ANIMAL PHYSIOLOGY

ASSIGNMENT

SUBMITTED BY –
Farheen Khan
Roll no –19MBS007
MSc. Biosciences
1st year (2nd semester)
Q1. Explain how the receptors in the semicircular canal
detect rotational acceleration and how the receptors in
the saccule and utricle detect linear acceleration.

Physiology of Equilibrium
There are two types of equilibrium (balance). Static equilibrium refers
to the maintenance of the position of the body (mainly the head) relative
to the force of gravity. Body movements that stimulate the receptors for
static equilibrium include tilting the head and linear acceleration or
deceleration, such as when the body is being moved in an elevator or in
a car that is speeding up or slowing down. Dynamic equilibrium is the
maintenance of body position (mainly the head) in response to rotational
acceleration or deceleration. Collectively, the receptor organs for
equilibrium are called the vestibular apparatus. These include the
saccule, utricle, and semicircular ducts.
Otolithic Organs: Saccule and Utricle
The walls of both the utricle and the saccule contain a small,thickened
region called a macula. The two maculae, which are perpendicular to
one another, are the receptors for static equilibrium. They provide
sensory information on the position of the head in space and are
essential for maintaining appropriate posture and balance. The maculae
also detect linear acceleration and deceleration. The maculae consist of
two kinds of cells: hair cells, which are the sensory receptors, and
supporting cells. Hair cells have on their surface 40–80 stereocilia
(which are actually microvilli) of graduated height, plus one kinocilium,
a conventional cilium anchored firmly to its basal body and extending
beyond the longest stereocilium. As in the cochlea, the stereocilia are
connected by tip links. Collectively, the stereocilia and kinocilium are
called a hair bundle. Scattered among the hair cells are columnar
supporting cells that probably secrete the thick, gelatinous, glycoprotein
layer, called the otolithic membrane, that rests on the hair cells. A layer
of dense calcium carbonate crystals, called otoliths extends over the
entire surface of the otolithic membrane. Because the otolithic
membrane sits on top of the macula, if you tilt your head forward, the
otolithic membrane is pulled by gravity. It slides “downhill” over the
hair cells in the direction of the tilt, bending the hair bundles. However,
if you are sitting upright in a car that suddenly jerks forward, the
otolithic membrane lags behind the head movement, pulls on the hair
bundles, and makes them bend in the other direction. Bending of the
hair bundles in one direction stretches the tip links, which pull open
transduction channels, producing depolarizing receptor potentials;
bending in the opposite direction closes the transduction channels and
produces hyperpolarization. As the hair cells depolarize and repolarize,
they release neurotransmitter at a faster or slower rate. The hair cells
with first-order sensory neurons in the vestibular branch of the
vestibulocochlear (VIII) nerve. These neurons fire impulses at a slow or
rapid pace depending on the amount of neurotransmitter present. Motor
neurons also synapse with the hair cells and sensory neurons. Evidently,
the motor neurons regulate the sensitivity of the hair cells and sensory
neurons.
Semicircular Ducts
The three semicircular ducts function in dynamic equilibrium. The
ducts lie at right angles to one another in three planes: The two vertical
ducts are the anterior and posterior semicircular ducts, and the
horizontal one is the lateral semicircular duct. This positioning permits
detection of rotational acceleration or deceleration. In the ampulla, the
dilated portion of each duct, is a small elevation called the crista. Each
crista contains a group of hair cells and supporting cells. Covering the
crista is a mass of gelatinous material called the cupula. When you
move your head, the attached semicircular ducts and hair cells move
with it. The endolymph within the ampulla, however, is not attached and
lags behind. As the moving hair cells drag along the stationary
endolymph, the hair bundles bend. Bending of the hair bundles produces
receptor potentials. In turn, the receptor potentials lead to nerve
impulses that pass along the vestibular branch of the
vestibulocochlear(VIII) nerve.

