5. Synapses, Receptor Cells, and Brain
5Synapses,
Receptor Cells, and Brain
5.1 INTRODUCTION
The focus of this book is primarily the electric activity of
nerve and muscle and the extracellular electric and magnetic fields that they
generate. It is possible to undertake such a study without considering the
functional role of nerve and muscle in physiology. But without some life science
background, the reader's evaluation of electrophysiological signals would
necessarily be handicapped. For that reason, we have included an overview, with
appropriate terminology, of relevant topics in physiology. This chapter is
therefore devoted to a survey of the organization of the nervous system and its
main components. It is hoped that the reader will find it helpful for
understanding of the physiological function of the excitable tissues discussed
in other chapters, and to know what to look for elsewhere. For further study, we
suggest the following texts: Jewett and Rayner (1984); Kuffler, Nicholls, and
Martin (1984); Nunez (1981); Patton et al. (1989); Schmidt (1981); Shepherd
(1988); all of which appear in the list of references. A discussion
of the nervous system might logically begin with sensory cells located at the
periphery of the body. These cells initiate and conduct signals to the brain and
provide various sensory inputs such as vision, hearing, posture, and so on.
Providing information on the environment to the body, these peripheral cells
respond to stimuli with action pulses, which convey their information through
encoded signals. These signals are conducted axonally through ascending
pathways, across synapses, and finally to specific sites in the brain. Other
neural cells in the brain process the coded signals, and direct the actions of
muscles and other organs in response to the various sensory inputs. The entire
circuit is recognized as a reflex arc, a basic unit in the nervous
system. In some cases it is entirely automatic, and in others it is under
voluntary control. No neurons
run directly from the periphery to the brain. Normally the initiated signal is
relayed by several intermediate neural cells. The interconnection between
neurons, called the synapse, behaves as a simple switch but also has a
special role in information processing. The junction (synapse) between a neural
cell and the muscle that it innervates, called the neuromuscular
junction, has been particularly well studied and provides much of our
quantitative understanding about synapses. Since it is impossible to discuss the
structure of the nervous system without including synapses, we begin our
discussion with an examination of that topic.
5.2 SYNAPSES
5.2.1 Structure and Function of the Synapse
The function of the synapse is to transfer electric activity
(information) from one cell to another. The transfer can be from nerve to nerve
(neuro-neuro), or nerve to muscle (neuro-myo). The region between the pre- and
postsynaptic membrane is very narrow, only 30-50 nm. It is called the
synaptic cleft (or synaptic gap). Direct electric communication
between pre- and postjunctional cells does not take place; instead, a chemical
mediator is utilized. The sequence of events is as follows:
An action pulse reaches the terminal endings of the presynaptic cell.
A neurotransmitter is released, which diffuses across the synaptic gap to
bind to receptors in specialized membranes of the postsynaptic cell.
The transmitter acts to open channels of one or several ion species,
resulting in a change in the transmembrane potential. If depolarizing,
it is an excitatory postsynaptic potential (EPSP); if
hyperpolarizing, an inhibitory postsynaptic potential (IPSP).
Figure 5.1 shows the synapse between a nerve and muscle cell, a
neuromuscular junction. In cardiac
muscle the intercellular space between abutting cells is spanned by gap
junctions, which provide a low-resistance path for the local circuit
currents and may be regarded as an electric (myo-myo) synapse. (The gap,
however, is not called a synaptic cleft.) This type of junction is
discussed in a later chapter. The
presynaptic nerve fiber endings are generally enlarged to form terminal
buttons or synaptic knobs. Inside these knobs are the vesicles that
contain the chemical transmitters. The arrival of the action pulse opens
voltage-gated Ca2+ channels that permit an influx of calcium ions.
These in turn trigger the release into the synaptic gap, by exocytosis,
of a number of the "prepackaged" vesicles containing the neurotransmitter.
On
average, each neuron divides into perhaps 1000 synaptic endings. On the other
hand, a single spinal motor neuron may have an average of 10,000 synaptic
inputs. Based on this data, it is not surprising that the ratio of synapse to
neurons in the human forebrain is estimated to be around 4×104. In
neuro-neuro synapses, the postjunctional site may be a dendrite or cell body,
but the former predominates.
