PHYSIOLOGY
AS THE SCIENCE.
BIOELECTRICAL
PHENOMENA IN NERVE CELLS.
Physiology is the
science about the regulation of organism vital activity in connection with the
external environment.
Tasks
of physiological subjects – a deep studying of the mechanisms of vital activity
of health man with the matter of expose the causes and characters‘breaches
of thease mechanisms in different diseases.
Connection of physiology with other
sciences
Connection
of physiology with anatomy course – the names, localization, functions of
nerves, muscles, bones, vessels, inner organs, endocrine glands; with histology
– the structure of nerves, muscles, bones, vessels, inner organs, endocrine
glands; with chemistry – osmotic and oncotic pressure, gradient of
concentration, with physics – electroconductivity,
with biology – blood groups inheridity. This is the
connection of physiology with the subject has been studied. The physiology is
necessary for pathologic physiology, pathologic anatomy, surgery, obstetric,
therapy.
Method of physiology
a)
Observation (This is the method in which the scientists don‘t mix in course of
vital processes. They only make use of vision and description of all changes.
On the base of this changes they make conclusions.)
b)
Experiment (There are two kinds of experiments: acute and chronic. Acute
experiment was doing with the helps of anesthesia. It
may be accompanied by cut off the nerves, introduction the different
substances. The chronic experiment was doing in vital animals, for example,
after the acute experiment scientists can used the observation.)
c)
Examination (This is the method of examine the patient with different diseases,
for example, with using the different apparatuses.)
d)
Simulation (We can simulation different processes as a laboratory simulation or
realistic simulation, for example, apparatus of artificial kidney or apparatus
of artificial circulation. It may be the simulation the different processes by
means of computers.)
History of physiology development
a)
Till 17 century (The first medicine used the knowledge about function of health
and ill person and animal, which was based on the observation method. This
summarizing of receiving results was doing by Hippocrates, Gallen,
Aristotel, Ibn Sina (Avicenna). One of the doctor was Akmean.
He come to the conclusion that brain is the organ of consciousness and answer
for memory, thought, filling. Empedocl determined
that the breathing are doing not only by nose and mouth, but through skin too. Pracsagor distinguished the arterial and venous vessels,
but it thought that they have air. Gallen considered
that arteries had blood, established the knowledge about the breathing,
described the nerves.)
b)
In 17-18 centuris (Garvey in 1628 published the work
about the small and big circles of blood circulation and about the heart as a engine of blood. Decart was the
author of the first text-book “About the Man”, developed the theory of pain,
hunger, thirst, digestion, vision, memory. The high of his physiology
investigation was the description of the organism‘s reaction on the external
irritations. Prokhaska considered that the reflex act
may arise in internal and external stimulus. Levenguk
and Malpigy described the capillaries. This development
widen the vision on blood circulation. Discovering Azelly
and Bartolini lymphatic vessels maintain the lymph
circulation. Galvani put the bases of electric physiology.)
c)
From 19 century to our days (In 19 century physiology separated of anatomy and
became the independent science. Majandi studied the
physiology of nerves system. Bernar studied the
physiology mechanisms of development of digestive juice and their digestion
properties, the role of liver in supporting the sugar level in blood, meaning
of constant of pupils‘ internal surrounding. Yung worked out the three
component theory of color perception. Gelmgolths
developed this theory and creation the theory of hear perception. Phylomaphytsky worked out the theory of cyclic functioning
of nerves system. Phylomaphytsky and Basov worked the
operation of suturing the gastric fistula on dogs. Phylomaphytsky
and Pirogov worked the method of anesthesia
intravenous. Gering worked out the theory of the color vision. Gering and Braier described the reflex of nervus vagus, which control the breathing. Boydich formulated the “all or none” low, which say that
cardiac muscle can contract in full or noncontract. In 1846 Ludvig
described the theory of uropoiesis. Kennon created the doctrine about homeostasis. G.Selye studied the stress-syndrome.)
d)
Standing of physiology in
Cell Membrane
The
membrane that surrounds the cell is a remarkable structure. It is not only
semipermeable, allowing some substances to pass through it and excluding
others, but its permeability can be varied. It is generally referred to as the
plasma membrane. The nucleus is also surrounded by a membrane, and the
organelles are surrounded by or made up of membrane.
Although
the chemical structure of membranes and their properties vary onsiderably from one location to another, they have certain
common features. They are generally about 7,5 nm (75 Angstrom units) thick.
