INTERNAL ASSESSMENT (II)

ANIMAL PHYSIOLOGY

SUBMITTED BY –
Farheen Khan
Roll no – 19MBS007
MSc. Biosciences
1st year (2nd semester)
Q1.DESCRIBE THE ELECTRICAL RESPONSE
PRODUCED BY RODS AND CONES AND
EXPLAIN HOW THESE RESPONSES ARE
PRODUCED
Physiology of Vision
Photoreceptors and Photopigments
Rods and cones were named for the different appearance of the outer
segment—the distal end next to the pigmented layer—of each of these
types of photoreceptors. The outer segments of rods are cylindrical or
rod-shaped; those of cones are tapered or cone-shaped. Transduction of
light energy into a receptor potential occurs in the outer segment of both
rods and cones. The photopigments are integral proteins in the plasma
membrane of the outer segment. In cones the plasma membrane is
folded back and forth in a pleated fashion; in rods the pleats pinch off
from the plasma membrane to form discs. The outer segment of each
rod contains a stack of about 1000 discs, piled up like coins inside a
wrapper.Photoreceptor outer segments are renewed at an astonishingly
rapid pace. In rods, one to three new discs are added to the base of the
outer segment every hour while old discs slough off at the tip and are
phagocytized by pigment epithelial cells. The inner segment contains
the cell nucleus, Golgi complex, and many mitochondria. At its
proximal end, the photoreceptor expands into bulblike synaptic
terminals filled with synaptic vesicles.
The first step in visual transduction is absorption of light by a
photopigment, a colored protein that undergoes structural changes
when it absorbs light, in the outer segment of a photoreceptor. Light
absorption initiates the events that lead to the production of a receptor
potential. The single type of photopigment in rods is rhodopsin (rhod-
rose; opsin- related to vision). Three different cone photopigments are
present in the retina, one in each of the three types of cones. Color
vision results from different colors of light selectively activating the
different cone photopigments. All photopigments associated with vision
contain two parts: a glycoprotein known as opsin and a derivative of
vitamin A called retinal. Vitamin A derivatives are formed from
carotene,the plant pigment that gives carrots their orange color. Good
vision depends on adequate dietary intake of carotene-rich vegetables
such as carrots, spinach, broccoli, and yellow squash, or foods that
contain vitamin A, such as liver. Retinal is the light-absorbing part of all
visual photopigments. In the human retina, there are four different
opsins, three in the cones and one in the rods (rhodopsin). Small
variations in the amino acid sequences of the different opsins permit the
rods and cones to absorb different colors (wavelengths) of incoming
light. Photopigments respond to light in the following cyclical process :
● In darkness, retinal has a bent shape, called cis-retinal, which fits
snugly into the opsin portion of the photopigment. When cis-retinal
absorbs a photon of light, it straightens out to a shape called trans-
retinal. This cis-to-trans conversion is called isomerization and is the
first step in visual transduction. After retinal isomerizes, several
unstable chemical intermediates form and disappear. These chemical
changes lead to production of a receptor potential
● In about a minute, trans-retinal completely separates from opsin. The
final products look colorless, so this part comple cycle is termed
bleaching of photopigment.
● An enzyme called retinal isomerase converts trans-retinal back to
cis-retinal.
● The cis-retinal then can bind to opsin, reforming a functional
photopigment. This part of the cycle—resynthesis of a photopigment—
is called regeneration.
The pigmented layer of the retina adjacent to the photoreceptors stores a
large quantity of vitamin A and contributes to the regeneration process
in rods. The extent of rhodopsin regeneration decreases drastically if the
retina detaches from the pigmented layer. Cone photopigments
regenerate much more quickly than the rhodopsin in rods and are less
dependent on the pigmented layer. After complete bleaching,
regeneration of half of the rhodopsin takes 5 minutes; half of the cone
photopigments regenerate in only 90 seconds. Full regeneration of ble
ached rhodopsin takes 30 to 40 minutes
Light and Dark Adaptation
When you emerge from dark surroundings (say, a tunnel) into the
sunshine, light adaptation occurs—your visual system adjusts in
seconds to the brighter environment by decreasing its sensitivity. On the
other hand, when you enter a darkened room such as a theater, your
visual system undergoes dark adaptation—its sensitivity increases
slowly over many minutes. The difference in the rates of bleaching and
regeneration of the photopigments in the rods and cones accounts for
some (but not all) of the sensitivity changes during light and dark
adaptation. As the light level increases, more and more photopigment is
bleached. While light is bleaching some photopigment molecules,
however, others are being regenerated. In daylight, regeneration of
rhodopsin cannot keep up with the bleaching process, so rods contribute
little to daylight vision. In contrast, cone photopigments regenerate
rapidly enough that some of the cis form is always present, even in very
bright light. If the light level decreases abruptly, sensitivity increases
rapidly at first and then more slowly. In complete darkness, full
regeneration of cone photopigments occurs during the first 8 minutes of
dark adaptation. During this time, a threshold (barely perceptible) light
flash is seen as having color. Rhodopsin regenerates more slowly, and
our visual sensitivity increases until even a single photon (the smallest
unit of light) can be detected. In that situation, although much dimmer
light can be detected, threshold flashes appear gray-white, regardless of
their color. At very low light levels, such as starlight, object appear as
shades of gray because only the rods are functioning.