RESPONSES TO ROTATIONAL ACCELERATION

Rotational acceleration in the plane of a given semicircular canal
stimulates its crista. The endolymph, because of its inertia is displaced
in a direction opposite to the direction of rotation. The fluid pushes on
the cupula, deforming it. This bends the processes of the hair cells.
When a constant speed of rotation is reached, the fluid spins at the same
rate as the body and the cupula swings back into the upright position.
When rotation is stopped, deceleration produces displacement of the
endolymph in the direction of the rotation, and the cupula is deformed
in a direction opposite to that during acceleration. It returns to mid
position in 25 to 30 s. Movement of the cupula in one direction
commonly causes an increase in the firing rate of single nerve fibers
from the crists, whereas movement in the opposite direction commonly
inhibits neural activity. Rotation causes maximal stimulation of the
semicircular canals most nearly in the plane of rotation. Because the
canals on one side of the head are a mirror image of those on the other
side, the endolymph is displaced toward the ampulla on one side and
away from it on the other. The pattern of stimulation reaching the brain
therefore varies with the direction as well as the plane of rotation.
Linear acceleration probably fails to displace the cupula and therefore
does not stimulate the cristae. However, there is considerable evidence
that when one part of the labyrinth is destroyed, other parts take over its
functions. The characteristic jerky movement of the eye observed at the
start and end of a period of rotation is called nystagmus. It is actually a
reflex that maintains visual fixation on stationary points while the body
rotates, although it is not initiated by visual impulses and is present in
blind individuals.

