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Saladin 5e Extended Outline
Chapter 12
Nervous Tissue
I. Overview of the Nervous System (pp. 442–443)
A. The study of the nervous system is neurobiology. (p. 442)
B. Two organ systems are dedicated to maintaining internal coordination: the endocrine system
and the nervous system. (p. 424) (Fig. 12.1)
C. The nervous system carries out its coordinating task in three basic steps. (p. 424)
1. Through sense organs and sensory nerve endings, it receives information about the
body and external environment and transmits messages to the spinal cord and brain.
2. The spinal cord and brain process this information, relate it to past experience, and
determine an appropriate response.
3. The spinal cord and brain issue commands to muscle and gland cells to carry out the
response.
C. The nervous system has two major anatomical subdivisions, the central nervous system and
peripheral nervous system; the latter has additional subdivisions. (pp. 442–443) (Fig. 12.2)
1. The central nervous system (CNS) consists of the brain and spinal cord, which are
enclosed and protected by the cranium and vertebral column.
a. Nerves emerge from the CNS through foramina in the skull and vertebral
column.
2. The peripheral nervous system (PNS) consists of all the nervous system except the
brain and spinal cord; it is composed of nerves and ganglia.
a. A nerve is a bundle of nerve fibers (axons) wrapped in connective tissue.
b. A ganglion (pl. ganglia) is a knotlike swelling in a nerve where the cell bodies
of neurons are concentrated.
3. The PNS is functionally divided into sensory and motor divisions.
a. The sensory (afferent) division carries sensory signals from receptors to the
CNS; this pathway informs the CNS of stimuli.
i. The somatic sensory division carries signals from receptors in the
skin, muscles, bones, and joints.
ii. The visceral sensory division carries signals from viscera of the
thoracic and abdominal cavities.
b. The motor (efferent) division carries signals from the CNS to gland and
muscle cells that carry out the body’s reponses; cells and organs that respond are
called effectors.
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i. The somatic motor division carries signals to the skeletal muscles,
producing muscular contractions that are under voluntary control as
well as involuntary contractions called somatic reflexes.
ii. The visceral motor division (autonomic nervous system) carries
signals to glands, cardiac muscle, and smooth muscle over which we
have no voluntary control; the responses are termed visceral reflexes.
c. The autonomic nervous system has two further divisions.
i. The sympathetic division tends to arouse the body for action; for
example, through accelerating the heartbeat and increasing respiratory
airflow and inhibiting digestion.
ii. The parasympathetic division tends to have a calming effect; for
example, slowing down the heartbeat and stimulating digestion.
II. Properties of Neurons (pp. 443–448)
A. Nerve cells, or neurons, have three fundamental physiological properties that enable them to
communicate with other cells. (pp. 443–444)
1. Excitability (irritability). All cells are excitable, that is, they respond to stimuli;
neurons have developed this property to the highest degree.
2. Conductivity. Neurons respond to stimuli by producing electrical signals that are
conducted to other cells.
3. Secretion. When the electrical signal reaches the end of a nerve fiber, the neuron
secretes a neurotransmitter that stimulates the next cell.
B. Neurons fall into three functional classes based on the three major aspects of nervous system
function. (p. 444) (Fig. 12.3)
1. Sensory (afferent) neurons are specialized to detect stimuli and transmit information
about them to the CNS. (Fig. 11.3a, b, d)
a. Sensory neurons begin in almost every organ of the body and end in the CNS.
b. Some receptors are themselves neurons, such as those for pain and smell; in
senses such as taste and hearing, the receptor is a separate cell that
communicates directly with a sensory neuron.
2. Interneurons (association neurons) lie entirely within the CNS.
a. They receive signals from many other neurons and carry out integrative
functions and “make decision” about response.
b. About 90% of neurons in the human body are interneurons.
c. The word interneuron refers to the fact that the lie between and interconnect
the the incoming sensory pathways and the outgoing motor pathways of the
CNS.
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3. Motor (efferent) neurons send signals predominantly to muscle and gland cells; they
are called motor neurons because most of them lead to muscle cells, and efferent because
they carry signals away from the CNS.
C. A motor neuron of the spinal cord illustrates general neuron structure. (pp. 444–447) (Fig. 12.4)
1. The control center is the soma, also called the neurosoma, cell body, or perikaryon.
a. It contains a single, centrally located nucleus with a large nucleolus.
b. The cytoplasm contains mitochondria, lysosomes, a Golgi complex, many
inclusions, and an extensive rough ER and cytoskeleton.
c. The cytoskeleton consists of a dense mesh of microtubules and neurofibrils,
bundles of actin filaments that compartmentalize the rough ER into darkstaining Nissl bodies. (Fig. 12.4c, d)
i. Nissl bodies are unique to neurons and help identify them in tissue
sections.
d. Mature neurons do not divide but have long lives; stem cells in the CNS,
however, can divide and develop into new neurons.
e. the major cytoplasmic inclusions are glycogen granules, lipid droplets,
melanin, and a golden brown pigment, lipofuscin.
i. Lipofuscin is produced when lysosomes digest worn-out organelles
and other products.
ii. Lipofuscin accumulates with age and pushes the nucleus to one side
of the cell; granules of lipofuscin are called wear-and-tear granules.