They are made up primarily of protein and lipids. The major lipids are phospholipids
such as phosphatidylcholine and phosphatidylethanolamine.
The head end of the molecule contains the phosphate portion, is positively
charged, and is quite soluble in water (polar, hydrophilic). The tails are
quite insoluble (nonpolar, hydrophobia). In the membrane, the hydrophilic ends
are exposed to the aqueous environment that bathes the exterior of the cells
and the aqueous cytoplasm; the hydrophobic ends meet in the water-poor interior
of the membrane. However, there is a degree of asymmetry in the distribution of
lipid in the membrane; in human red cells, for example, there is more phosphatidylethanolamine and phosphatidylserine
in the inner lamella and more lecithin and sphingomyelin
in me outer lamella. The significance of this asymmetry is unknown. In
prokaryotes (cells like bacteria in which there is no nucleus), phospholipids
are generally the only membrane lipids, but in eukaryotes (cells containing
nuclei), cell membranes also contain cholesterol (in animals) or other steroids
(in plants). The cholesterol/phospholipid ratio in the membrane is inversely
proportionate to the fluidity of the membrane. Variations in the ratio lead to
abnormalities of cell function. In healthy animals, the ratio is maintained at
a nearly constant level by a variety of regulatory mechanisms.
There
are many different proteins embedded in the membrane. They exist as separate
globular units and stud the inside and outside of the membrane in a random
array. Some are located in the inner surface of the membrane; some are located
on the outer surface; and some extend through the membrane (through and through
proteins). In general, the uncharged, hydrophobic portions of the protein
molecules are located in the interior of the membrane and the charged,
hydrophilic portions are located on the surfaces. Some of the proteins contain
lipids (lipoproteins) and some contain arbohydrates
(glycoproteins). There are 5 types of proteins in the membrane. In addition to
structural proteins, there are proteins that function as pumps, actively
transporting ions across the membrane. Other proteins function as passive
channels for ions that can be opened or closed by changes in the conformation
of the protein. A fourth group of proteins functions as receptors that bind
neurotransmitters and hormones, initiating physiologic changes inside the cell.
A fifth group functions as enzymes, catalyzing reactions at the surfaces of the
membrane.
The
protein structure – and particularly the enzyme content – of biologic membranes
varies not only from cell to cell but also within the same cell. For example,
there are different enzymes embedded in cell membranes than in mitochondrial
membranes; in epithelial cells, the enzymes in the cell membrane on the mucosal
surface differ from those in the cell membrane on the lateral margins of the
cells. The membranes are dynamic structures, and their constituents are being
constantly renewed at different rates. In addition, some proteins move
laterally in the membrane. For example, receptors move in the membrane and
aggregate at sites of endocytosis. There is evidence that the lateral movement
of components in the membrane is not random but is controlled by mtracellular mechanisms that probably involve
microfilaments and nucrotubules.
Underlying
most cells is a thin, fuzzy layer plus some fibrils that collectively make up
the basement membrane or, more properly, the basal lamina. The material that
makes up the basal lamina has been shown to be made up of a collagen derivative
plus 2 glycoproteins.
The
Sodium-Potassium Pump
The
sodium-potassium pump responsible for the coupled active transport of Na+ out
of cells and K+ into cells is a unique protein in the cell membrane Figure 1.
This protein is also an adenosine triphosphatase, ie, an enzyme that catalyzes the hydrolysis of ATP to
adenosine diphosphate (ADP), and it is activated by
Na+ and K+. Consequently, it is known as sodium-potassium-activated adenosine triphosphatase (Na+-K+ ATPase). The ATP provides the energy
for transport. The pump extrudes three Na+ from the cell for each two K+ it
takes into the cell, ie, it has a coupling ratio of
3/2. Its activity is inhibited by ouabain and related
digitalis glycosides used in the treatment of heart failure. It is made up of
two a subunits, each with a molecular weight of about 95,000, and two b
subunits, each with a molecular weight of about 40,000. Separation of the
subunits leads to loss of ATPase activity.
The
a subunits contain binding sites for ATP and ouabain,
whereas the b subunits are glycoproteins. Application of ATP by micropipette to
the inside of the membrane increases transport, whereas application of ATP to
the outside of the membrane has no effect. Conversely, ouabain
inhibits transport when applied to the outside but not to the inside of the
membrane. Consequently, the a subunits must extend through the cell membrane.