AMPULLARY RESPONSE TO ROTATION

RESPONSES TO LINEAR ACCELERATION

In mammals, the utricular and saccular maculae respond to linear
acceleration. In general, the utricle responds to horizontal acceleration
and the saccule to vertical acceleration. The otoliths are more dense than
the endolymph, and acceleration in any direction causes them to be
displaced in the opposite direction, distorting the hair cell processes and
generating activity in the nerve fibers. The maculae also discharge
tonically in the absence of head movement, because of the pull of
gravity on the otoliths. The impulses generated from these receptors are
partly responsible for labyrinth righting reflexes. These reflexes are a
series of responses integrated for the most part in the nuclei of the
midbrain. The stimulus for the reflex is tilting of the head, which
stimulates the otolithic organs; the response is compensatory contraction
of the neck muscles to keep the head level. In cats, dogs, and primates,
visual cues can initiate optical righting reflexes that right the animal in
the absence of labyrinthine or body stimulation. In humans, the
operation of these reflexes maintains the head in a stable position and
the eyes fixed on visual targets despite movements of the body and the
jerks and jolts of everyday life. The responses are initiated by vestibular
stimulation, stretching of neck muscles, and movement of visual images
on the retina, and the responses are the vestibulo-ocular reflex and other
remarkably precise reflex contractions of the neck and extraocular
muscles. Although most of the responses to stimulation of the maculae
are reflex in nature, vestibular impulses also reach the cerebral cortex.
These impulses are presumably responsible for conscious perception of
motion and supply part of the information necessary for orientation in
space. Vertigo is the sensation of rotation in the absence of actual
rotation and is a prominent symptom when one labyrinth is inflamed.
Q2. Discuss the gross neuroanatomy of the spinal chord.
SPINAL CORD ANATOMY
Protective Structures
Two types of connective tissue coverings—bony vertebrae and tough,
connective tissue meninges—plus a cushion of cerebrospinal fluid
(produced in the brain) surround and protect the delicate nervous tissue
of the spinal cord.
Vertebral Column
The spinal cord is located within the vertebral canal of the vertebral
column. The vertebral foramina of all the vertebrae, stacked one on top
of the other, form the vertebral canal. The surrounding vertebrae
provide a sturdy shelter for the enclosed spinal cord. The vertebral
ligaments, meninges, and cerebrospinal fluid provide additional
protection.
Meninges
The meninges are three connective tissue coverings that encircle the
spinal cord and brain. The spinal meninges surround the spinal cord
and are continuous with the cranial meninges, which encircle the
brain . The most superficial of the three spinal meninges, the dura mater
is composed of dense, irregular connective tissue. It forms a sac from
the level of the foramen magnum in the occipital bone, where it is
continuous with the dura mater of the brain, to the second sacral
vertebra. The spinal cord is also protected by a cushion of fat and
connective tissue located in the epidural space, a space between the dura
mater and the wall of the vertebral canal. The middle meninx is a
vascular covering called the arachnoid mater because of its spider’s web
arrangement of delicate collagen fibers and some elastic fibers. It is
deep to the dura mater and is continuous with the arachnoid mater of the
brain. Between the dura mater and the arachnoid mater is a thin
subdural space, which contains interstitial fluid. The innermost meninx
is the pia mater, a thin transparent connective tissue layer that adheres to
the surface of the spinal cord and brain. It consists of squamous to
cuboidal cells within interlacing bundles of collagen fibers and some
fine elastic fibers. Within the pia mater are many blood vessels that
supply oxygen and nutrients to the spinal cord. Between the arachnoid
mater and the pia mater is the sub-arachnoid space, which contains
cerebrospinal fluid that serves as a shock absorber and suspension
system for the spinal cord and brain. All three spinal meninges cover
the spinal nerve roots up to the point where they exit the spinal column
through the intervertebral foramina. Triangular-shaped membranous
extensions of the pia mater suspend the spinal cord in the middle of its
dural sheath. These extensions, called denticulate ligaments are
thickenings of the pia mater. They project laterally and fuse with the
arachnoid mater and inner surface of the dura mater between the
anterior and posterior nerve roots of spinal nerves on either side.
Extending all along the length of the spinal cord, the denticulate
ligaments protect the spinal cord against sudden displacement that could
result in shock.
External Anatomy of the Spinal Cord
The spinal cord, although roughly cylindrical, is flattened slightly
anteriorly and posteriorly. In adults, it extends from the medulla
oblongata, the inferior part of the brain, to the superior border of the
second lumbar vertebra . In newborn infants, it extends to the third or
fourth lumbar vertebra. During early childhood, both the spinal cord and
the vertebral column grow longer as part of overall body growth.
Elongation of the spinal cord stops around age 4 or 5, but growth of the
vertebral column continues. Thus, the spinal cord does not extend the
entire length of the adult vertebral column.The length of the adult spinal
cord ranges from 42 to 45 cm(16–18 in.). Its diameter is about 2 cm
(0.75 in.) in the midathoracic region, somewhat larger in the lower
cervical and midlumbar regions, and smallest at the inferior tip. When
the spinal cord is viewed externally, two conspicuous enlargements can
be seen. The superior enlargement, the cervical enlargement, extends