2. The soma gives rise to a few thick processes that branch into a vast number of
dendrites.
a. Dendrites are the primary site for receiving signals from other neurons.
b. Their number varies from one to thousands, depending on the neuron.
c. As tangled as multiple dendrites may seem, they provide highly precise
pathways.
3. The axon (nerve fiber) originates on a mound on the soma called the axon hillock.
a. The axon is cylindrical and relatively unbranched for most of its length,
although it may give rise to axon collaterals along the way.
b. Most axons branch extensively at their distal end.
c. An axon is specialized for rapid conduction of nerve signals to points remote
from the soma.
i. Its cytoplasm is the axoplasm and its membrane is the axolemma.
ii. A neuron never has more than one axon, and some have none.
iii. Schwann cells and a myelin sheath are associated with the axon.
(Fig. 12.4)
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d. Somas range from 5–135 μm in diameter, while axons range from 1–20 μm
and from a few millimeters to more than a meter in length.
e. At the distal end an axon usually has a terminal arborization of fine branches.
i. Each branch ends in a synaptic knob (terminal button) that forms a
junction (synapse) with the next cell.
ii. The synapse contains synaptic vesicles full of neurotransmitter.
4. Neuron structure varies, and they are classified according to the number of processes
extending from the stroma. (Fig. 12.5)
a. Multipolar neurons are those with one axon and multiple dendrites; they are
the most common type.
b. Bipolar neurons have one axon and one dendrite; examples include olfactory
cells, neurons of the retina, and sensory neurons of the inner ear.
c. Unipolar neurons have only a single process leading away from the soma;
they are represented by the neurons that carry sensory signals to the spinal cord.
i. They are also called pseudounipolar because they start out
embryonically as bipolar neurons but their two processes fuse as the
neuron matures.
ii. A short distance from the soma, the process branches like a T, with a
peripheral fiber bringing signals from a source of sensation and a
central fiber continuing into the spinal cord.
iii. The dendrites are the branching receptive endings; the rest of the
fiber is considered to be the axon because of the presence of myelin and
the sbility to produce action potentials.
d. Anaxonic neurons have multiple dendrites but no axon; they communicate
through their dendrites and do not produce action potentials, and some are found
in the brain, retina, and adrenal medulla.
D. Axonal transport refers to the passage of proteins, organelles, and other materials along an
axon, to and from the cell soma. (p. 447)
1. Movement from the soma down the axon is called anterograde transport, and
movement up the axon toward the soma is called retrograde transport.
2. Materials travel along microtubules of the cytoskeleton.
3. The motor protein for anterograde transport is kinesin; the motor protein for retrograde
transport is dynein. They act somewhat like the myosin heads of muscle to crawl along
the microtubules.
4. The two types of axonal transport are fast and slow.
a. Fast axonal transport occurs at a rate of 20 to 400 mm per day and may be
anterograde or retrograde.
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i. Fast anterograde transport moves mitochondria, synaptic vesicles,
other organelles, axolemma components, calcium ions, enzymes, etc.
toward the distal end of the axon.
ii. Fast retrograde transport returns used synaptic vesicles to the soma
and informs the soma of conditions at the axon terminals
iii. Some pathogens, such as the tetanus toxin and certain viruses
invade the nervous system by entering the distal tips of axons and being
transported to the soma by fast retrograde transport.
b. Slow axonal transport (axoplasmic flow) occurs at a rate of 0.5 to 10 mm per
day and is always anterograde.
i. Slow axonal transport moves enzymes and cytoskeletal components
down the axons, renews worn-out axoplasmic component in mature
neurons, and supplies new axoplasm for developing or regenerating
neurons.
ii. Damaged nerve fibers regenerate at a speed governed by slow axonal
transport.
III. Supportive Cells (Neuroglia) (pp. 448–453)
A. Neurons are outnumbered by as much as 50 to 1 by supportive cells called neuroglia, or glial
cells. Glia means glue, and one of the roles of these cells is to bind neurons and form a supportive
framework. (p. 448)
B. There are six types of neuroglia, each of which has a unique function; four types occur only in
the CNS (pp. 448–449) (Fig. 12.6) (Table 12.1)
1. Oligodendrocytes somewhat resemble an octopus with as many as 15 armlike
processes. (CNS)
a. Each process spirals around a nerve fiber like electrical tape, wrapping the
fiber with the insulating myelin sheath.
b. This sheath speeds up nerve conduction.
2. Ependymal cells resemble cuboidal epithelium lining internal cavities of the brain and
spinal cord; however, they have no basement membrane and have rootlike process that
penetrate the underlying tissues. (CNS)
a. Ependymal cells produce cerebrospinal fluid (CSF), which bathes the CNS
and fills its internal cavities.
b. These cells have cilia that helps to circulate CSF.