Fig. 5.1. The neuromuscular (synaptic) junction. Many
features of this junction are also seen in the nerve-nerve synapse. The
terminal ending of the prejunctional cell contains many vesicles, which are
packages of the neurotransmitter acetylcholine (ACh). The gap between the pre-
and postjunctional membrane is on the order of 15-30 nm. The transmitter is
released by the arrival of an action impulse in the nerve; it diffuses and
binds to receptors on the postjunctional muscle membrane, bringing about an
EPSP and the initiation of a muscle action potential.
5.2.2 Excitatory and Inhibitory Synapses
In the neuromuscular junction, upon arrival of an action pulse
at the motor neuron ending, acetylcholine (ACh) is released into the
cleft. It diffuses across the gap to the muscle membrane where it binds to
specialized receptors, resulting in a simultaneous increase in membrane
permeability to both sodium and potassium ions. Because the relative effect on
sodium exceeds that of potassium (described quantitatively later in this
section), the membrane depolarizes and a postsynaptic action potential results.
The process is always excitatory. Furthermore, arrival of a single action
potential at the prejunctional site always results in sufficient release of
transmitter to produce a transthreshold depolarization and initiate an
action potential in the muscle. Synaptic
inhibition occurs at nerve-nerve (neuro-neuro) junctions when presynaptic
activity releases a transmitter that hyperpolarizes the postsynaptic membrane
(i.e., makes its membrane voltage more negative). In theory, hyperpolarization
could result from elevation of either potassium or chloride permeability because
the equilibrium potential of each is more negative than the normal resting
potential (which is influenced in the positive direction by the presence of
sodium). In actuality, however, inhibition is due to elevated chloride
permeability. In contrast with the neuromuscular (neuro-myo) junction, a single
excitatory input to a neuro-neuro synapse is completely inadequate to depolarize
the postjunctional membrane to threshold. In fact, with perhaps thousands of
both excitatory and inhibitory inputs on the postjunctional cell, a
spatial and temporal summation is continually taking place, and
the membrane voltage will fluctuate. When, finally, a threshold of perhaps 10-15
mV is reached, an action potential results. In this way, an important
integrative process takes place at the inputs to each nerve cell. The reader
with computer science experience can appreciate the tremendous possibilities for
information processing that can (and do!) take place, particularly when one
considers that there are perhaps 1012 neurons and 1015
synapses in the human brain. This is indeed a neural net. Presynaptic inhibition is another inhibition mechanism. In this
case an inhibitory nerve ending (from another axon known as the presynaptic
inhibitor) is synapsed to an excitatory presynaptic terminal. The
inhibitory nerve releases a transmitter that partially depolarizes the
presynaptic cell. As a consequence, activation arising in the presynaptic fiber
is diminished, hence the release of transmitter is reduced. As a result, the
degree of excitation produced in the postsynaptic cell is reduced (hence
an inhibitory effect). The
falling phase of the EPSP is characterized by a single time
constant - that is, the time required for the response to a single
excitatory stimulus to diminish to 1/e of its maximum. This is an
important value. If a sequence of afferent stimuli occurs in a very short time
interval, then temporal summation of the EPSPs occurs, yielding a growing
potential. Similarly, if activity occurs at more than one synaptic knob
simultaneously (or within the length of the aforementioned time constant), then
spatial summation results. The additive effect on a synapse is nonlinear.
Furthermore, the individual synapses interact in an extremely complicated way
(Stevens, 1968). Despite these complexities, it has been shown experimentally
that both spatial and temporal summation generally behave in a simple linear
manner (Granit, Haase, and Rutledge, 1960; Granit and Renkin, 1961). Synaptic
transmission has been compared to an electric information transfer circuit in
the following way: In the nerve axon the information is transferred by means of
nerve impulses in "digital" or, more accurately, "pulse-code modulated" form. In
the synapse, information is conducted with the transmitter substance in analog
form, to be converted again in the next neuron into "digital" form. Though this
analogy is not correct in all aspects, it illustrates the character of the
neural information chain.