PHOTOTRANSDUCTION
Visual or phototransduction is the process by which light energy is
converted into receptor potential in visual receptors. Resting
membrane potential in other sensory receptor cells is usually between –
70 and –90 mV. However, in the visual receptors during darkness,
negativity is reduced and resting membrane potential is about –40 mV.
It is because of influx of sodium ions. Normally in dark, sodium ions
are pumped out of inner segments of rod cell to ECF. However, these
sodium ions leak back into the rod cells through membrane of outer
segment and reduce the electronegativity inside rod cell. Thus, sodium
influx maintains a decreased negative potential up to –40 mV. This
potential is constant and it is also called dark current. In darkness,
sodium ions flow into photoreceptor outer segments through ligand-
gated Na+ channel. The ligand that holds these channels open is cyclic
GMP (guanosine monophosphate) or cGMP. The inflow of Na ions ,
called the “dark current,” partially depolarizes the photoreceptor. As a
result, in darkness the membrane potential of a photoreceptor is about –
30 mV. This is much closer to zero than a typical neuron’s resting
membrane potential of –70mV. The partial depolarization during
darkness triggers continual release of neurotransmitter at the synaptic
terminals. The neurotransmitter in rods, and perhaps in cones, is the
amino acid glutamate (glutamic acid). At synapses between rods and
some bipolar cells, glutamate is an inhibitory neurotransmitter: It
triggers inhibitory postsynaptic potentials (IPSPs) that hyperpolarize the
bipolar cells and prevent them from sending signals onto the ganglion
cells.
When light strikes the retina and cis-retinal undergoes isomerization,
enzymes are activated that break down cGMP. As a result, some cGMP-
gated sodium ion channels close, Na inflow decreases, and the
membrane potential becomes more negative approaching –70 mV. This
sequence of events produces a hyperpolarizing receptor potential that
decreases the release of glutamate. Dim lights cause small and brief
receptor potentials that partially turn off glutamate release; brighter
lights elicit larger and longer receptor potentials that more completely
shut down neurotransmitter release. Thus, light excites the bipolar cells
that synapse with rods by turning off the release of an inhibitory
neurotransmitter. The excited bipolar cells subsequently stimulate the
ganglion cells to form action potentials in their axons. Thus, the process
of receptor potential in visual receptors is unique in nature. When other
sensory receptors are excited, the electrical response is in the form of
depolarization (receptor potential). But, in visual receptors, the
response is in the form of hyperpolarization.
Q2.DESRCRIBE THE STRUCTURE AND
FUNCTION OF LIMBIC SYSTEM
The concept that was previously known as the “Visceral brain” and
denoted a complex anatomical and physiological association, started
being called the “limbic system” in 1952. Today, we still know it as the
limbic system of the limbic lobe of our brain. The inner and lower
surfaces of the brain hemispheres unite in the so-called limbic
(marginal) cortex together with the almond-shaped nucleus from the
group of subcortical nuclei, the olfactory tract and the bulb, frontal,
temporal, and parietal lobes of the cerebral hemisphere, as well as the
subarticular region and reticular formation of the trunk. The limbic
cortex is combined into one functional system – the limbic-reticular
complex. The girdle and the hippocampal (parahippocampal) gyrus
combine into the limbic region, which has numerous connections with
structures of the reticular formation, forming with it the limbic-reticular
complex that provides a wide range of physiological and psychological
processes. The limbic lobe is commonly attributed to elements of
the old bark (archiocortex), which cover the dentate gyrus and
hippocampal gyrus; the ancient cortex (paleocortex) of the anterior
hippocampus; as well as the middle, or middle, mesocortex cingulate
gyrus.The term “Limbic system” includes components of the limbic
lobe and related structures – amygdala, hippocampus, thalamus,
hypothalamus, basal ganglia, and cingulate gyrus.