3. Microglia are small macrophages that develop from white blood cells called
monocytes; they wander through the CNS, constantly probing for cellular debris or other
problems. (CNS)
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a. They are thought to perform a complete checkup on the brain tissue several
times a day, phagocytizing dead tissue, microorganism, etc.
b. They become concentrated in areas damaged by infection, trauma, or stroke,
and pathologists look for clusters in brain tissue as a clue to injury.
4. Astrocytes are the most abundant glia and constitute over 90% of the tissue in some
brain areas; they are named for their many-branched starlike shape. They have the most
diverse functions of any glia. (CNS)
a. They form a supportive framework for nervous tissue.
b. They have extensions called perivascular feet that contact blood capillaries
and stimulate them to form a tight seal called the blood–brain barrier.
c. They convert blood glucose to lactate and supply it to the neurons.
d. They secrete nerve growth factors, proteins that promote neuron growth and
synapse formation.
e. They communicate electrically with neurons and may influence signaling.
f. They regulate the chemical composition of the tissue fluid, absorbing
neurotransmitters and potassium ions so that they do not reach excessive levels.
g. They form hardened scar tissue when neurons are damaged, a process called
astrocytosis or sclerosis.
5. Schwann cells envelope nerve fibers of the PNS. (PNS)
a. The Schwann cell winds repeatedly around a nerve fiber, producing a myelin
sheath similar to the one produced by oligodendrocytes in the CNS.
b. Schwann cells also assist in regeneration of damaged fibers.
6. Satellite cells surround the neurosomas in ganglia of the PNS; they provide electrical
insulation around the soma and regulate the chemical environment. (PNS).
Insight 12.1 Glial Cells and Brain Tumors
C. The myelin sheath is an insulating layer around a nerve fiber, somewhat like the rubber
insulation on a wire. (p. 450)
1. Because myelin is the plasma membrane of glial cells, its composition is like that of
the membrane with about 20% protein and 80% mixed lipids.
2. Production of the myelin sheath is called myelination; it begins in the fourteenth week
of fetal development, proceeds rapidly in infancy, and isn’t completed until late
adolescence.
a. Children under 2 years old must not be put on low-fat diets because this could
interfere with myelination.
3. In the PNS, a Schwann cell spirals repeatedly around a single nerve fiber, laying down
as many as a hundred compact layers of its membrane with almost no cytoplasm. (Fig.
12.7a)
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a. The Schwann cell spirals outward, finally ending with a thick outermost coil
called the neurilemma, which contains the body of the Schwann cell with its
nucleus and most of its cytoplasm.
b. External to the neurilemma is a basal lamina and then a thin sleeve of fibrous
connective tissue called the endoneurium.
4. In the CNS, each oligodendrocyte reaches out to myelinate several nerve fibers in its
immediate vicinity. (Fig. 12.7b)
a. Because it is anchored to multiple nerve fibers, it cannot migrate around them,
so it pushes newer layers of myelin under the older ones.
b. Myelination spirals inward toward the nerve fiber.
c. Nerve fibers of the CNS have no neurilemma or endoneurium.
5. In both the PNS and CNS, many Schwann cells or oligodendrocytes are needed to
cover a single nerve fiber
a. The myelin sheath is therefore segmented, and the gaps between the
segments are called the nodes of Ranvier.
b. The myelin-covered segments from one gap to the next are called internodes;
they are 0.2 to 1.0 mm long. (Fig. 12.4)
c. The short section of nerve fiber between the axon hillock and the first glial
cell is called the initial segment; the axon hillock plus initial segment constitute
the trigger zone.
Insight 12.2 Diseases of the Myelin Sheath
D. Many nerve fibers in the CNS and PNS are unmyelinated, but in the PNS, even unmyelinated
fibers are enveloped in Schwann cells.(p. 450–452)
1. One Schwann cell harbors from 1 to 12 small unmyenlinated fibers in grooves in its
surface. (Fig. 12.8)
a. The Schwann cell’s plasma membrane does not spiral around the fiber, but
folds once and somewhat overlaps at the edges.
i. This wrapping is the neurilemma (also called a mesaxon in
unmyelinated fibers).
b. Most nerve fibers have individual channels, but small fibers are sometimes
bundled.
c. A basal lamina surrounds the entire Schwann cell and fibers.
E. The speed at which nerve signals are conducted along a nerve fiber depends on the diameter of
the fiber and the presence of absence of myelin. (p. 452)
1. Signal conduction occurs along the surface of a fiber, not in the axoplasm.
2. Large fibers have more surface area and conduct more rapidly than do small fibers.
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a. Nerve signals travel about 0.5 to 2.0 m/sec in small unmyelinated fibers and 3
to 15 m/sec in myelinated fibers of the same size.
b. In large myelinated fibers, nerve signals travel as fast as 120 m/sec.