5.2.3 Reflex Arc
The driver of a car receives visual signals via photoreceptors
that initiate coded afferent impulses that ascend nerve fibers and terminate in
the visual cortex. Once the brain has processed the information, it sends
efferent signals to the muscles in the foot and hands. Thus the car is slowed
down and can make a right turn. But if our hand is mistakenly brought to rest on
a hot surface, a set of signals to the hand and arm muscles result that are
not initiated in the higher centers; cognition comes into play only after
the fact. We say that a reflex path is involved in both of these
examples. The first is complex and involves higher centers in the central
nervous system, whereas the second describes a simpler reflex at a lower level.
In fact, a great deal of reflex activity is taking place at all times of
which we are unaware. For example, input signals are derived from internal
sensors, such as blood pressure, or oxygen saturation in the blood, and so on,
leading to an adjustment of heart rate, breathing rate, etc. The reflex
arc, illustrated above, is considered to be the basic unit of integrated
neural activity. It consists essentially of a sensory receptor, an afferent
neuron, one or more synapses, an efferent neuron, and a muscle or other
effector. The connection between afferent and efferent pathways is found,
generally, in the spinal cord or the brain. The simplest reflex involves only a
single synapse between afferent and efferent neurons (a monosynaptic
reflex); an example is the familiar knee jerk reflex. Homeostasis refers to the various regulatory processes in the
body that maintain a normal state in the face of disturbances. The autonomic
nervous system is organized to accomplish this automatically with regard to
many organs of the body; its activity, like that of the somatic nervous system,
is based on the reflex arc. In this case signals, which arise at visceral
receptors, are conveyed via afferent neurons to the central nervous system,
where integration takes place, resulting in efferent signals to visceral
effectors (in particular, smooth muscle) to restore or maintain normal
conditions. Integration of signals affecting blood pressure and respiration
takes place in the medulla oblongata; those controlling pupillary
response to light are integrated in the midbrain, whereas those
responding to body temperature are integrated in the hypothalamus - to
give only a few examples.
5.2.4 Electric Model of the Synapse
At the neuromuscular junction, Fatt and Katz (1951) showed that
acetylcholine significantly increases the permeability of the cell membrane to
small ions, whereas Takeuchi and Takeuchi (1960) demonstrated that chloride
conductance was unaffected (in fact, gCl 0).
What happens if the membrane becomes equally permeable to sodium and potassium
ions? Such a condition would alter the membrane potential from near the
potassium Nernst potential to a value that approximates the average of the
sodium and potassium equilibrium potentials. (This potential, in turn, is close
to zero transmembrane voltage and is entirely adequate to initiate an
activation.) If the postsynaptic region is voltage-clamped, the value that
reduces the membrane current to zero during transmitter release is called the
reversal voltage Vr. One can show that it equals the
average Nernst potential of sodium and potassium, as mentioned above. In the
neuromuscular junction in skeletal muscle, this reversal voltage is about -15
mV. The electric behavior at a synapse can be estimated by examining an
equivalent circuit of the postsynaptic membrane, such as that shown in Figure
5.2. Two regions are identified: One represents the membrane associated with
receptors sensitive to the transmitter, and the other the normal excitable
membrane of the cell. In Figure 5.2 these two regions are represented by
discrete elements, but in reality these are distributed along the structure that
constitutes the actual cell. This figure depicts a neuromuscular junction, where
the release of acetylcholine results in the elevation of sodium and potassium
conductance in the target region, which is in turn depicted by the closing of
the ACh switch. Upon closure of this switch,
DINa = DGNa(Vm -
VNa)
(5.1)
DIK = DGK(Vm -
VK)
(5.2)
where
INa, IK
=
sodium and potassium ion currents [µA/cm²]
DGNa, DGK
=
additional sodium and potassium conductances following activation by
ACh (i.e., nearly equal large conductances) [mS/cm²]
VNa, VK
=
the Nernst voltages corresponding to the sodium and potassium
concentrations [mV]
Vm
=
membrane voltage [mV]
Fig. 5.2. (A) Electric model of the postsynaptic cell
with excitatory synapse (a neuromuscular junction is specifically
represented). Most of the cell is bounded by normal excitable membrane, as
described on the left. In addition, a specialized postsynaptic region
(end-plate) exists that is sensitive to the chemical transmitter ACh. When the
ACh is released, it diffuses to receptor sites on the postjunctional membrane,
resulting in the opening of potassium and sodium gates. This effect is
mimicked in the model through closing of the switch, hence introducing the
high transmembrane potassium and sodium conductance (DGNa and DGK). (B) The corresponding model
with an inhibitory synapse.