The Amygdala
The amygdala is a small almond-shaped structure; there is one located
in each of the left and right temporal lobes. Known as the emotional
center of the brain, the amygdala is involved in evaluating the
emotional valence of situations (e.g., happy, sad, scary). It helps the
brain recognize potential threats and helps prepare the body for fight-
or-flight reactions by increasing heart and breathing rate. The
amygdala is also responsible for learning on the basis of reward or
punishment. Due to its close proximity to the hippocampus, the
amygdala is involved in the modulation of memory consolidation,
particularly emotionally-laden memories. Emotional arousal following a
learning event influences the strength of the subsequent memory of that
event, so that greater emotional arousal following a learning event
enhances a person’s retention of that memory. In fact, experiments have
shown that administering stress hormones to individuals immediately
after they learn something enhances their retention when they are tested
two weeks late
The Hippocampus
The hippocampus is found deep in the temporal lobe, and is shaped like
a seahorse. It consists of two horns curving back from the amygdala.
Psychologists and neuroscientists dispute the precise role of the
hippocampus, but generally agree that it plays an essential role in the
formation of new memories about past experiences. Some researchers
consider the hippocampus to be responsible for general declarative
memory (memories that can be explicitly verbalized, such as
memory of facts and episodic memory). Damage to the hippocampus
usually results in profound difficulties in forming new memories
(anterograde amnesia), and may also affect access to memories formed
prior to the damage (retrograde amnesia). Although the retrograde
effect normally extends some years prior to the brain damage, in some
cases older memories remain intact; this leads to the idea that over time
the hippocampus becomes less important in the storage of memory.

The Thalamus and Hypothalamus

Both the thalamus and hypothalamus are associated with changes in
emotional reactivity. The thalamus, which is a sensory “way-station”
for the rest of the brain, is primarily important due to its connections
with other limbic-system structures. The hypothalamus is a small part of
the brain located just below the thalamus on both sides of the third
ventricle. Lesions of the hypothalamus interfere with several
unconscious functions (such as respiration and metabolism) and some
so-called motivated behaviors like sexuality, combativeness, and
hunger. The lateral parts of the hypothalamus seem to be involved with
pleasure and rage, while the medial part is linked to aversion,
displeasure, and a tendency for uncontrollable and loud laughter.
The Cingulate Gyrus
The cingulate gyrus is located in the medial side of the brain next to the
corpus callosum. There is still much to be learned about this gyrus, but
it is known that its frontal part lin smells and sights with pleasant
memories of previous emotions. This region also participates in our
emotional reaction to pain and in the regulation of aggressive behaviour.

The Basal Ganglia

The basal ganglia is a group of nuclei lying deep in the subcortical
white matter of the frontal lobes that organizes motor behavior.
The caudate, putamen, and globus pallidus are major components of
the basal ganglia. The basal ganglia appears to serve as a gating
mechanism for physical movements, inhibiting potential movements
until they are fully appropriate for the circumstances in which they are
to be executed. The basal ganglia is also involved with:
 rule-based habit learning (e.g., initiating, stopping, monitoring,
temporal sequencing, and maintaining the appropriate movement);
 inhibiting undesired movements and permitting desired ones;
 choosing from potential actions;
 motor planning;
 sequencing;
 predictive control;
 working memory;
 attention.
Damage to the structures of the limbic lobe and the limbic-reticular
complex, in general, can be accompanied by different clinical
symptoms. Those include pronounced changes in the emotional sphere
of permanent and paroxysmal nature, anorexia or bulimia, sexual
disorders, memory impairment, and especially signs of the Korsak
syndrome, in which the patient loses the ability to remember current
events. Moreover, the symptoms of the limbic system damage include
vegetative-endocrine disorders, sleep disorders, psychosensory
disorders in the form of illusions and hallucinations, changes in
consciousness, clinical manifestations of akinetic mutism, and seizures.