The protein could exist in 2 conformational states. In one, three Na+ bind to
sites accessible only from the inside of the membrane. This triggers hydrolysis
of ATP, and the protein changes its conformation so that the three Na+ are
extruded into the ECP. In the second conformation, two K+ bind to sites
accessible only from the outside of the membrane. This triggers a return to the
original conformation while extruding two K+ into the interior of the cell. It
appears that Na+ binding is associated with phosphorylation of the protein and
K+ binding with dephosphorylation.
Effects
of Na+ & K+ Transport
It
should be noted that since Na+-K+ ATPase transports three Na+ out of the cell
for each two K+ it transports in, it is an electrogenic
pump, ie, it produces net movement of positive charge
out of the cell. The amount of Na+ provided to the pump can be the
rate-limiting factor in its operation; consequently, the amount of Na+ extruded
by the cell is partly regulated in a feedback fashion by the amount of Na+ in
the cell.
The
enzyme described above is found in all parts of the body. In some tissues, the
active transport of Na+ is coupled to the transport of other substances
(secondary active transport). For example the membranes of mucosal cells in the
small intestine contain a cotransport protein (symport) that transports glucose into the cell only if Na+
binds to the protein and is transported down its electrochemical gradient at
the same time. The electrochemical gradient is maintained by the active
transport of Na+ out of the mucosal cell into ECF. Other nutrients are
reabsorbed in a similar fashion. In the brain transport by Na+-K+ ATPase is
coupled to the reuptake of neurotransmitters. In the heart Na+-K+ ATPase
indirectly affects Ca2+ transport because an exchange protein (antiport) in the membranes of cardiac muscle cells
exchanges intracellular Ca2+ for extracellular Na+ on an electrically neutral 1
for 2 basis. The rate of this exchange is proportionate to the concentration
gradient for Na+ across the cell membrane. If the operation of the Na+-K+
ATPase is inhibited (eg, by ouabam),
less intracellular Ca2+ is extruded and intracellular Ca2+ is increased. This
facilitates the contraction of cardiac muscle and is the probable explanation
of the positively inotropic effect of digitalis glycosides.
Active
transport of Na+ and K+ is one of the major energy-using processes in the body
and probably accounts for a large part of the basal metabolism. Furthermore,
there is a direct link between Na+ and K+ transport and metabolism; the greater
the rate of pumping, the more ADP is formed and the available supply of ADP
determines the rate at which ATP is formed by oxidative phosphorylation.
In
animals, the maintenance of normal cell volume and pressure depend on Na+ and
K+ pumping In the absence of such pumping, Cl- and
Na+ would enter the cells down their concentration gradients, and water would
follow along the osmotic gradient thus created, causing the cells to swell
until the pressure inside them balanced the influx. This does not occur, and
the osmolality of the cells remains the same as that of the interstitial fluid
because Na+ and K+ are actively transported. The membrane potential is
maintained, and [Cli- ], the Cl-
concentration inside the cells, remains low.
Proteins
closely related to Na+-K+ ATPase transport Ca2+ out of cells (Ca2+ ATPase) and
extrude H+ from cells in exchange for K+ (H+-K+ ATPase). No other extramitochondrial membrane pumps have been described that
can convert energy directly into transportation of ions against concentration
gradients, and all other known examples of net extrusion or accumulation of
substances across an animal cell membrane against a concentration gradient have
been attributed to secondary active transport, ie,
they depend on an electrochemical gradient created by Na+-K+ ATPase
In
certain situations proteins enter cells, and a number of hormones and other
substances secreted by cells are proteins or large polypeptides. Proteins and
other large molecules enter cells by the process of endocytosis and are
secreted by exocytosis. These processes provide an explanation of how large
molecules can enter and leave cells without disrupting cell membranes.