If we now introduce and maintain the reversal voltage across
the postsynaptic membrane through a voltage clamp, Equations 5.1 and 5.2 are
replaced by:
DINa = DGNa(VR -
VNa)
(5.3)
DIK = DGK(VR -
VK)
(5.4)
since the transmembrane voltage Vm takes the
value VR, the reversal voltage. For the
conditions described by Equations 5.3 and 5.4, since the total current at the
reversal voltage is zero, it follows that the sodium and potassium ion currents
are equal and opposite in sign (i.e., DINa = -DIK). Consequently, applying this
condition to Equations 5.3 and 5.4 results in the following:
DGNa(VR -
VNa) = - DGK(VR -
VK)
(5.5)
Collecting terms in Equation 5.5 gives
(DGNa + DGK) VR = DGNaVNa - DGKVK
(5.6)
and solving for the reversal voltage results in
(5.7)
From Equation
5.7 it is easy to see that if the introduction of ACh causes an equal increase
in the sodium and potassium conductances - that is, if
(5.8)
then
(5.9)
as noted previously. For the frog's neuromuscular junction the
reversal voltage comes to around -25 mV. In practice, the reversal voltage is a
little closer to zero, which means that ACh increases the sodium conductance a
little more than it does the potassium conductance. It is also clear that the
increase of these sodium and potassium conductances must occur simultaneously.
The differences in the mechanisms of the membrane activation and synaptic
voltages are described in Table 5.1.
Table 5.1. Comparison of the mechanisms of membrane activation
with synaptic voltage change for the post-synaptic neuromuscular
junction.
Feature
Membrane region
Synaptic region
Early effect
depolarization
arrival of acetylcholine
Changes in membrane conductance during
-
rising phase
specific increase in GNa
simultaneous increase in GNa and
GK
-
falling phase
specific increase in GK
passive decay
Equilibrium voltage of active membrane
VNa = +50 mV
reversal voltage close to 0 mV
Other features
regenerative ascent followed by refractory
period
no evidence for regenerative action or
refractoriness
Pharmacology
blocked by TTX, not influenced by curare
blocked by curare, not influenced by
TTX
Source: After Kuffler, Nicholls and Martin,
1984.
Returning to
Figure 5.2, and applying Thevenin's theorem, we can simplify the receptor
circuit to consist of a single battery whose emf is the average of
VNa and VK (hence VR), and
with a conductivity gR = gNa +
gK. Its effect on the normal membrane of the postsynaptic cell
can be calculated since the total current at any node is necessarily zero - that
is, there are no applied currents. Consequently,
GR (Vm -
VR) + GK(Vm -
VK) + GNa(Vm -
VNa) = 0
(5.10)
The chloride path in Figure 5.2 is not included in Equation
5.10, since gCl 0 , as noted above. Solving for the postsynaptic potential
Vm results in
(5.11)
This expression is only approximate since the distributed
membrane is represented by a discrete (lumped) membrane. In addition, if the
membrane is brought to or beyond threshold, then the linear circuit
representation of Figure 5.2 becomes invalid. Nevertheless, Equation 5.11 should
be a useful measure of whether the postsynaptic potential is likely to result in
excitation of the postsynaptic cell.
5.3 RECEPTOR CELLS
5.3.1 Introduction
To begin the overview of the nervous system, we consider the
sensory inputs to the body and how they are initiated. There are many
specialized receptor cells, each characterized by a modality to which it is
particularly sensitive and to which it responds by generating a train of action
pulses. We are particularly interested in the structure and function of these
receptor cells and focus on the Pacinian corpuscle as an example.