from the fourth cervical vertebra to the first thoracic vertebra. Nerves to
and from the upper limbs arise from the cervical enlargement. The
inferior enlargement, called the lumbar enlargement, extends from the
ninth to the twelfth thoracic vertebra. Nerves to and from the lower
limbs arise from the lumbar enlargement. Inferior to the lumbar
enlargement, the spinal cord terminates as a tapering, conical structure
called the conus medullaris, which ends at the level of the intervertebral
disc between the first and second lumbar vertebrae in adults. Arising
from the conus medullaris is the filum terminale an extension of the pia
mater that extends inferiorly and blends with the arachnoid mater and
dura mater and anchors the spinal cord to the coccyx.
Spinal nerves are the paths of communication between the spinal cord
and specific regions of the body. The spinal cord appears to be
segmented because the 31 pairs of spinal nerves emerge at regular
intervals from intervertebral foramina . Indeed, each pair of spinal
nerves is said to arise from a spinal segment. Within the spinal cord
there is no obvious segmentation but, for convenience, the naming of
spinal nerve based on the segment in which they are located. There are
8 pairs of cervical nerves( C1–C8), 12 pairs of thoracic nerves (T1–
T12), 5 pairs of lumbar nerves (L1–L5), 5 pairs of sacral nerves (S1–
S5), and 1 pair of coccygeal nerves (Co1). Spinal nerves C1–C7 exit the
vertebral canal above their corresponding vertebrae. Spinal nerve C8
exits the vertebral canal between vertebrae C7 and T1. Spinal nerves
T1–L5 exit the vertebral canal below their corresponding vertebrae.
From the spinal cord, the roots of the sacral spinal nerves (S1–S5) and
the coccygeal spinal nerves (Co1) enter the sacral canal, the part of the
vertebral canal in the sacrum. Subsequently, spinal nerves S1–S4 exit
the sacral canal via the four pairs of anterior and posterior sacral
foramina and spinal nerves S5 and Co1 exit the sacral canal via the
sacral hiatus. Because the spinal cord is shorter than the vertebral
column, nerves that arise from the lumbar, sacral, and coccygeal regions
of the spinal cord do not leave the vertebral column at the same level
they exit the cord. The roots of these spinal nerves angle inferiorly in
the vertebral canal from the end of the spinal cord like wisps of hair.
Appropriately, the roots of these nerves are collectively named the
cauda equina meaning “horse’s tail” . Two bundles of axons, called
roots, connect each spinal nerve to a segment of the cord by even
smaller bundles of axons called rootlets. The posterior (dorsal) root
and rootlets contain only sensory axons, which conduct nerve impulses
from sensory receptors in the skin, muscles, and internal organs into the
central nervous system. Each posterior root has a swelling, the posterior
root ganglion, which contains the cell bodies of sensory neurons. The
anterior (ventral) root and rootlets contain axons of motor neurons,
which conduct nerve impulses from the CNS to effectors (muscles and
glands).
Internal Anatomy of the Spinal Cord
A freshly dissected section of the spinal cord reveals regions of white
matter that surround an inner core of gray matter. The white matter of
the spinal cord consists primarily of bundles of myelinated axons of
neurons. Two grooves penetrate the white matter of the spinal cord and
divide it into right and left sides. The anterior median fissure is a wide
groove on the anterior side. The posterior median sulcus is a narrow
furrow on the posterior side. The gray matter of the spinal cord is
shaped like the letter H or a butterfly; it consists of dendrites and cell
bodies of neurons, unmyelinated axons, and neuroglia. The gray
commissure forms the crossbar of the H. In the center of the gray
commissure is a small space called the central canal; it extends the
entire length of the spinal cord and is filled with cerebrospinal fluid. At
its superior end, the central canal is continuous with the fourth ventricle
in the medulla oblongata of the brain. Anterior to the gray commissure
is the anterior white commissure, which connects the white matter of the
right and left sides of the spinal cord. The gray matter on each side of
the spinal cord is subdivided into regions called horns. The posterior
gray horns contain cell bodies and axons of interneurons as well as
axons of incoming sensory neurons.The anterior gray horns contain
somatic motor nuclei, which are clusters of cell bodies of somatic motor
neurons that provide nerve impulses for contraction of skeletal muscles.
Between the posterior and anterior gray horns are the lateral gray horns,
which are present only in thoracic and upper lumbar segments of the
spinal cord. The lateral gray horns contain autonomic motor nuclei,
which are clusters of cell bodies of autonomic motor neurons that
regulate activity of cardiac muscle, smooth muscle, and glands. The
white matter of the spinal cord, like the gray matter, is organized into
regions. The anterior and posterior gray horns divide the white matter
on each side into three broad areas called anterior white columns,
posterior white columns, and lateral white columns. Each column in
turn contains distinct bundles of axons having a common origin or
destination and carrying similar information. These bundles, which may
extend long distances up or down the spinal cord, are called tracts.
Sensory(ascending) tracts consist of axons that conduct nerve impulses
toward the brain. Tracts consisting of axons that carry nerve impulses
from the brain are called motor (descending) tracts. Sensory and motor
tracts of the spinal cord are continuous with sensory and motor tracts in
the brain
Q3. Explain how light rays in the environment are
brought to a focus on the retina and the role of
accommodation in the process
The Formation of Images on the Retina