Q3.INSULIN IS SOMETIME DESCRIBED AS ”THE

HORMONE OF PLENTY” AND GLUCAGON AS
THE “ HORMONE OF STARVATION ”. DISCUSS
THE APPROPRIATENESS OF THESE TERMS IN
THE CONTEXT OF THE PHYSIOLOGIC EFFECTS
OF EACH HORMONE AND THEIR
INTERACTIONS
Each pancreatic islet includes four types of hormone-secreting cells:
1. Alpha or A cells constitute about 17% of pancreatic islet cells and
secrete glucagon.
2. Beta or B cells constitute about 70% of pancreatic islet cells and
secrete insulin
3. Delta or D cells constitute about 7% of pancreatic islet cells and
secrete somatostatin (identical to the growth hormone inhibiting
hormone secreted by the hypothalamus).
4. F cells constitute the remainder of pancreatic islet cells and secrete
pancreatic polypeptide
In essence, insulin signals the fed state that is why it is “Hormone of
Plenty”—it stimulates the storage of fuels and the synthesis of proteins
in a variety of ways. For instance, insulin initiates protein kinase
cascades—it stimulates glycogen synthesis in both muscle and the liver
and suppresses gluconeogenesis by the liver. Insulin also accelerates
glycolysis in the liver, which in turn increases the synthesis of fatty
acids.
The liver helps to limit the amount of glucose in the blood during times
of plenty by storing it as glycogen so as to be able to release glucose in
times of scarcity. the excess blood glucose present after a meal
removed by the uptake of blood glucose into the liver by GLUT2. The
level of glucose in the liver rises because only then do the catalytic sites
of glucokinase become filled with glucose. Glucokinase is active only
when blood-glucose levels are high. Consequently, the liver forms
glucose more rapidly as the blood-glucose level rises. The increase in
glucose 6-phosphate coupled with insulin action leads to a buildup of
glycogen stores. The hormonal effects on glycogen synthesis and
storage are reinforced by a direct action of glucose
itself. Phosphorylase a is a glucose sensor in addition to being the
enzyme that cleaves glycogen. When the glucose level is high, the
binding of glucose to phosphorylase a renders the enzyme susceptible to
the action of a phosphatase that converts it into phosphorylase b, which
does not readily degrade glycogen. Thus, glucose allosterically shifts
the glycogen system from a degradative to a synthetic mode.
The high insulin level in the fed state also promotes the entry of glucose
into muscle and adipose tissue. Insulin stimulates the synthesis of
glycogen by muscle as well as by the liver. The action of insulin also
extends to amino acid and protein metabolism. Indeed, insulin has a
general stimulating effect on protein synthesis, which favors a building
up of muscle protein. In addition, it inhibits the intracellular degradation
of proteins.