5.3.2 Various Types of Receptor Cells
One of the most important properties required to maintain the
life of the living organism is the ability to react to external stimuli. Sense
organs are specialized for this task. The essential element of these organs is
the receptor cell, which responds to physical and chemical stimuli by sending
information to the central nervous system. In general, a receptor cell may
respond to several forms of energy, but each is specialized to respond primarily
to one particular type. For instance, the rods and cones in the
eye (photoreceptors) can respond to pressure, but they have a particularly low
threshold to electromagnetic energy in the certain frequency band of
electromagnetic radiation, namely visible light. In fact, they are the only
receptor cells with such low thresholds to light stimulus. There are at
least a dozen conscious sense modalities with which we are familiar. In
addition, there are other sensory receptors whose information processing goes on
without our awareness. Together these may be classified as (1)
extroreceptors, which sense stimuli arising external to the body; (2)
introreceptors, which respond to physical or chemical qualities within
the body; and (3) proprioceptors, which provide information on the body's
position. Examples in each of these categories include the following:
Extroreceptors
Photoreceptors in the retina for, vision
Chemoreceptors for sensing of smell and taste
Mechanoreceptors for sensing sound, in the cochlea, or in the
skin, for touch sensation
Thermoreceptors (i.e., Krause and Ruffini cells), for sensing
cold and heat
Introreceptors
Chemoreceptors in the carotid artery and aorta, responding to the
partial pressure of oxygen, and in the breathing center, responding to the
partial pressure of carbon dioxide
Mechanoreceptors in the labyrinth
Osmoreceptors in the hypothalamus, registering the osmotic
pressure of the blood
Proprioceptors
Muscle spindle, responding to changes in muscle length
Golgi tendon organ, measuring muscle tension
The sensory
receptor contains membrane regions that respond to one of the various forms of
incident stimuli by a depolarization (or hyperpolarization). In some cases the
receptor is actually part of the afferent neuron but, in others it consists of a
separate specialized cell. All receptor cells have a common feature: They are
transducers - that is, they change energy from one form to another. For
instance, the sense of touch in the skin arises from the conversion of
mechanical and/or thermal energy into the electric energy (ionic currents) of
the nerve impulse. In general, the receptor cells do not generate an activation
impulse themselves. Instead, they generate a gradually increasing potential,
which triggers activation of the afferent nerve fiber to which they are
connected. The electric events in receptors may be separated into two distinct
components:
Development of a receptor voltage, which is the graded response of
the receptor to the stimulus. It is the initial electric event in the
receptor.
Subsequent buildup of a generator voltage, which is the electric
phenomenon that triggers impulse propagation in the axon. It is the final
electric event before activation, which, in turn, follows the "all-or-nothing"
law.
These voltage
changes are, however, one and the same in a receptor such as the Pacinian
corpuscle, in which there are no specialized receptor cells. But in cases like
the retina where specialized receptor cells (i.e., the rods and cones) do exist,
these voltages are separate. In the following, we consider the Pacinian
corpuscle in more detail (Granit, 1955). Because the
neural output is carried in the form of all-or-nothing action pulses, we must
look to another form of signal than one that is amplitude modulated. In fact,
the generator or receptor potentials cause repetitive firing of action pulses on
the afferent neuron, and the firing rate (and rate of change) is reflective of
the sensory input. This coded signal can be characteristic of the modality being
transduced. In a process of adaptation, the frequency of action potential
firing decreases in time with respect to a steady stimulus. One can separate the
responses into fast and slow rates of adaptation, depending on how quickly the
frequency reduction takes place (i.e., muscle spindle is slow whereas touch is
fast).
5.3.3 The Pacinian Corpuscle
The Pacinian corpuscle is a touch receptor which, under the
microscope, resembles an onion (see Figure 5.3). It is 0.5-1 mm long and 0.3-0.7
mm thick and consists of several concentric layers. The center of the corpuscle
includes the core, where the unmyelinated terminal part of the afferent neuron
is located. The first node of Ranvier is also located inside the core. Several
mitochondria exist in the corpuscle, indicative of high energy production.
Fig. 5.3. The Pacinian corpuscle consists of a
myelinated sensory neuron whose terminal portion is unmyelinated. The
unmyelinated nerve ending and the first node lie within a connective tissue
capsule, as shown.
Werner R.
Loewenstein (1959) stimulated the corpuscle with a piezoelectric crystal and
measured the generator voltage (from the unmyelinated terminal axon) and the
action potential (from the nodes of Ranvier) with an external electrode. He
peeled off the layers of the corpuscle, and even after the last layer was
removed, the corpuscle generated signals similar to those observed with the
capsule intact (see recordings shown in Figure 5.4).