3. Slow unmyelinated fibers are sufficient for many processes; fast myelinated fibers
occur where speed is vital, such as in motor commands to skeletal muscles
F. Nerve fibers of the PNS are vulnerable to trauma, but may regenerate of the soma is intact and
at least some neurilemma. (pp. 452–453) (Fig. 12.9)
1. The regeneration process in a somatic motor neuron may be conceptualized as having
the following steps:
a. When a nerve fiber is cut, the fiber distal to the injury cannot survive because
it cannot synthesize protein.
i. Protein-synthesis organelles are limited to the soma.
ii. Schwann cells of the distal fiber also degerenate.
iii. Macrophages clean up tissue debris at the point of injury and
beyond.
b. The soma also undergoes abnormalities.
i. The soma swells and its ER breaks up; Nissl bodies disperse.
ii. The nucleus moves off center.
iv. Some neurons die at this stage.
c. The axon stump may sprout multiple growth processes while the distal end
degenerates.
d. Muscle fibers deprived of nerve supply shrink, a process called denervation
atrophy.
e. Near the injury, Schwann cells, the basal lamina, and the neurilemma form a
regeneration tube.
i. Schwann cells produce cell-adhesion molecules and nerve growth
factors that enable to neuron to regrow.
ii. When one axon growth process finds its way into the tube, it grows
rapidly (3–5 mm/day).
f. The regeneration tube guides the growing sprout back to the original target
cells, reestablishing synaptic contact.
g. When contact is established, the soma shrinks and returns to its original
appearance, and the reinnervated muscle fibers regrow.
2. Regeneration is not perfect, as some nerve fibers may connect to the wrong muscle
fibers or never find a muscle fiber; some damaged motor neurons simply die.
3. Nerve injury is therefore often followed by some degree of functional deficit.
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4. Damaged nerve fibers in the CNS cannot regenerate at all, but being enclosed in bone
helps protect the CNS.
IV. Electrophysiology of Neurons (pp. 453–462)
A. Santiago Ramon y Cajal demonstrated in the late 1800s that the nervous pathway is not a
continuous “wire” or tube, but a series of cells separated by gaps that we now call synapses; this is
known as the neuron doctrine. (pp. 453–454)
B. Two key issues in neurophysiology are (1) How does a neuron generate and electrical signal,
and (2) How does it transmit a meaningful message to the next cell? (p. 454)
Insight 12.3 Nerve Growth Factor—From Bedroom Laboratory to Nobel Prize (Fig. 12.10)
C. An electrical potential is a difference in the concentration of charged particles between one
point and another; an electrical current is a flow of charged particles from one point to another.
(pp. 454–455).
1. When an electrical potential exists between two points, such as between poles of a
battery, they are said to exhibit a polarized state.
2. Living cells are polarized because a charge difference, the resting membrane potential
(RMP), exists across the plasma membrane.
a. The membrane potential is –70 mV in a resting neuron; the negative value
means more negative charges are on the inside of the membrane than on the
outside.
3. Electrical currents in the body are created by the flow of ions such as Na+ and K+
through gated channels.
D. The resting membrane potential exists because electrolytes are unequally distributed between
the ECF and the ICF. (p. 455)
1. Three factors collectively determine the RMP:
a. Diffusion of ions down their concentration gradients through the membrane.
b. Selective permeability of the membrane, allowing some ions to pass more
easily than others.
c. Electrical attraction of cations and anions to each other.
2. Potassium ions (K+) have the greatest influence on RMP because the plasma is more
permeable to K+ than to any other ion.
a. Many cytoplasmic anions cannot escape from the cell because of their size or
charge, so that diffusion of K+ out of the cell down its concentration gradient
leaves the ICF with a net negative charge. (Fig. 12.11)
b. The negative ICF attracts K+ back into the cell, so that eventually equilibrium
is reached between concentration-driven diffusion and electrical attraction; at
this point, the net diffusion of K+ stops.
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i. At equilibrium K+ is 40 times as concentrated in the ICF as in the
ECF.
ii. If K+ were the only ion involved, the RMP would be about –90 mV.
3. Sodium ions (Na+) also influence the RMP.
a. Na+ is 12 times more concentrated in the ECF than in the ICF.
b. Although the resting membrane is less permeable to Na+, it does diffuse down
the concentration gradient into the cell and is attracted by the anions of the ICF.
(Fig. 12.11)
4. The Na+–K+ pump continually compensates for the leakage of Na+ and K+ into and out
of the cell.
a. For every 1 ATP consumed by the Na+–K+ pump, 3 Na+ are pumped out of
the cell and 2 K+ are brought in.
b. The Na+–K+ pump accounts for about 70% of the ATP requirement of the
nervous system and it works continually, which is why the nervous system
consumes so much glucose and oxygen.
5. The net effect of K diffusion outward, Na diffusion inward, and the action of the Na–K
pump is the RMP of –70 mV.