Because light rays diverge in all directions from their source, the set of
rays from each point in space that reach the pupil must be focused. The
formation of focused images on the photoreceptors of the retina depends
on the refraction (bending) of light by the cornea and the lens.The
cornea is responsible for most of the necessary refraction, a contribution
easily appreciated by considering the hazy out-of-focus images
experienced when swimming underwater. Water, unlike air, has a
refractive index close to that of the cornea; as a result, immersion in
water virtually eliminates the refraction that normally occurs at the
air/cornea interface. The lens has considerably less refractive power
than the cornea; however, the refraction supplied by the lens is
adjustable, allowing objects at various distances from the observer to be
brought into sharp focus on the retinal surface. Images focused on the
retina are inverted (upside down). They also undergo right-to-left
reversal; that is, light from the right side of an object strikes the left side
of the retina, and vice versa. The reason the world does not look
inverted and reversed is that the brain “learns” early in life to coordinate
visual images with the orientations of objects. The brain stores the
inverted and reversed images we acquired when we first reached for and
touched objects and interprets those visual images as being correctly
oriented in space. About 75% of the total refraction of light occurs at the
cornea. The lens provides the remaining 25% of focusing power and
also changes the focus to view near or distant objects. When an object is
6 m (20 ft) or more away from the viewer, the light rays reflected from
the object are nearly parallel to one another.The lens must bend these
parallel rays just enough so that they fall exactly focused on the central
fovea, where vision is sharpest. Because light rays that are reflected
from objects closer than 6 m (20 ft) are divergent rather than parallel.,
the rays must be refracted more if they are to be focused on the retina.
This additional refraction is accomplished through a process called
accommodation.
ACCOMMODATION
When the ciliary muscle is relaxed, parallel light rays striking the
optically normal (emmetropic) eye are brought to a focus on the retina.
As long as this relaxation is maintained, rays from objects closer than 6
m from the observer are brought to a focus behind the retina, and
consequently the objects appear blurred. The problem of bringing
diverging rays from close objects to a focus on the retina can be solved
by increasing the distance between the lens and the retina or by
increasing the curvature or refractive power of the lens. In bony fish, the
problem is solved by increasing the length of the eyeball, a solution
analogous to the manner in which the images of objects closer than 6 m
are focused on the film of a camera by moving the lens away from the
film. In mammals, the problem is solved by increasing the curvature of
the lens. The process by which the curvature of the lens is increased is
called accommodation. At rest, the lens is held under tension by the
lens ligaments. Because the lens substance is malleable and the lens
capsule has considerable elasticity, the lens is pulled into a flattened
shape. When the gaze is directed at a near object, the ciliary muscle
contracts. This decreases the distance between the edges of the ciliary
body and relaxes the lens ligaments, so that the lens springs into a more
convex shape. The change is greatest in the anterior surface of the lens.
In young individuals, the change in shape may add as many as 12
diopters to the refractive power of the eye. The relaxation of the lens
ligaments produced by contraction of the ciliary muscle is due partly to
the sphincter like action of the circular muscle fibers in the ciliary body
and partly to the contraction of longitudinal muscle fibers that attach
anteriorly, near the corneoscleral junction. When these fibers contract,
they pull the whole ciliary body forward and inward. This motion brings
the edges of the ciliary body closer together. Changes in
accommodation with age In addition to accommodation, the visual axes
converge and the pupil constricts when an individual looks at a near
object. This three-part response—accommodation, convergence of the
visual axes, and pupillary constriction—is called the near response.