Fig. 5.4. Loewenstein's experiments with the Pacinian
corpuscle. (A) The normal response of the generator voltage for increasing
applied force (a)-(e). (B) The
layers of the corpuscle have been removed, leaving the nerve terminal intact.
The response to application of mechanical force is unchanged from A. (C) Partial
destruction of the core sheath does not change the response from A or B.
(D) Blocking the first node of Ranvier eliminates the initiation of
the activation process but does not interfere with the formation of the
generator voltage. (E)
Degeneration of the nerve ending prevents the creation of the generator
voltage.
The
generator voltage has properties similar to these of the excitatory
postsynaptic voltage. (The generator voltage is a graded response whereby a weak
stimulus generates a low generator voltage whereas a strong stimulus generates a
large generator voltage.) Even partial destruction of the corpuscle did not
prevent it from producing a generator voltage. But when Loewenstein destroyed
the nerve ending itself, a generator voltage could no longer be elicited. This
observation formed the basis for supposing that the transducer itself was
located in the nerve ending. The generator voltage does not propagate on the
nerve fiber (in fact, the nerve ending is electrically inexcitable) but, rather,
triggers the activation process in the first node of Ranvier by electrotonic
(passive) conduction. If the first node is blocked, no activation is initiated
in the nerve fiber. The ionic
flow mechanism underlying the generator (receptor) voltage is the same as that
for the excitatory postsynaptic voltage. Thus deformation of the Pacinian
corpuscle increases both the sodium and potassium conductances such that their
ratio (PNa/PK) increases and depolarization
of the membrane potential results. As a result, the following behavior is
observed:
Small (electrotonic) currents flow from the depolarized
unmyelinated region of the axon to the nodes of Ranvier.
On the unmyelinated membrane, local graded generator voltages are produced
independently at separate sites.
The aforementioned separate receptor voltages are summed in the first node
of Ranvier.
The summed receptor voltages, which exceed threshold at the first node of
Ranvier, generate an action impulse. This is evidence of spatial
summation, and is similar to the same phenomenon observed in the
excitatory postsynaptic potential.
5.4 ANATOMY AND PHYSIOLOGY OF THE BRAIN
5.4.1 Introduction
Action pulses generated at the distal end of sensory neurons
propagate first to the cell body and then onward, conveyed by long axonal
pathways. These ascend the spinal cord (dorsal root) until they reach the lower
part of the central nervous system. Here the signals are relayed to other
neurons, which in turn relay them onward. Three or four such relays take place
before the signals reach particular loci in the cerebral cortex. Signal
processing takes place at all levels, resulting in the state of awareness and
conscious recognition of the various signals that characterize human physiology.
The important integrative activity of the brain has been the subject of intense
study, but its complexity has slowed the rate of progress. In this section a
brief description is given of both the anatomy and the physiology of the brain.
5.4.2 Brain Anatomy
The brain consists of 1010-1011 neurons
that are very closely interconnected via axons and dendrites. The neurons
themselves are vastly outnumbered by glial cells. One neuron may receive stimuli
through synapses from as many as 103 to 105 other neurons
(Nunez, 1981). Embryologically the brain is formed when the front end of the
central neural system has folded. The brain consists of five main parts, as
described in Figure 5.5:
The cerebrum, including the two cerebral hemispheres
The interbrain (diencephalon)
The midbrain
The pons Varolii and cerebellum
The medulla oblongata
Fig. 5.5. The anatomy of the brain.
The entire
human brain weighs about 1500 g (Williams and Warwick, 1989). In the brain the
cerebrum is the largest part. The surface of the cerebrum is strongly
folded. These folds are divided into two hemispheres which are separated by a
deep fissure and connected by the corpus callosum. Existing within
the brain are three ventricles containing cerebrospinal fluid. The
hemispheres are divided into the following lobes: lobus frontalis, lobus
parietalis, lobus occipitalis, and lobus temporalis. The surface area
of the cerebrum is about 1600 cm², and its thickness is 3 mm. Six layers, or
laminae, each consisting of different neuronal types and populations, can
be observed in this surface layer. The higher cerebral functions, accurate
sensations, and the voluntary motor control of muscles are located in this
region. The interbrain or diencephalon is surrounded by the
cerebrum and is located around the third ventricle. It includes the
thalamus, which is a bridge connecting the sensory paths. The
hypothalamus, which is located in the lower part of the interbrain, is
important for the regulation of autonomic (involuntary) functions. Together with
the hypophysis, it regulates hormonal secretions. The midbrain is
a small part of the brain. The pons Varolii is an interconnection of
neural tracts; the cerebellum controls fine movement. The medulla
oblongata resembles the spinal cord to which it is immediately connected.
