utveckligen generellt från barn till tonåren.

Emotioner

Orsaker till beteende Motivation är ett tillstånd inuti som startar

och driver ett beteende. Två grupper av
Överlevnad- kopplas till evolutionär påverkan
motiverade beteende:
Belöning- kan också kopplas till miljöpåverkan
Reglerat beteende
; stimuli och respons. Apa gör allt för att se
banan genom en lucka.  Homeostatiska mekanismer: Huttra
(non volontary ) eller sätt på jacka
Jaga-döda instinkt i en katt->Belöning från
verkar ”volontär”Behåller samma
hjärnkretsar->Försäkrar överlevnad och
nivå. Temp, kroppsvätska(törst),
motiverar beteende. Sinnen påverkar
hunger- glucos. Hypthalamus är
sökandet på belöning. Lukt på pizza. Andra
väldigt involverade med sina
hjärnkretsar reglerar vår reaktion på det
hormoner och neurotrasmittor
stimulus.
 Motiveras av att kroppen vill
Innate releasing mechanism(IRM) överlevna

Ett nätverk av neuroner , tar emot ett specifikt Icke-reglerat beteende

stimuli och de utlöser ett specikt beteende .
Stimuli matchar en medfödd mall för ett visst
beteende och vi agera på ett visst sätt.
Evolutionära faktorer (överleva, naturligt
urval) och faktorer från miljön kan påverka
aktivitet i olika hjärnbanor,
Miljö och erfarenhet kan reglera hur vi
regerar. Mamma ler och bebis ler tillbaka
omedvetet. Mamma ler och slår barnet->barn
gråter när hen ser leendet. Picasso katt
matchar inte ”äkta” katt>ingen respons
Motiverat beteende
 Beteende som inte är livsviktiga
/uppfyller de grundläggande
överlevnadsbehoven. EX: Sex
(Hypothalamus involverad) Läsning,
nyfiken påverkas mycket av frontala
loben.
 Ej homoestatiska och starkt påverkad
av yttre stimuli. Du t.ex ser/luktar och
du gör.
Hypotalamus funktion och Feedback
Involverad i homeostas genom sina hormoner
via ANS->Reglering av temp,puls,socker,
cortisol Får feedback vid hög/låg nivåer
3 regioner: Lateral. Medial och Petrivetrikulär
styr:
Vårt Beroende på substanser, impuls
beteende; --; Behagliga känslor och
anknytning
Generar beteende: Kamp/flykt, äta och
dricka, reproduktivt,. Tänk på
Symp/Parasymp--. Eg Råttan ”På” och ”av”
grävande
Definition av Emotioner
- Känsla som är din upplevelse (jag är arg) +
Emotionellt uttryck är din reaktion (rynkar
pannan) =Emotion
-Det är en kortvarig upplevelse som
involverar förändringar i kroppen och hjärnan.
Orsak och riktning.
Syfte med emotioner
 Riktar vårt fokus ,motiverar oss och
orienterar.
 Minne och inlärning fästpunkt,
 Hot kognition och rationella beslut
Emotioners komponenter
-Fysiologisk reaktion (aktivering)- Händer i
kroppen, svettas, puls. ANS!!
-Uttrycksfulla beteende(motorik)- Yttre
Kroppsliga signaler/rörelser som kopplas till
olika emotioner. Ex: Ansiktsuttryck och
handlingar
-Medveten/omedveten upplevelser: Märker
eller ej att en viss stimulus orsakar min
reaktion. Självrapporter. Annars svårt att
mäta subjektiva upplevelsen ”sorg etc”. Fråga!
Dimensioner på emotioner i i ett kordinat
system : X +Arousal , -No arousal ; Y-Pleasant ,
+Unpleasant. Placera ut grundemotioner i
systemet.
TRE Synsätt på Emotioner
1) Modulär- 6 grundläggande emotions
Anses vara medfödda ; Rädsla,ilska,
glädje, sorg, äckdel och förvåning-
>Blandas=Komplex emotioner. Glädje
m.m ger INTE specifik hjärnaktivitet
2) Reaktivt- Bedömningsteorier
-Vi upplever emotioner i händelser
beroende på vår synpunkt,
erfarenheter och fysiologiska
förändringar. Att bedöma är
funktionen som ”är” medfödd-Det är
reaktion=stimuli- respons.
3) Prediktivt sätt- Konstruktvistiska
teorier
Känslor och emotioner är något
hjärna skapar för att tolka och
förklara situationer (inkl
människor)och förutsäga handlingar.
Kategoriserar baserad på
erfarenheter. Inte inre + yttrre om 2)
Men konstruerad.
Emotioner på Ansiktet: Utgick från
stereotyper för ansiktsuttryck och emotioner-
>Upptäckt samma ansiktsuttryck överallt.
Bevis för 6 emotioner. Ansiktsmuskler kanske
kan påverka vårt inre tillstånd och ANS. Glad,
penna i munnen<-Kan vi manipulera den?
OBS! Inkludera andra kropsspråk
Vad händer i kroppen? Emotioner
Fysiologiska reaktioner:
Händelse blir ett stimuli för hjärnan->
1) Sympa- systemet och Endokri-
larmas->
2) Muskler agerar=beteende->
3) Feedback till hjärnan skapar
emotion. Ex: En clown->vi är rädda -
Stress system-> Blod till muskler ger
kalla fötter. Arga- varm hud och vi
svettas. Rädsla och spänning ger
samma fysiologisk reaktion. High road