Autonomic Control of Accommodation and Pupillary Aperture

Autonomic Nerves to the Eyes: The eye is innervated by both
parasympathetic and sympathetic nerve fibers. The parasympathetic
preganglionic fibers arise in the Edinger-Westphal nucleus (the visceral
nucleus portion of the third cranial nerve) and then pass in the third
nerve to the ciliary ganglion, which lies immediately behind the eye.
There, the preganglionic fibers synapse with postganglionic
parasympathetic neurons, which in turn send fibers through ciliary
nerves into the eyeball. These nerves excite the ciliary muscle that
controls focusing of the eye lens and the sphincter of the iris that
constricts the pupil.The sympathetic innervation of the eye originates in
the intermediolateral horn cells of the first thoracic segment of the
spinal cord. From there, sympathetic fibers enter the sympathetic chain
and pass upward to the superior cervical ganglion, where they synapse
with postganglionic neurons. Postganglionic sympathetic fibers from
these then spread along the surfaces of the carotid artery and
successively smaller arteries until they reach the eye. There, the
sympathetic fibers innervate the radial fibers of the iris (which open the
pupil) as well as several extraocular muscles of the eye.
Control of Accommodation (Focusing the Eyes)
The accommodation mechanism—that is, the mechanism that focuses
the lens system of the eye—is essential for a high degree of visual
acuity. Accommodation results from contraction or relaxation of the eye
ciliary muscle. Contraction causes increased refractive power of the
lens, and relaxation causes decreased power. How does a person adjust
accommodation to keep the eyes in focus all the time? Accommodation
of the lens is regulated by a negative feedback mechanism that
automatically adjusts the refractive power of the lens to achieve the
highest degree of visual acuity. When the eyes have been focused on
some far object and must then suddenly focus on a near object, the lens
usually accommodates for best acuity of vision within less than 1
second. Although the precise control mechanism that causes this rapid
and accurate focusing of the eye is unclear, some of the known features
are the following. First, when the eyes suddenly change distance of the
fixation point, the lens changes its strength in the proper direction to
achieve a new state of focus within a fraction of a second. Second,
different types of clues help to change the lens strength in the proper
direction:
1. Chromatic aberration appears to be important. That is, red light rays
focus slightly posteriorly to blue light rays because the lens bends blue
rays more than red rays. The eyes appear to be able to detect which of
these two types of rays is in better focus, and this clue relays
information to the accommodation mechanism whether to make the lens
stronger or weaker.
2. When the eyes fixate on a near object, the eyes must converge. The
neural mechanisms for convergence cause a simultaneous signal to
strengthen the lens of the eye.
3. Because the fovea lies in a hollowed-out depression that is slightly
deeper than the remainder of the retina, the clarity of focus in the depth
of the fovea is different from the clarity of focus on the edges. It has
been suggested that this also gives clues about which way the strength
of the lens needs to be changed.
4. It has been found that the degree of accommodation of the lens
oscillates slightly all the time at a frequency up to twice per second. The
visual image becomes clearer when the oscillation of the lens strength is
changing in the appropriate direction and becomes poorer when the lens
strength is changing in the wrong direction. This could give a rapid clue
as to which way the strength of the lens needs to change to provide
appropriate focus. The brain cortical areas that control accommodation
closely parallel those that control fixation movements of the eyes, with
analysis of the visual signals in Brodmann’s cortical areas 18 and 19
and transmission of motor signals to the ciliary muscle through the
pretectal area in the brain stem, then through the Edinger-Westphal
nucleus, and finally by way of parasympathetic nerve fibers to the eyes.
Accommodation & Aging
Accommodation is an active process, requiring muscular effort, and can
therefore be tiring. Indeed, the ciliary muscle is one of the most used
muscles in the body. The degree to which the lens curvature can be
increased is limited, and light rays from an object very near the
individual cannot be brought to a focus on the retina, even with the
greatest of effort. The nearest point to the eye at which an object can be
brought into clear focus by accommodation is called the near point of
vision. The near point recedes throughout life, slowly at first and then
rapidly with advancing age, from approximately 9 cm at age 10 to
approximately 83 cm at age 60. This recession is due principally to
increasing hardness of the lens, with a resulting loss of accommodation
due to the steady decrease in the degree to which the curvature of the
lens can be increased. By the time a normal individual reaches age 40–
45, the loss of accommodation is usually sufficient to make reading and
close work difficult. This condition, which is known as presbyopia, can
be corrected by wearing glasses with convex lenses. As a person grows
older, the lens grows larger and thicker and becomes far less elastic,
partly because of progressive denaturation of the lens proteins. The
ability of the lens to change shape decreases with age. The power of
accommodation decreases from about 14 diopters in a child to less than
2 diopters by the time a person reaches 45 to 50 years; it then decreases
to essentially 0 diopters at age 70 years. Thereafter, the lens remains
almost totally nonaccommodating, a condition known as “presbyopia.”
Once a person has reached the state of presbyopia, each eye remains
focused permanently at an almost constant distance; this distance
depends on the physical characteristics of each person’s eyes. The eyes
can no longer accommodate for both near and far vision. To see clearly
both in the distance and nearby, an older person must wear bifocal
glasses with the upper segment focused for far-seeing and the lower
segment focused for near-seeing (e.g., for reading).
Horner’s Syndrome
The sympathetic nerves to the eye are occasionally interrupted.
Interruption frequently occurs in the cervical sympathetic chain. This
causes the clinical condition called Horner’s syndrome, which consists
of the following effects: First, because of interruption of sympathetic
nerve fibers to the pupillary dilator muscle, the pupil remains
persistently constricted to a smaller diameter than the pupil of the
opposite eye. Second, the superior eyelid droops because it is normally
maintained in an open position during waking hours partly by
contraction of smooth muscle fibers embedded in the superior eyelid
and innervated by the sympathetics. Therefore, destruction of the
sympathetic nerves makes it impossible to open the superior eyelid as
widely as normally. Third, the blood vessels on the corresponding side
of the face and head become persistently dilated. Fourth, sweating
(which requires sympathetic nerve signals) cannot occur on the side of
the face and head affected by Horner’s syndrome.

Q4.Destinguish between myelinated and unmyelinated

neurons.Describe the chemical nature of myelin and
summarize the differences in the ways in which myelinated
and unmyelinated neurons conduct nerve impulses.