Many reflex centers, such as the vasomotor center and the breathing center, are
located in the medulla oblongata. In the
cerebral cortex one may locate many different areas of specialized brain
function (Penfield and Rasmussen, 1950; Kiloh, McComas, and Osselton, 1981). The
higher brain functions occur in the frontal lobe, the visual center is located
in the occipital lobe, and the sensory area and motor area are located on both
sides of the central fissure. There are specific areas in the sensory and motor
cortex whose elements correspond to certain parts of the body. The size of each
such area is proportional to the required accuracy of sensory or motor control.
These regions are described in Figure 5.6. Typically, the sensory areas
represented by the lips and the hands are large, and the areas represented by
the midbody and eyes are small. The visual center is located in a different part
of the brain. The motor area, the area represented by the hands and the speaking
organs, is large.
Fig. 5.6. The division of sensory (left) and motor (right)
functions in the cerebral cortex. (From Penfield and Rasmussen, 1950.)
5.4.3 Brain Function
Most of the information from the sensory organs is communicated
through the spinal cord to the brain. There are special tracts in both spinal
cord and brain for various modalities. For example, touch receptors in the trunk
synapse with interneurons in the dorsal horn of the spinal cord. These
interneurons (sometimes referred to as second sensory neurons) then usually
cross to the other side of the spinal cord and ascend the white matter of the
cord to the brain in the lateral spinothalamic tract. In the brain they synapse
again with a second group of interneurons (or third sensory neuron) in the
thalamus. The third sensory neurons connect to higher centers in the cerebral
cortex. In the area of vision, afferent fibers from the photoreceptors carry
signals to the brain stem through the optic nerve and optic tract to synapse in
the lateral geniculate body (a part of the thalamus). From here axons pass to
the occipital lobe of the cerebral cortex. In addition, branches of the axons of
the optic tract synapse with neurons in the zone between thalamus and midbrain
which is the pretectal nucleus and superior colliculus. These, in turn, synapse
with preganglionic parasympathetic neurons whose axons follow the oculomotor
nerve to the ciliary ganglion (located just behind the eyeball). The reflex loop
is closed by postganglionic fibers which pass along ciliary nerves to the iris
muscles (controlling pupil aperture) and to muscles controlling the lens
curvature (adjusting its refractive or focusing qualities). Other reflexes
concerned with head and/or eye movements may also be initiated. Motor signals
to muscles of the trunk and periphery from higher motor centers of the cerebral
cortex first travel along upper motor neurons to the medulla oblongata. From
here most of the axons of the upper motor neurons cross to the other side of the
central nervous system and descend the spinal cord in the lateral corticospinal
tract; the remainder travel down the cord in the anterior corticospinal tract.
The upper motor neurons eventually synapse with lower motor neurons in the
ventral horn of the spinal cord; the lower motor neurons complete the path to
the target muscles. Most reflex motor movements involve complex neural
integration and coordinate signals to the muscles involved in order to achieve a
smooth performance. Effective
integration of sensory information requires that this information be collected
at a single center. In the cerebral cortex, one can indeed locate specific areas
identified with specific sensory inputs (Penfield and Rasmussen, 1950; Kiloh,
McComas, and Osselton, 1981). While the afferent signals convey information
regarding stimulus strength, recognition of the modality depends on pinpointing
the anatomical classification of the afferent pathways. (This can be
demonstrated by interchanging the afferent fibers from, say, auditory and
tactile receptors, in which case sound inputs are perceived as of tactile origin
and vice versa.) The higher
brain functions take place in the frontal lobe, the visual center is in the
occipital lobe, the sensory area and motor area are located on both sides of the
central fissure. As described above, there is an area in the sensory cortex
whose elements correspond to each part of the body. In a similar way, a part of
the brain contains centers for generating command (efferent) signals for control
of the body's musculature. Here, too, one finds projections from specific
cortical areas to specific parts of the body.