E. A change in local potential, which is a short-range change in voltage, may occur when a neuron
is stimulated. (pp. 455–456)
1. Typically, a neuron’s response begins at the dendrite, spreads through the soma, travels
down the axon, and ends at the synaptic knobs. (Fig. 12.12)
2. A stimulus at the dendrite binds to receptors that open Na+ gates in the membrane so
that Na+ flows into the cell, neutralizing some of the negative charge.
a. Any change that shifts the membrane voltage to a less negative value is
termed depolarization.
3. Incoming Na+ ions diffuse for a short distance and produce a current (local potential)
that travels from the stimulus point toward the cell’s trigger zone.
4. Four characteristics distinguish local potentials from action potentials. (Table 12.2)
a. Local potentials are graded; they vary in magnitude depending on strength of
stimulus.
b. Local potentials are decremental; they get weaker as they spread from the
point of stimulation.
c. Local potentials are reversible if stimulation ceases.
d. Local potentials can be either excitatory or inhibitory; the result of inhibitory
local potentials is hyperpolarization (increase in negative potential).
F. An action potential is a rapid up-and-down shift in membrane voltage produced by voltageregulated ion gates in the plasma membrane. (p. 457–459) (Fig. 12.13)
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1. Action potentials occur only when there is a high enough density of voltage-regulated
gates; most of the soma cannot generate action potentials.
a. The trigger zone contains 350 to 500 voltage-regulated gates per μm2,
compared to 50 to 75 gates per μm2 in most of the soma.
2. If a local potential spreads all the way to the trigger zone and is still strong enough, it
can open the gates and generate an action potential.
3. The sequence of events in an action potential are as follows. (Fig. 12.14)
a. Na+ arrives at the axon hillock and depolarize the membrane as a local
potential.
b. The local potential must rise to the threshold (about –55 mV) to open the
voltage-regulated gates.
c. The neuron produces an action potential; the voltage regulated Na+ gates open
quickly, while K+ gates open more slowly, and the membrane depolarizes
further in a positive feedback cycle.
d. As the rising membrane potential passes 0 mV, Na + gates are inactivated and
begin closing; by the time they all close, the voltage peaks at about +35 mV.
e. By the time the voltage peaks, the slow K+ gates are fully open, and K+ now
exits the cell, which acts to repolarize the membrane.
f. K+ gates stay open longer than Na+ gates, so slightly more K+ leaves the cell
than the amount of Na+ that entered; the membrane voltage drops to 1 or 2 mV
more negative than the original RMP, a condition called hyperpolarization or
afterpotential.
g. Na+ diffusion into the cell and (in CNS) removal of extracellular K + by
astrocytes gradually restore RMP.
4. Only about 1 ion in a million crosses the membrane to produce and action potential,
and an action potential affects distribution only in a thin layer near the membrane.
5. Action potentials differ from local potentials in the following ways. (Table 12.2)
a. Action potentials follow an all-or-none law and are not graded; if threshold is
not reached, no action potential is generated.
b. Action potentials are nondecremental; they do not get weaker with distance.
c. Action potentials are irreversible; once initiated, an action potential goes to
completion and cannot be stopped.
G. During an action potential and for a few milliseconds after, the neuron cannot be stimulated to
fire again; this period is called the refractory period. (p. 459)
1. The refractory period has two phases: absolute refractory period and relative refractory
period. (Fig. 12.15)
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a. During the absolute refractory period, no stimulus of any strength will trigger
a new action potential; this period lasts from the start of the action potential until
the return to RMP (i.e., for as long as the Na + gates are open).
b. During the relative refractory period, an unusually strong stimulus will trigger
a new action potential; this period lasts until hyperpolarization ends (i.e., for as
long as the K+ gates are still open).
2. The refractory period is present only in a small patch of membrane where an action
potential has already begun, not to the entire neuron.
H. Signal conduction is somewhat different in unmyelinated fibers compared to conduction in
myelinated fibers. (p. 459–461)
1. An unmyelinated fiber has voltage-regulated ion gates along its entire length. (Fig.
12.16)
a. When an action potential occurs at the trigger zone, Na+ enters the axon, and
the resulting depolarization excites voltage-regulated gates distal to the action
potential.
b. This chain reaction continues to the end of the axon.
c. An action potential does not travel along an axon, but rather, it stimulates the
production of a new action potential just ahead of it.
i. An action potential is therefore different from a nerve signal, which is
a traveling wave of excitation produced by the self-propagation of
action potentials.
ii. No one action potential travels to the end of an axon; a nerve signal
is a chain reaction of action potentials.
d. Action potentials do not travel backward because the membrane behind the
nerve signal is still in its refractory period.
e. A nerve signal is not like a current in a wire: It moves much more slowly, and
the last action potential has the same voltage as the first one.