The early fasting state- The blood-glucose level begins to drop several
hours after a meal, leading to a decrease in insulin secretion and a rise
in glucagon secretion; glucagon is secreted by the α cells of the
pancreas in response to a low blood-sugar level in the fasting
state. Just as insulin signals the fed state, glucagon signals the
starved state.. That is why glucagon is “Hormome of Starvation” It
serves to mobilize glycogen stores when there is no dietary intake of
glucose. The main target organ of glucagon is the liver. Glucagon
stimulates glycogen breakdown and inhibits glycogen synthesis.
Glucagon also inhibits fatty acid synthesis. In addition, glucagon
stimulates gluconeogenesis in the liver and blocks glycolysis. All
known actions of glucagon are mediated by protein kinases that are
activated by cyclic AMP. The large amount of glucose formed by the
hydrolysis of glucose 6-phosphate derived from glycogen is then
released from the liver into the blood. The entry of glucose into muscle
and adipose tissue decreases in response to a low insulin level. The
diminished utilization of glucose by muscle and adipose tissue also
contributes to the maintenance of the blood glucose level. The net
result of these actions of glucagon is to markedly increase the release
of glucose by the liver.
Both muscle and liver use fatty acids as fuel when the blood-glucose
level drops. Thus, the blood-glucose level is kept at or above 80 mg/dl
by three major factors: (1) the mobilization of glycogen and the release
of glucose by the liver, (2) the release of fatty acids by adipose tissue,
and (3) the shift in the fuel used from glucose to fatty acids by muscle
and the liver
The refed state- what are the biochemical responses to a hearty
breakfast? Fat is processed exactly as it is processed in the normal fed
state. However, this is not the case for glucose. The liver does not
initially absorb glucose from the blood, but rather leaves it for the
peripheral tissues. Moreover, the liver remains in a gluconeogenic
mode. Now, however, the newly synthesized glucose is used to
replenish the liver's glycogen stores. As the blood-glucose levels
continue to rise, the liver completes the replenishment of its glycogen
stores and begins to process the remaining excess glucose for fatty acid
synthesis.
Q4.OUTLINE THE STEPS INVOLVED IN
SPERMATOGENESIS FROM THE PRIMITIVE
GERM CELLS TO MATURE MOTILE
SPERMATOZOA
SPERMATOGONIA
In humans, spermatogenesis takes 65–75 days. It begins with the
spermatogonia, which contain the diploid (2n) number of chromosomes.
Spermatogonia are types of stem cells; when they undergo mitosis,
some spermatogonia remain near the basement membrane of the
seminiferous tubule in an undifferentiated state to serve as a reservoir of
cells for future cell division and subsequent sperm production. The rest
of the spermatogonia lose contact with the basement membrane,squeeze
through the tight junctions of the blood–testis barrier, undergo
developmental changes, and differentiate into primary spermatocytes
Primary spermatocytes, like spermatogonia, are diploid (2n); that is,
they have 46 chromosomes.Shortly after it forms, each primary
spermatocyte replicates its DNA and then meiosis begins. In meiosis I,
homologous pairs of chromosomes line up at the metaphase plate,and
crossing-over occurs. Then, the meiotic spindle pulls one (duplicated)
chromosome of each pair to an opposite pole of the dividing cell.
SPERMATOCYTES/MEIOSIS
Primary Spermatocytes
Meiosis starts with DNA synthesis of type B spermatogonia which lose
contact with the basal lamina (preleptotene). After completion of DNA
synthesis, each chromosome consists of two chromatids. These cells are
named primary spermatocytes, and the DNA content is tetraploid.
Primary spermatocytes undergo the first meiotic division. The prophase
of the first meiotic division takes about 1 –3 weeks and is divided into
several stages: the leptotene, zygotene, pachytene and diplotene
stages.The leptotene stage is characterized by DNA condensation
resulting in the appearance of thin filaments within the nucleus. In the
zygotene stage, condensation of chromosomes proceeds, and pairing of
homologous chromosomes takes place due to the formation of the
“synaptonemal complexes” which are only visible using an electron
microscope. In the pachytene stage,there is an exchange of genetic
material derived from maternal and paternal sources between sister
chromatids of homologous chromosomes involving DNA breakage and
repair in autosomes but not in the heterosomes “x” and “y”. The pairing
of chromosomes leads to a “crossover” of adjacent sister chromatids.
When the chromosomes start to separate in the pachytene stage, these
sites become visible and are termed “chiasmata”. In the diplotene stage,
chromosomes separate with the exception of the chiasmata sites. The
end of the meiotic prophase is recognized as “diakinesis”, when
chromosomes shorten and the four separate chromatids become visible.
Finally, the nuclear membrane disappears and chromosomes are
subsequently arranged in the metaphase plate. After formation of the
spindle apparatus, chromosomes move to opposite poles, but in contrast
to mitotic division, chromatids remain interconnected. Thus the number
of chromosomes in resulting secondary spermatocytes is haploid, but
the DNA content is still diploid
Secondary Spermatocytes
Secondary spermatocytes undergo the second meiotic division after a
short interphase of about 6 h in the human without DNA synthesis. By
this division, chromatids are finally separated leading to round
spermatids with a haploid number of chromosomes and DNA content
SPERMATIDS/SPERMIOGENESIS
Early round spermatids are postmitotic cells, exhibit a nucleus with a
homogenous chromatin pattern and can be identified by the perinuclear
acrosome vesicle, which can easily be seen after periodic acid Schiff
(PAS)reaction on formalin, or Bouin-fixed paraffin-embedded sections
or at the ultrastructural level.The transformation of conventional round
cell spermatids into spermatozoa with the capacity for motility and
fertilization of an egg includes a complex sequence of events: (1)
formation of the acrosome, (2) condensation of the nucleus, (3)
development of the sperm tail, (4) reorganization of cellular organelles
such as mitochondria and centrioles and (5) reduction of the
cytoplasm.The synthesis of many acrosome-specific proteolytic
enzymes starts as early as in pachytene spermatocytes. These proteins,
such as proacrosin, are packed into electron-dense vesicles:
proacrosomal granules (PAGs) derive from the trans-Golgi complexes.
They start to fuse after completion of meiotic divisions in step1
spermatids. The growing acrosome forms a cap-like structure that
covers about 30 –50% of the nuclear surface. Nuclear condensation in
the human is due to replacement of about 85% of the DNA-associated
lysine rich histones by transition proteins, and finally by arginine-rich
protamines. In contrast to histones, which form a loop-like association
with DNA(nucleosomes),protamines are associated with the grooves of
the DNAhelix, leading to extreme condensation and finally to a
reduction to about 10% of the original nuclear size . Transition proteins
are believed to be involved in DNArepair mechanisms during histone to
protamine ex-change. Associated with the increased exchange of
nuclear proteins is a decrease in and cessation of gene transcription.
Thus, in spermatids gene transcription and protein translation are
temporally uncoupled, together with the temporal storage of mRNA in
spermatid-specific nucleoprotein complexes, which were described at
the ultrastructural level by Holstein and Roosen-Runge(1981).The
formation of the tail (flagellum) starts early in spermiogenesis. The
axoneme shows the typical “9+2” arrangement This is the common
pattern of eukaryotic cilia and derives from one of the pair of centrioles.
These centrioles are placed in a nuclear fossa opposite the acrosome.
The distal centriole gives rise to the flagellum. The other structures of
the flagellum, the fibrous sheet and outer dense fibres are developed
when spermiogenesis takes place.Mitochondria from the periphery of
the spermatid aggregate around the proximal part of the flagellum in a
helical manner forming the latter’s mid-piece. At the end, the
spermatid’s cytoplasm is shed by active involvement of the adjacent
Sertoli cell, and this “residual body” is phagocytosed by Sertoli cells.
The events described occur either simultaneously or with a degree of
overlap. For practical reasons, depending on the development and
formation of the acrosome, the whole process of spermiogenesis can be
divided as follows:

