Ganong's Review of Medical Physiology, 23rd Edition

CHAPTER 6Synaptic & Junctional Transmission 127

difficulty has been reduced by administration of neurotro-
phins. For example, sensory neurons torn when dorsal nerve
roots are avulsed from the spinal cord regrow and form func-
tional connections in the spinal cord if experimental animals
are treated with NGF, neurotrophin 3, or GDNF.
Hypersensitivity is limited to the structures immediately
innervated by the destroyed neurons and fails to develop in neu-

rons and muscle farther downstream. Suprasegmental spinal

cord lesions do not lead to hypersensitivity of the paralyzed

skeletal muscles to acetylcholine, and destruction of the

preganglionic autonomic nerves to visceral structures does

not cause hypersensitivity of the denervated viscera. This fact

has practical implications in the treatment of diseases due to

spasm of the blood vessels in the extremities. For example, if

the upper extremity is sympathectomized by removing the

upper part of the ganglionic chain and the stellate ganglion,

the hypersensitive smooth muscle in the vessel walls is stimu-

lated by circulating norepinephrine, and episodic vasospasm

continues to occur. However, if preganglionic sympathectomy

of the arm is performed by cutting the ganglion chain below

the third ganglion (to interrupt ascending preganglionic

fibers) and the white rami of the first three thoracic nerves, no

hypersensitivity results.

Denervation hypersensitivity has multiple causes. As noted

in Chapter 2, a deficiency of a given chemical messenger gen-

erally produces an upregulation of its receptors. Another fac-

tor is lack of reuptake of secreted neurotransmitters.

CHAPTER SUMMARY

■ Presynaptic terminals are separated from the postsynaptic

structure by a synaptic cleft. The postsynaptic membrane con-

tains many neurotransmitter receptors and usually a postsynap-

tic thickening called the postsynaptic density.

■ At chemical synapses, an impulse in the presynaptic axon causes

secretion of a chemical that diffuses across the synaptic cleft and

binds to postsynaptic receptors, triggering events that open or

close channels in the membrane of the postsynaptic cell. At elec-

trical synapses, the membranes of the presynaptic and postsyn-

aptic neurons come close together, and gap junctions form

FIGURE 6–15 Endings of postganglionic autonomic neurons on smooth muscle. Neurotransmitter, released from varicosities along the
branched axon, diffuses to receptors on smooth muscle cell plasma membranes. (From Widmaier EP, Raff H, Strang KT: Vanders Human Physiology. McGraw-Hill, 2008.)

Varicosity

Synaptic

vesicles

Mitochondrion

Autonomic

nerve fiber

Varicosities

Sheet of

cells

FIGURE 6–16 Summary of changes occurring in a neuron
and the structure it innervates when its axon is crushed or cut at
the point marked X. Hypersensitivity of the postsynaptic structure to
the transmitter previously secreted by the axon occurs largely due to
the synthesis or activation of more receptors. There is both orthograde
(wallerian) degeneration from the point of damage to the terminal and
retrograde degeneration of the axon stump to the nearest collateral
(sustaining collateral). Changes also occur in the cell body, including
chromatolysis. The nerve starts to regrow, with multiple small branch-
es projecting along the path the axon previously followed (regenera-
tive sprouting).

Axon branch

(sustaining collateral)

Receptor

Receptor

hypersensitive

Retrograde

degeneration

Site of injury

Retrograde

reaction:

chromatolysis

Regenerative

sprouting

Orthograde

(wallerian)

degeneration

X