2. In myelinated fibers, voltage-regulated ion gates are scarce in the myelin-covered
internodes (fewer than 25/μm2 compared with 2,000 to 12,000/μm2 in nodes of Ranvier).
a. A nerve signal travels through an internode as Na+ diffuses down the fiber
under the axolemma; this flow is very fast but is decremental. (Fig. 12.17a)
b. A node of Ranvier occurs every millimeter or less along the axon, however,
with an abundance of voltage-regulated gates.
c. When the diffusing ions reach a node, these gates are opened and a new action
potential is generated; this process of jumping from node to node is called
saltatory conduction. (Fig. 12.17b)
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d. Saltatory conduction is the reason that myelinated fibers transmit signals at
120 m/sec as compared to 2 m/sec in unmyelinated fibers.
V. Synapses (pp. 462–467)
A. A synapse exists at the end of an axon; in synapses between two neurons, the first neuron is the
presynaptic neuron (releases neurotransmitter) and the second is the postsynaptic neuron (responds
to neurotransmitter). (p. 462)
B. A presynaptic neuron may form an axodentritic, axosomatic, or axoaxonic synapse. (Fig.
12.18b)
C. A single neuron may have an enormous number of synapses; a spinal motor neuron is covered
with about 10,000 synaptic knobs from other neurons, and a neuron of the cerebellum may have as
many as 100,000 synapses. (Fig. 12.19)
D. The first neurotransmitter discovered was acetylcholine, which Otto Loewi detected
experimentally in 1921.
1. Electrical communication between cells was not considered possible because of the
synaptic cleft; however, we now know that some excitatory cells, such as cardiac muscle,
have electrical synapses via gap junctions.
2. Most other synapses are chemical synapses relying on neurotransmitters.
E. The structure of a chemical synapse includes the synaptic knob, a part of the presynaptic neuron
that contains synaptic vesicles. (pp. 421–423) (Fig. 12.20)
1. Many of the presynaptic neuron’s vesicles are docked at the membrane, while others
farther away constitute a reserve pool.
2. The postsynaptic neuron has no synaptic vesicles in the synapse and cannot release
neurotransmitters; the membrane does contain receptor proteins and ligand-regulated ion
gates.
F. More than 100 confirmed or suspected neurotransmitters have been identified. (pp. 463–464)
(Fig. 12.21)
1. Neurotransmitters fall into four major categories according to composition. (Table
12.3)
a. Acetylcholine, in a class by itself, is formed from acetic acid and choline.
b. Amino acid neurotransmitters include gylcine, glutamate, aspartate, and γaminobutyric acid (GABA).
c. Monoamines (biogenic amines) are synthesized from amino acids by removal
of the —COOH group; the major monoamines are epinephrine, norepinephrine,
dopamine, histamine, and serotonin. The first three are in a subclass called
catecholamines.
d. Neuropeptides are chain of 2 to 40 amino acids; examples are b-endorphin
and substance P.
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i. Neuropeptides typically act in lower concentrations and have longer
lasting effects than other neurotransmitters and are stored in larger
secretory granules (dense-core vesicles).
ii. Some also function as hormones or as neuromodulators.
iii. Some are produced not only by neurons but also by the digestive
tract (gut–brain peptides).
2. Traditionally, neurotransmitters have been considered as small organic compounds that
function at the synapse in the following ways:
a. They are synthesized by the presynaptic neuron.
b. They are released in response to stimulation.
c. They bind to specific receptors on the postsynaptic cell.
d. They alter the physiology of that cell.
3. Neuropeptides are an exception to small size, and neurons may communicate by other
means, such as the gas nitric oxide.
4. A given neurotransmitter may not have the same effect everywhere in the body, and
there are multiple receptor types for a particular neurotransmitter.
G. Neurotransmitters have diverse actions; three examples of different modes of action are
illustrated by an excitatory cholinergic synapse, an inhibitory GABA-ergic synapse, and an
excitatory adrenergic synapse.
1. A cholinergic synapse employs acetylecholine (ACh) as its neurotransmitter; in an
excitatory synapse, the steps in transmission are as follows. (Fig. 12.22)
a. The arrive of a nerve signal at the synaptic knob opens voltage-regulated
calcium gates.
b. Ca2+ enters the knob and triggers exocytosis of synaptic vesicles, releasing
ACh.
c. Empty vesicles drop back into the cytoplasm to be refilled, and synaptic
vesicles in the reserve pool move to the active sites and release ACh.
d. ACh diffuses across the cleft and binds to ligand-regulated gates, which open
to allow Na+ to enter the cell and K+ to leave.
e. Na+ spreads out along the inside of the membrane producing a local potential
called the postsynaptic potential; if strong and persistent enough, this triggers an
action potential.
2. A GABA-ergic synapse employs γ-aminobutyric acid as its neurotransmitter; in an
inhibitory synapse:
a. The release of GABA by the presynaptic neuron and its binding to ion gates is
a similar mechanism as for cholinergic synapses.
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b. The GABA receptor, however, is a chloride channel, and when it opens, Cl –
enters the cell, increasing the negative membrane potential and inhibiting firing.