or low perspective.
Emotionsteorier
James-lange : Vi uppfattar ett stimuli genom
våra sinnen. #1-Förändringar sker i vår kropp
ex pulsen ökar. Då signaleras hjärnan att det
är samma sak som rädsla, nervositet. Just att
förändringarna i kroppen är och föregår
emotionen.
Cannon-Bard teorin: Den känslomässiga
upplevelsen sker oberoende av fysiologisk
förändring. Han menar att sorg och gråt kan är
oberoende av varandra men sker oftast
samtidigt. Vi blir rädda och vi märker att
hjärta börjar slå. Feeling doesnt depend on
fysiological changes. Oberoende av somatisa
systemet : Du kan vara arg även när du är
förlamad. (Händer tillsammans?)
Schachter-Singers two faktor teori: Vi
uppfattar ett Stimulus den ger en
kroppsaktivering + Hur vi tolkar och
beskriver det ”KONTEXT” kognitivt avgör
vilken emotion vi har. Det leder till
motsvarande handling. Ex: Du får adrenalin
och hjärtat slår. Du kanske tolkar pulsen som
rädsla eller andra emotioner.
Emotion och Kognition, High & Low way:
Vi kan reagera direkt på stimuli utan att vi
hunnit tolka den. Speciellt när impulsen går
talamus-Amygdala snarare än Talamus-
Sensoriska kortex- Amygdala vid respons. Vs
High way- Tänka 1st på känslor
Somatiska Markörer:
Skador: Ju högre upp i ryggmärgen desto
mindre intensitet på upplevelse av emotioner.
Pga färre kroppsliga reaktioner. Somatisk info
utnyttjas inte 100% .
Kroppsliga responsen i situationer hjälper att
fatta ”bättre “beslut. Ju mindre fysiologisk
feedback som vi känner från kroppen desto
sämre blir vi på att basera vår beslut på
känslor.-Hot kognition och sociala beslut
nedsätts Skada på frontal lob utesluter
emotioner från kognition.
Neuroanatomi och Emotioner
Essentiella Strukturer:
1) Hypotalamus- Input alla andra
strukturer passerar här- Ger
motivation och emotion i beteende.
1b) Hypofysen, homeostatiska
mekanismer
2) Limbiska Systemet: Under
neocortex-”Allocortex”
 Amygdala: Får info från flera
sensoriska system
(multimodala). Många
synapser från visuella cortex-
>Tidig upptäck av faror i
världen. Ångest med sina
reaktioner från barndom kan
lagras här.
 El. Stimuleras -> ilska,
aggression.
Emotionens via amygdala :
1) Sinne->Amygdala.
2) Amygdala->3a) Hypotalamus=> ANS
respons. Och till Hjärnstam-> respons
ex beteende 3b)-> Cerebral Cortex-
Emotionell upplevelse
Kluver Bucy Syndrom-Ingen rädsla, litar på
främlingar, har mindre emotionella uttryck
eller känna igen ansikte. Problem att reagera
men man kommer ihåg stimuli.
 Hippocampus: Långtidsminne
kodas och formas här. Minnas
associationer till emotioner.
T.ex. rädsla pga clownen
Möjliggör inlärning.
 Mamilarkropparna : För över
minnet till Hippo (& hypo) till
C.cortex. Minne av dagliga
händelser.
Gyrus Cingulum: Kogniticva konflikter.
o För Självreglering emotioner.
o Relästation för Info från Talamus- tiill
->Hippocampus.
o Koppla lukt och smärta till minne.
o Stödjer fokus på emotionella
händelser.
Prefrontala Cortex
  Input från ALLA sensoriska cortex (alla
sinne) + Amygdala + talamus.
 Konkretisar och bedömer lämpliga för
beteende. Skickar vidare till resten av
motor system + Basal ganglia och
ACTION!
 Även till alla essentiella strukturer. Ex
Amygdala och Hypothalamus-
>ANS&ENS
Skador på PFrontala Cortex:
Svårt att tala och förstå andras talmelodi, läsa
av, nedsatt fokus och motorik, icke-adaptiv
beteende och beslut
Dorsolateralt Syndrom:
Pseudo depression- Planlös Energilös, , Auto-
handlingar
Oribital/ventromedial syndrom:
Pseudo psykopati-Impulsiv, Självcentrerad,
ansvarlöS.
Socialt smärta = fysiskt smärta enligt hjärnan

Motiverat beteende : Styrs av Hypothalamus. Reglerat:Jämvikt inom satta ramar temp,

vätskebalans,. Kallt: Ofrivlliga beteende att skaka eller välja att klä på sig.

Hypotalamus ser till att de celebra regioner är aktiva när de behöver vara det. Producerar beteende

Rädsla eller glädje-> Håll undan fara eller nära det som ökar överlevnad.

Emotioner har format alltså evolutionen.

Sinnerörelse=emotioner. Emotion: inifrån SUBJETIKV, affekt när sett utifrån. Emotioner är kortvariga

Inre/ytre stimuli påverkar emotion.

Olika emotionerkomponenter: Uttyckt—vad vi kopplar till olika emotioner

Arousal= kroppsaktiviering
Grundemotioner kan blandas och skapa komplexa emotioner. Kritisk mot att de är relaterad till en
sprcifik hjärnaktivitet.

Olika känslor->olika ansiktysuttryck. Vice versa #nyans