CELL
MEMBRANE & RESTING MEMBRANE POTENTIALS
Membrane
Potentials
There
is a potential difference across the membranes of most if not all cells, with
the inside of the cells negative to the exterior. By convention, this resting
membrane potential (steady potential) is written with a minus sign, signifying
that the inside is negative relative to the exterior. Its magnitude vanes
considerably from tissue to tissue, ranging from -9 to –100 mV
Cell
membranes are practically impermeable to intracellular protein and other
organic anions, which make up most of the intracellular anions and are usually
represented by the symbol A-. However, they are moderately permeable to Na+ and
rather freely permeable to Cl- and K+. K+
permeability is 50-100 times greater than Na+ permeability. Particle size
affects the movement of ions across cell membranes, and it should be noted that
the ions in the body are hydrated. Thus, although the atomic weight of
potassium (39) is greater than the atomic weight of sodium (23), the hydrated
sodium ion – ie, Na+ with its full complement of
water – is larger than the hydrated potassium ion. However, it is clear that
ions cross membranes via ion channels rather than simple pores. These channels
are usually passages through protein molecules, and charge configurations
around them and related variables make them relatively specific. Thus, for
example, there are separate Na+ channels, K+ channels, and Cl-
channels. The ease with which ions pass through some of these channels is controlled
(gated) by voltage or by agents such as neurotransmitters. Thus, for example,
passage of Na+ through the Na+ channels in excitable tissues (nerve and muscle)
is greatly increased by a decrease in membrane potential, ie,
they are voltage-gated. At synaptic junctions and elsewhere, many ion channels
are chemically gated, ie, their ability to pass ions
is increased by the binding of a given neurotransmitter or hormone to receptors
associated with them.
Latent
Period
If
the axon is stimulated and a conducted impulse occurs, a characteristic series
of potential changes is observed as the impulse passes the exterior electrode.
When the stimulus is applied, there is a brief irregular deflection of the
baseline, the stimulus artifact. This artifact is due to current leakage from
the stimulating electrodes to the recording electrodes. It usually occurs
despite careful shielding, but it is of value because it marks on the
cathode-ray screen the point at which the stimulus was applied.
The
stimulus artifact is followed by an isopotential
interval (latent period) that ends with the next potential change and
corresponds to the time it takes the impulse to travel along the axon from the
site of stimulation to the recording electrodes. Its duration is proportionate
to the distance between the stimulating and recording electrodes and the speed
of conduction of the axon. If the duration of the latent period and the
distance between the electrodes are known, the speed of conduction in the axon
can be calculated. For example, assume that the distance between the cathodal stimulating electrode and the exterior electrode
is
The
first manifestation of the approaching impulse is a beginning depolarization of
the membrane. After an initial 15 mV of depolarization, the rate of
depolarization increases. The point at which this change in rate occurs is
called the firing level. Thereafter, the tracing on the oscilloscope rapidly
reaches and overshoots the isopotential (zero
potential) line to approximately +35 mV. It then reverses and falls rapidly
toward the resting level. When repolarization is about 70 % completed, the rate
of repolarization decreases and the tracing approaches the resting level more
slowly. The sharp rise and rapid fall are the spike potential of the axon, and
the slower fall at the end of the process is the after-depolarization. After
reaching the previous resting level, the tracing overshoots slightly in the
hyperpolarizing direction to form the small but prolonged
after-hyperpolarization. The after-depolarization is sometimes called the
negative after-potential and the after-hyperpolarization the positive
after-potential, but the terms are now rarely used. The whole sequence of
potential changes is called the action potential. It is a monophasic action
potential because it is primarily in one direction. Before electrodes could be
inserted in the axons, the response was approximated by recording between an
electrode on intact membrane and an electrode on an area of nerve that had been
damaged by crushing, destroying the integrity of the membrane. The potential
difference between an intact area and such a damaged area is called a
demarcation potential.
The
proportions of the tracing are intentionally distorted to illustrate the
various components of the action potential. Note that the rise of the action
potential is so rapid that it fails to show clearly the change in
depolarization rate at the firing level, and also that the
after-hyperpolarization is only about 1-2 mV in amplitude although it lasts
about 40 ms. The duration of the afterdepolarization
is about 4 ms in this instance. It is shorter and less prominent in many other
neurons. Changes may occur in the after-polarization without changes in the
rest of the action potential. For example, if the nerve has been conducting
repetitively for a long time, the after-hyperpolarization is usually quite
large.
Conduction
in myelinated axons depends upon a similar pattern of
circular current flow. However, myelin is an effective insulator, and current
flow through it is negligible. Instead, depolarization in myelinated
axons jumps from one node of Ranvier to the next, with the current sink at the
active node serving to electrotonically depolarize to
the firing level the node ahead of the action potential. This jumping of
depolarization from node to node is called saltatory
conduction. It is a rapid process, and myelinated
axons conduct up to 50 times faster than the fastest unmyelinated
fibers. Indeed, myelination saves considerable space in the nervous system,
because in unmyelinated neurons conduction velocity
increases with the square root of the diameter of the axon, whereas in myelinated axons the conduction velocity increases directly
with the diameter of the axon. Thus, a nervous system made up of unmyelinated axons would have to be many times larger.