3. An adrenergic synapse employs norepinephrine (NE) as a neurotransmitter; its receptor
is not an ion gate but a transmembrane protein associated with a G protein in a secondmessenger system. (Fig. 12.23)
a. Binding of NE to the recetpro causes the G protein to dissociate from it.
b. The G protein binds to adenlyate cyclase, inducing it to convert ATP to cyclic
AMP (cAMP).
c. Cyclic AMP can induce several alternative effects inside the cell.
i. One effect is to produce an internal chemical that binds to a ligandregulated ion gate from inside the membrane, opening the gate.
ii. Another is to activate preexisting cytoplasmic enzymes that affect
metabolism.
iii. Yet another is to induce genetic transcription, so that new enzymes
are produced.
d. Although slower to respond than cholinergic and GABA-ergic synapses,
adrenergic synapsis have the advantage of enzyme amplification, that is, a single
NE molecule can induce formation of many cAMPs, which in turn can activate
many molecules, and so on.
4. Synaptic events require only 0.5 msec or so, an interval called synaptic delay.
H. Cessation of a signal occurs when neurotransmitter stops being released and when
neurotransmitter already present in the synaptic cleft is removed. ( p. 467)
1. The cessation of action potentials in the presynaptic nerve fiber stop the release of
neurotransmitter.
2. The removal of neurotransmitter from the synaptic cleft is accomplished in three ways.
a. Diffusion. Neurotransmitter leaves the synapse and enters the ECF. In the
CNS, astrocytes absorb it and return it to neurons.
b. Reuptake. The synaptic knob reabsorbs amino acids and monoamines by
endocytosis and breaks them down with monoamine oxidase (MAO).
c. Degradation. The enzyme acetylcholinesterase (AChE) breaks down ACh into
acetate and choline, the latter of which is reabsorbed by the synaptic knob.
I. Neuromodulators are hormones, neuropeptides, and other messengers that modify synaptic
transmission. ( p. 467)
1. The enkephalins, a family of neuromodulators, consist of small peptides that inhibit
spinal interneurons from transmitting pain signals to the brain.
2. Nitric oxide (NO) is a gas released by postsynaptic neurons in some areas of the brain;
here it stimulates the presynaptic neuron to release more neurotransmitter.
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VI. Neural Integration (pp. 467–475)
A. The ability of neurons to process information, store and recall it, and make decisions is called
neural integration. (pp. 467–468)
B. Neural integration is based on the postsynaptic potentials produced by neurotransmitters. (p.
468)
1. Any voltage change that raises the membrane potential closer to the threshold (from –
an RMP of 70 mV to a threshold of –55 mV) is termed and excitatory postsynaptic
potential (EPSP). (Fig. 12.24a)
2. Any voltage change that hyperpolarizes the membrane and makes it more negative
than the RMP is termed an inhibitory postsynaptic potential (IPSP). (Fig. 12.24b)
3. Because of ion leakage, all neurons fire at a certain background rate even when not
being stimulated; EPSPs and IPSPs only change the rate of firing.
4. Glutamate and aspartate produce EPSPs (excitatory); glycine and GABA produce
IPSPs (inhibitory); and acetylecholine and norepinephrine are excitatory for some cells
and inhibitory for others.
C. Summation, facilitation, and inhibition are mechanisms that influence a neuron’s integration of
multiple inputs. ( p. 468–469)
1. Summation is the process of adding up ESPSs and ISPSs and responding to their net
effect; it occurs in the trigger zone.
a. Summation enables the nervous system to make decisions.
b. A single action potential does not produce enough activity to lead to firing; at
least 30 EPSPs are needed for a postsynaptic cell to reach threshold and fire.
c. ESPSs can be added up in two ways, which may occur simultaneously.
i. Temporal summation occurs when a single synapse generates EPSPs
very quickly so that they have a cumulative effect. (Figs. 12.25a, 12.26)
ii. Spatial summation occurs when EPSPs from several different
synapses add up to threshold at the axon hillock. (Fig. 12.25b)
d. Neurons routinely work in groups to modify each other’s actions.
i. Facilitation is a process in which one neuron enhances the effect of
another; for example, when two neurons working cooperatively are
able to induce firing.
ii. Presynaptic inhibition is a mechanism by which one presynaptic
neuron suppresses the action of another, often by blocking with an
inhibitory nuerotransmitter. (Fig. 12.27)
D. The way in which the nervous system converts information to a mueaningful pattern of action
potentials is called neural coding. (pp. 470–471)
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1. The most important mechanism is the labeled line code: Each nerve fiber to the brain
leads from a receptor that recognized a particular stimulus type, such as optic nerve fibers
that carry signals only from light receptors in the eye.