BASIS OF MYELINATED NERVE UNMYELINATED

COMPARISO FIBER   NERVE FIBER
N
Description Myelinated Nerve Fibers are Unmyelinated Nerve
nerve fibers that are fibers are nerve fibers
insulated by a myelin sheath. that do not have a
myelin sheath. 
Color The myelinated nerve fibers The unmyelinated
are white in color.   nerve fibers are gray
in color.  
Nodes of The myelinated nerve fibers Unmyelinated nerve
Ranvier have nodes of Ranvier.   fibers do not have
nodes of Ranvier.
Speed of Due to presence of nodes of Unmyelinated nerve
Transmission Ranvier on myelinated nerve fibers do not have
fibers, the speed of myelin insulations,
transmission of nerve and therefore, the
impulses is high in speed of the
myelinated nerve fibers.  transmission of the
nerve impulses is low.
Location Most neurons in the central Unmyelinated
and peripheral nervous neurons can be found
system are myelinated in both the peripheral
because they require fast and central nervous
conduction speed such as system in the group c
neuron involved in spinal nerve fibers,
reflexes. responsible for
transmission of
secondary pain or
itch.  
Impulse Due to presence of myelin Unmyelinated nerve
Conduction sheath, myelinated nerves do fibers can lose the
not lose the impulse during nerve impulse during
conduction conduction.  
Axons The nerve fibers with long The short axon nerve
axons are myelinated. fibers are
unmyelinated.  