Resting membrane potential
a)
Common characteristic (There is a potential difference across the membranes of
most if not all cells, with the inside of the cells negative to the exterior.
By convention, this resting membrane potential (steady potential) is written
with a minus sign, signifying that the inside is negative relative to the
exterior. Its magnitude vanes considerably from tissue to tissue, ranging from
-9 to –100 mV. When 2 electrodes are connected through a suitable amplifier to
a CRO and placed on the surface of a single axon, no potential difference is
observed. However, if one electrode is inserted into the interior of the cell,
a constant potential difference is observed, with the inside negative relative
to the outside of the cell at rest. This
resting membrane potential is found in almost all cells. In neurons, it is
usually about –70 mV.)
b)
Mechanism of development (There are two kind of ion’s transport: active and
passive. Active transport is doing due to the energy of ATP. The sodium-potassium pump responsible for the coupled active transport of Na+
out of cells and K+ into cells is a unique protein in the cell
membrane. This protein is also an adenosine triphosphatase,
ie, an enzyme that catalyzes the hydrolysis of ATP to
adenosine diphosphate (ADP), and it is activated by
Na+ and K+. Consequently, it is known as sodium-potassium-activated adenosine triphosphatase (Na+-K+ ATPase). The
ATP provides the energy for transport. The pump extrudes three Na+
from the cell for each two K+ it takes into the cell, ie, it has a coupling ratio of 3/2. Its activity is
inhibited by ouabain and related digitalis glycosides
used in the treatment of heart failure. It is made up of two a subunits, each with a
molecular weight of about 95,000, and two b subunits,
each with a molecular weight of about 40,000. Separation of the subunits leads
to loss of ATPase activity. The a subunits contain
binding sites for ATP and ouabain, whereas the b subunits are glycoproteins.
Application of ATP by micropipette to the inside of the membrane increases
transport, whereas application of ATP to the outside of the membrane has no
effect. Conversely, ouabain inhibits transport when
applied to the outside but not to the inside of the membrane. Consequently, the
a subunits must
extend through the cell membrane. The protein could exist in 2 conformational
states. In one, three Na+ bind to sites accessible only from the
inside of the membrane. This triggers hydrolysis of ATP, and the protein
changes its conformation so that the three Na+ are extruded into the
ECP. In the second conformation, two K+
bind to sites accessible only from the outside of the membrane. This triggers a
return to the original conformation while extruding two K+ into the
interior of the cell. It appears that Na+ binding is associated with
phosphorylation of the protein and K+
binding with dephosphorylation.)
Ionic
Basis of Resting Membrane Potential
In
nerves, as in other tissues, Na+ is actively transported out of the cell and K+
is actively transported in. K+ diffuses back out of the cell down its
concentration gradient, and Na+ diffuses back in, but since the permeability of
the membrane to K+ is much greater than it is to Na+ at rest, the passive K+
efflux is much greater than the passive Na+ influx. Since the membrane is
impermeable to most of the anions in the cell, the K+ efflux is not accompanied
by an equal flux of anions and the membrane is maintained in a polarized state,
with the outside positive relative to the inside.
In
nerve, as in other tissues, a slight decrease in resting membrane potential
leads to increased movement of K+ out of and C1- into the cell, restoring the
resting membrane potential. In nerve and muscle, however, there is a unique
change in the cell membrane when depolarization exceeds 7 mV. This change is a
voltage-dependent increase in membrane permeability to Na+, so that the closer
the membrane potential is to the firing level the greater the Na+ permeability.
The electrical and concentration gradients for Na+ are both directed inward.
During the local response, Na+ permeability is slightly increased, but K+
efflux is able to restore the potential to the resting value. When the firing
level is reached, permeability is great enough so that Na+ influx further
lowers the membrane potential and Na+ permeability is further increased. The
consequent Na+ influx swamps the repolarizing processes, and runaway
depolarization results, producing the spike potential.
The
equilibrium potential for Na+ in mammalian neurons, calculated by using the Nemst equation, is about +60 mV. With the great increase in
Na+ permeability at the start of the action potential, the membrane potential
approaches this value. It does not reach it, however, primarily because the
change in Na+ permeability is short-lived. Na+ permeability starts to return to
the resting value during the rising phase of the spike potential, and Na+
conductance is decreased during repolarization. In addition, the direction of
the electrical gradient for Na+ is reversed during the overshoot because the
membrane potential is reversed. These factors limit Na+ influx and help bring
about repolarization.