■ Golgi phase - Development of the acrosome vesicle

■ Cap phase - Formation of the acrosomal cap together with the start of
nuclear condensation and development of the flagellum
■ Acrosome phase - Differentiation of the acrosome, and elongation of
the nucleus and cell body
■ Maturation phase - Differentiation of the species-specific form of
the acrosome and sperm head; completion of nuclear condensation, and
the reduction of cytoplasm. The release of fully differentiated
spermatids into the lumen of the seminiferous tubule, which is triggered
by the Sertoli cell, is termed “spermiation”. The haploid germ cell
within the seminiferous epithelium is termed the “spermatid” (round,
elongating,elongated). The haploid germ cell after spermiation is a
“spermatozoon” (sperm).
SPERMATOZOON
The length of the human spermatozoon measures about 60 µm. The flat
and oval head (diameter: 3 µm,length: 5 µm) consists of the acrosome
and the extremely condensed nucleus. The acrosome covers the head
surface, and contains numerous proteolytic enzymes, i.e. hyaluronidase,
collagenase, neuraminidase, phospholipase A, acrosin and others. The
release of these enzymes, the so-called acrosome reaction, enables the
spermatozoon to penetrate the “corona radiata” of follicle cells and the
zona pellucida of the egg. Some nuclear vacuoles are common. The
flagellum measures about 55 µm in length. It possesses the central
axoneme and is divided into:
■ The neck/connecting piece (1 µm). It contains the basal and striated
bodies and is the point of articulation between the sperm head and the
flagellum.
■ The mid-piece (6 µm). It contains the mitochondria and the nine
doublets of microtubules, which are associated with outer dense fibres,
each consisting of at least 14 polypeptides. Outer dense fibres are
believed to maintain the passive elastic structure for flagellar bending
and also to protect it from shearing forces during epididymal transit and
ejaculation.
■ The principal piece (45 µm). In addition to the outer dense fibres, the
flagellum contains a fibrous sheet.
■ The end-piece (5 µm) only contains microtubules . Spermatozoa
acquire motility during epididymal passage and their competence for
fertilization during the passage of the female genital tract (capacitation).
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