5.5 CRANIAL NERVES
In the central nervous system there are 12 cranial
nerves. They leave directly from the cranium rather than the spinal cord.
They are listed in Table 5.2 along with their functions. The following cranial
nerves have special importance: the olfactory (I) and optic (II)
nerves, which carry sensory information from the nose and eye; and the
auditory-vestibular (VIII) nerve, which carries information from the ear
and the balance organ. Sensory information from the skin of the face and head is
carried by the trigeminal (V) nerve. Eye movements are controlled by
three cranial nerves (III, IV, and VI). The vagus nerve (X) controls
heart function and internal organs as well as blood vessels.
Table 5.2. The cranial nerves
Number
Name
Sensory/Motor
Functions
Origin or terminusin the
brain
I
olfactory
s
smell
cerebral hemispheres (ventral part)
II
optic
s
vision
thalamus
III
oculomotor
m
eye movement
midbrain
IV
trochlear
m
eye movement
midbrain
V
trigeminal
m
masticatory movements
midbrain and pons
s
sensitivity of face and tongue
medulla
VI
abducens
m
eye movements
medulla
VII
facial
m
facial movement
medulla
VIII
auditory
s
hearing
medulla
vestibular
s
balance
IX
glossopharyngeal
s,m
tongue and pharynx
medulla
X
vagus
s,m
heart, blood vessels, viscera
medulla
XI
spinal accessory
m
neck muscles and viscera
medulla
XII
hypoglossal
m
medulla
REFERENCES
Fatt P, Katz B (1951): An analysis of the end-plate potential
recorded with an intracellular electrode. J. Physiol. (Lond.) 115:
320-70.
Granit R, Haase J, Rutledge LT (1960): Recurrent inhibition in
relation to frequency of firing and limitation of discharge rate of extensor
motoneurons. J. Physiol. (Lond.) 154: 308-28.
Granit R, Renkin B (1961): Net depolarization and discharge
rate of motoneurons, as measured by recurrent inhibition. J. Physiol.
(Lond.) 158: 461-75.
Hille B (1970): Ionic channels in nerve membranes. Prog.
Biophys. Mol. Biol. 21: 1-32.
Loewenstein WR (1959): The generation of electric activity in a
nerve ending. Ann. N.Y. Acad. Sci. 81: 367-87.
Schmidt RF (ed.) (1981): Fundamentals of Sensory
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Stevens CF (1968): Synaptic physiology. Proc. IEEE
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membrane during the action of transmitter. J. Physiol. (Lond.) 154:
52-67.
REFERENCES, BOOKS
Granit R (1955): Receptors and Sensory Perception, 369
pp. Yale University Press, New Haven.
Hille B (1992): Ionic Channels of Excitable Membranes,
2nd ed., 607 pp. Sinauer Assoc., Sunderland, Mass. (1st ed., 1984)
Jewett DL, Rayner MD (1984): Basic Concepts of Neuronal
Function, 411 pp. Little Brown, Boston.
Kiloh LG, McComas AJ, Osselton JW (1981): Clinical
Electroencephalography, 4th ed., 239 pp. Butterworth, London.
Kuffler SW, Nicholls JG, Martin AR (1984): From Neuron to
Brain, 2nd ed., 651 pp. Sinauer Assoc., Sunderland, Mass.
Nunez PL (1981): Electric Fields of the Brain: The
Neurophysics of EEG, 484 pp. Oxford University Press, New York.
Patton HD, Fuchs AF, Hille B, Scher AM, Steiner R (eds.)
(1989): Textbook of Physiology, 21st ed., 1596 pp. W. B. Saunders,
Philadelphia.
Penfield W, Rasmussen T (1950): The Cerebral Cortex of Man:
A Clinical Study of Localization of Function, 248 pp. Macmillan, New York.
Schmidt RF (ed.) (1981): Fundamentals of Sensory
Physiology, 2nd ed., 286 pp. Springer-Verlag, New York, Heidelberg, Berlin.
Shepherd GM (1988): Neurobiology, 689 pp. Oxford
University Press, New York.
Williams PL, Warwick R (eds.) (1989): Gray's Anatomy,
37th ed., 1598 pp. Churchill Livingstone, Edinburgh.
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