Another
important factor producing repolarization of the nerve membrane is the increase
in K+ permeability that follows the increase in Na+ permeability. The change in
K+ permeability starts more slowly and reaches a peak during the falling phase
of the action potential. The increase in permeability decreases the barrier to
K+ diffusion, and K+ consequently leaves the cell. The resulting net transfer
of positive charge out of the cell completes repolarization.
The
changes in membrane permeability during the action potential have been
documented in a number of ways, perhaps most clearly by the voltage clamp
technique. This research technique, the details of which are beyond the scope
of this book, has made it possible to measure changes in the conductance of
then membrane for various ions. The conductance of an ion is the reciprocal of
its electrical resistance in a membrane and is a measure of membrane
permeability to that ion. There is no change in C1- conductance. Decreasing the
external Na+ concentration decreases the size of the action potential but has
little effect on the resting membrane potential. The lack of much effect on the
resting membrane potential would be predicted from the Goldman equation, since
the permeability of the membrane to Na+ at rest is relatively low. Conversely,
increasing the external K+ concentration decreases the resting membrane
potential.
The
Na+ and K+ channels in the axon are separate, and both are voltage-gated. The
Na+ channel is a protein with a molecular weight of about 275,000 and a pore
diameter of about 0,5 nm. There are many charged groups on the surface of the
channel, and these groups shift when the channel moves from the closed to the
open position. Opening of the channel is also known as sodium channel
activation. The voltage differences across the membrane that cause the channel to
open also drive it more slowly into a special closed state called the
inactivated state. The channel remains in the inactivated state for a few
milliseconds before returning to the resting state. Na+ channels can be blocked
by a poison called tetrodotoxin (TTX) without
affecting the K+ channels. Conversely, the K+ channels can be blocked by tetraethylammonium (TEA) without any changes in Na+
conductance.
Although
Na+ enters the nerve cell and K+ leaves it during the action potential, the
number of ions involved is not large relative to the total numbers present. The
fact that the nerve gains Na+ and loses K+ during activity has been
demonstrated experimentally, but significant differences in ion concentrations
can be measured only after prolonged, repeated stimulation.
As
noted above, the after-depolarization and the after-hyperpolarization represent
restorative processes in the cell that are separate from those causing the
action potential. Relatively little is known about their origin. The
after-depolarization is reduced by agents that inhibit metabolism. The
after-hyperpolarization is also reduced, and it now seems clear that it is due
to the electrogenic action of the sodium pump. The
net flux of Na+ to the exterior hyperpolarizes the membrane until equilibrium
conditions are restored.
A
decrease in extracellular Ca2+ increases the excitability of nerve and muscle
cells by decreasing the amount of depolarization necessary to initiate the
changes in the Na+ and K+ conductance that produce the action potential.
Conversely, an increase in extracellular Ca2+ “stabilizes the membrane” by
decreasing excitability. The concentration and electrical gradients for Ca2+
are directed inward, and Ca2+ enters neurons during the action potential. The
early phase of Ca2+ entry is blocked by TTX, and it appears that even though
Na+ permeability is much greater than Ca2+ permeability, Ca2+ is entering via
the Na+ channels. An additional late phase of Ca2+ entry is unaffected by TTX
and TEA and apparently occurs via a separate voltage-sensitive Ca2+ pathway.
Ca2+ entering during the delayed phase plays an important role in the secretion
of synaptic transmitters, a Ca2+-dependent process. In addition, Ca2+ entry
contributes to depolarization, and in some instances in invertebrates it is
primarily responsible for the action potential.
The
central nervous system contains more than 100 billion neurons. Figure 1 shows a
typical neuron of a type found in the brain motor cortex. The incoming signals
enter the neuron through synapses mainly on the neuronal dendrites, but also on
the cell body. For different types of neurons, there may be only a few hundred
or as many as 200,000 such synaptic connections from the input fibers.
Conversely, the output signal travels by way of a single axon leaving the
neuron, but this axon has many separate branches to other parts of the nervous
system or peripheral body.
A
special feature of most synapses is that the signal normally passes only in the
forward direction (from axon to dendrites). This allows the signal to be
conducted in the required directions for performing necessary nervous
functions. We shall also see that the neurons are arranged into a multitude of
differently organized neural networks that determine the functions of the
nervous system.