2. Quantitative information about intensity of a stimulus is encoded in two ways.
a. In recruitment, additional neurons are brought into play as a stimulus becomes
stronger, enabling the nervous system to judge stimulus strength by which and
how many neurons are firing.
b. Another mechanism depends on the fact that the more strongly a neuron is
stimulated, the more frequently it fires, so that the nervous system can judge
stimulus strength from the firing frequency of afferent neurons. (Fig. 12.28)
i. The absolute refractory period sets an upper limit to how often a
neuron can fire.
ii. The theoretical limit of firing frequency is 2,000 action potentials per
second, but the highest frequencies observed are 500–1,000 per second.
E. Neurons function in ensembles called neural pools, which may contain thousands to millions of
interneurons; the functions of a neural pool are partly deteremined by its neural circuit. (pp. 471–
472)
1. Information arrives at a neural pool through one or more input neurons.
a. Within the discharge zone of an input neuron, that neuron can make the
postsynaptic cells fire. (Fig. 12.29)
b. In a braoder facilitated zone, the neuron synapses with still other neurons in
the pool and can stimulate them only with the assistance of other input neurons.
2. A neural pool’s neural circuit consists of the pathways among its neurons; a wide
variety of neural functions result from the operation of four principal kinds of neural
circuits. (Fig. 12.30)
a. In a diverging circuit, one nerve fiber branches and synapses with several post
synaptic cells, so that input from one neuron may produce output through
hundreds of neurons.
b. In a converging circuit, input from many different never fibers is funneled to
one neuron or neural pool; this type of circuit allows input from different
sensory systems to be evaluated, such as correcting balance.
c. In a reverberating circuit, neurons are stimulated in a linear fashion, but some
have an axon collateral leading back to the initial neuron and restimulates it.
e. In a parallel after-discharge circuit, an input neuron diverges to stimulate
several neuron chains that eventually reconverge on a single output neuron;
these chains different in total synaptic delay, meaning that their signals arrive on
the output neuron at different time.
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i. The output neuron may continue to fire after the stimulus stops, as
signals continue to arrive.
ii. There is no feedback loop, and once all neurons have fired, output
ceases.
F. The physical basis of memory is a pathway through the brain called a memory trace (engram); it
is based on the ability of synapses to be added, taken away, or modified, which is called synaptic
plasticity. (pp. 472–475)
1. During learning, synapses in a certain pathway become modified so that signals travel
more easily across them; this process is called synaptic potentiation.
2. Immediate memory is one of the three classes of memory; it is the ability to hold
something in mind for just a few seconds.
a. Immediate memory is necessary for continuity of events and is especially
important in reading.
b. It might be based on reverberating circuits.
3. Short-term memory (STM) lasts from a few seconds to a few hours.
a. Working memory is a form of STM that allows us to hold an idea in mind
long enough to carry out an action such as calling a telephone number we just
looked up; it might be based on reverberating circuits.
b. Somewhat longer-lasting memories probably involve synaptic facilitation,
which is induced by tetanic stimulation.
i. Rapid arrival of signals means that Ca2+ accumulates in the synaptic
knob, causing SPSPs to become stronger and stronger.
c. Memories lasting for a few hours may involve posttetanic potentiation.
i. The Ca2+ level stays elevated for so long that another signal releases a
burst of neurotransmitter, jogging the memory of an event from several
hours earlier.
4. Long-term memory (LTM) lasts up to a lifetimes and is less limited that STM in the
amount of information it can store; the two forms of LTM are declarative memory and
procedural memory.
a. Declarative memory is the retention of facts and events that can be put into
words.
b. Procedural memory is the retention of motor skills.
c. Some LTM involves physical remodeling of synapses or formation of new
ones through growth and branching of axon terminals and dendrites.
d. LTM can also involve long-term potentiation in which NMDA receptors that
bind glutamate are simultaneously subjected to tetanic stimulation, allowing
entry of Ca2+ as a second messenger in pyramidal cells with three effects.
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i. The neuron produces more NMDA receptors, making it more
sensitive to glutamate in the future.
ii. It synthesizes proteins concerned with remodeling synapses.
iii. It released nitric oxide, which trigger more glutamate release in the
presynaptic neuron.
Insight 12.4 Alzheimer and Parkinson Diseases (Fig. 12.31)
Connective Issues: Nervous System Interactions
Cross References
Additional information on topics mentioned in Chapter 12 can be found in the chapters listed below.
Chapter 2: Anaerobic and aerobic ATP synthesis
Chapter 3: Kinesin and dynein in cilia and flagella
Chapter 3: Sodium–potassium pump
Chapters 3 and 11: Gated channels in membranes
Chapter 4: Complexity of the genetic code
Chapter 11: Membrane potential
Chapter 11: The neuromuscular junction
Chapter 14: Parts of the brain
Chapter 14: Anatomical sites of memory
Chapter 14: Ependymal cells and cerebrospinal fluid
Chapter 14: The blood–brain barrier
Chapter 15: Different effects of a single neurotransmitter
Chapter 15: Drugs that inhibit monoamine oxidase.
Chapter 16: Role of enkephalins
Chapter 26: Action of neurotransmitters on food cravings