Myelinated Nerve Fiber

Nerve fiber which is insulated by myelin sheath is called myelinated
nerve fibers. Axons surrounded by a multilayered lipid and protein
covering, called the myelin sheath, are said to be myelinated. The sheath
electrically insulates the axon of a neuron and increases the speed of
nerve impulse conduction. Axons without such a covering are said to be
unmyelinated
MYELIN SHEATH
Myelin sheath is a thick lipoprotein sheath that insulates the myelinated
nerve fiber. Myelin sheath is not a continuous sheath. It is absent at
regular intervals. The area where myelin sheath is absent is called nodes
of Ranvier. Segment of the nerve fiber between two nodes is called
internode. Myelin sheath is responsible for white color of nerve fibers.
Chemistry of Myelin Sheath
Myelin sheath is formed by concentric layers of proteins, alternating
with lipids. The lipids are cholesterol, lecithin and cerebroside
(sphingomyelin).
Formation of Myelin Sheath – Myelinogenesis
Formation of myelin sheath around the axon is called the
myelinogenesis. Two types of neuroglia produce myelin sheaths:
Schwann cells (in the PNS) and oligodendrocytes (in the CNS).
Schwann cells begin to form myelin sheaths around axons during fetal
development. Each Schwann cell wraps about 1 millimeter (1 mm - 0.04
in.) of a single axon’s length by spiraling many times around the axon.
Eventually, multiple layers of glial plasma memmbrane surround the
axon, with the Schwann cell’s cytoplasm and nucleus forming the
outermost layer. The inner portion, consisting of up to 100 layers of
Schwann cell membrane, is the myelin sheath. The outer nucleated
cytoplasmic layer of the Schwann cell, which encloses the myelin
sheath, is the neurolemma (sheath of Schwann). A neurolemma is found
only around axons in the PNS. When an axon is injured, the
neurolemma aids regeneration by forming a regeneration tube that
guides and stimulates regrowth of the axon. Gaps in the myelin sheath,
called nodes of Ranvier , appear at intervals along the axon. Each
Schwann cell wraps one axon segment between two nodes. In the CNS,
an oligodendrocyte myelinates parts of several axons. Each
oligodendrocyte puts forth about 15 broad, flat processes that spiral
around CNS axons, forming a myelin sheath. A neurolemma is not
present, however, because the oligodendrocyte cell body and nucleus do
not envelop the axon. Nodes of Ranvier are present, but they are fewer
in number. Axons in the CNS display little regrowth after injury. This is
thought to be due, in part, to the absence of a neurolemma, and in part to
an inhibitory influence exerted by the oligodendrocytes on axon
regrowth. The amount of myelin increases from birth to maturity, and
its presence greatly increases the speed of nerve impulse conduction. An
infant’s responses to stimuli are neither as rapid nor as coordinated as
those of an older child or an adult, in part because myelination is still in
progress during infancy.
Functions of Myelin Sheath
1. Faster conduction
Myelin sheath is responsible for faster conduction of impulse through
the nerve fibers. In myelinated nerve fibers, the impulses jump from one
node to another node. This type of transmission of impulses is called
saltatory conduction
2. Insulating capacity
Myelin sheath has a high insulating capacity. Because of this quality,
myelin sheath restricts the nerve impulse within single nerve fiber and
prevents the stimulation of neighboring nerve fibers
CONDUCTION OF NERVE IMPULSES
Propagation of the Action Potential
The action potential is initiated at the beginning of the axon, at what is
called the initial segment. There is a high density of voltage-gated
Na+ channels so that rapid depolarization can take place here. Going
down the length of the axon, the action potential is propagated because
more voltage-gated Na+ channels are opened as the depolarization
spreads. This spreading occurs because Na+ enters through the channel
and moves along the inside of the cell membrane. As the Na+ moves, or
flows, a short distance along the cell membrane, its positive charge
depolarizes a little more of the cell membrane. As that depolarization
spreads, new voltage-gated Na+ channels open and more ions rush into
the cell, spreading the depolarization a little fArther. Because voltage-
gated Na+ channels are inactivated at the peak of the depolarization,
they cannot be opened again for a brief time. Because of this,
depolarization spreading back toward previously opened channels has
no effect. The action potential must propagate toward the axon
terminals; as a result, the polarity of the neuron is maintained.
Propagation, as described above, applies to unmyelinated axons. When
myelination is present, the action potential propagates differently.
Continuous And Saltatory Action
There are two types of propagation: continuous conduction and saltatory
conduction. The type of action potential propagation described so far is
continuous conduction, which involves step-by-step depolarization and
repolarization of each adjacent segment of the plasma membrane. In
continuous conduction, ions flow through their voltage-gated channels
in each adjacent segment of the membrane. Note that the action
potential propagates only a relatively short distance in a few
milliseconds. Continuous conduction occurs in unmyelinated axons and
in muscle fibers.
Action potentials propagate more rapidly along myelinated axons than
along unmyelinated axons. Saltatory conduction, the special mode of
action potential propagation that occurs along myelinated axons, occurs
because of the uneven distribution of voltage-gated channels. Few
voltage-gated channels are present in regions where a myelin sheath
covers the axolemma. By contrast, at the nodes of Ranvier (where there
is no myelin sheath), the axolemma has many voltage-gated channels.
Hence, current carried by Na and K flows across the membrane mainly
at the nodes. When an action potential propagates along a myelinated
axon, an electric current (carried by ions) flows through the extracellular
fluid surrounding the myelin sheath and through the cytosol from one
node to the next. The action potential at the first node generates ionic
currents in the cytosol and extracellular fluid that depolarize the
membrane to threshold, opening voltage-gated Na channels at the
second node. The resulting ionic flow through the opened channels
constitutes an action potential at the second node. Then, the action
potential at the second node generates an ionic current that opens
voltage-gated Na,– channels at the third node, and so on. Each node
repolarizes after it depolarizes.
The flow of current across the membrane only at the nodes of Ranvier
has two consequences.
1. The action potential appears to “leap” from node to node as each
nodal area depolarizes to threshold, thus the name “saltatory.” Because
an action potential leaps across long segments of the myelinated
axolemma as current flows from one node to the next, it travels much
faster than it would in an unmyelinated axon of the same diameter.
2. Opening a smaller number of channels only at the nodes, rather than
many channels in each adjacent segment of membrane, represents a
more energy-efficient mode of conduction.Because only small regions
of the membrane depolarize and repolarize, minimal inflow of Na and
outflow of K occurs each time an action potential passes by. Thus, less
ATP is used by sodium–potassium pumps to maintain the low
intracellular concentration of Na and the low extracellular concentration
of K
Factors That Affect The Speed of Propagation
The speed of propagation of an action potential is affected by three
major factors: amount of myelination, axon diameter, and temperature.
1. Amount of myelination. As you have just learned, action potentials
propagate more rapidly along myelinated axons than along
unmyelinated axons.
2. Axon diameter. Larger-diameter axons propagate action potentials
faster than smaller ones due to their larger surface areas.
3. Temperature. Axons propagate action potentials at lower speeds
when cooled.