Ganong's Review of Medical Physiology, 23rd Edition

118
SECTION II
Physiology of Nerve & Muscle Cells

achieved by advancing a microelectrode through the ventral
portion of the spinal cord. Puncture of a cell membrane is sig-
naled by the appearance of a steady 70-mV potential differ-
ence between the microelectrode and an electrode outside the
cell. The cell can be identified as a spinal motor neuron by
stimulating the appropriate ventral root and observing the
electrical activity of the cell. Such stimulation initiates an anti-
dromic impulse (see Chapter 4) that is conducted to the soma

and stops at this point. Therefore, the presence of an action

potential in the cell after antidromic stimulation indicates that

the cell that has been penetrated is an

α

-motor neuron. Stim-

ulation of a dorsal root afferent (sensory neuron) can be used

to study both excitatory and inhibitory events in

α

-motor

neurons (Figure 6–6).

When an impulse reaches the presynaptic terminals, an

interval of at least 0.5 ms, the

synaptic delay,

occurs before a

response is obtained in the postsynaptic neuron. It is due to

the time it takes for the synaptic mediator to be released and

to act on the membrane of the postsynaptic cell. Because of it,

conduction along a chain of neurons is slower if many syn-

apses are in the chain than if there are only a few. Because the

minimum time for transmission across one synapse is 0.5 ms,

it is also possible to determine whether a given reflex pathway

is monosynaptic or polysynaptic (contains more than one

synapse) by measuring the delay in transmission from the

dorsal to the ventral root across the spinal cord.

A single stimulus applied to the sensory nerves character-

istically does not lead to the formation of a propagated action

potential in the postsynaptic neuron. Instead, the stimulation

produces either a transient partial depolarization or a tran-

sient hyperpolarization. The initial depolarizing response

produced by a single stimulus to the proper input begins

about 0.5 ms after the afferent impulse enters the spinal

cord. It reaches its peak 11.5 ms later and then declines

exponentially. During this potential, the excitability of the

neuron to other stimuli is increased, and consequently the

potential is called an

excitatory postsynaptic potential

(EPSP)

(Figure 6–6)

.

FIGURE 6–4
Small synaptic vesicle cycle in presynaptic nerve terminals.
Vesicles bud off the early endosome and then fill with neu-
rotransmitter (NT; top left). They then move to the plasma membrane, dock, and become primed. Upon arrival of an action potential at the ending,
Ca
2+
influx triggers fusion and exocytosis of the granule contents to the synaptic cleft. The vesicle wall is then coated with clathrin and taken up
by endocytosis. In the cytoplasm, it fuses with the early endosome, and the cycle is ready to repeat.
(Reproduced with permission from Sdhof TC: The
synaptic vesicle cycle: A cascade of proteinprotein interactions. Nature 1995;375:645. Copyright by Macmillan Magazines.)

Early endosome

ATP

NT

NT uptake

Translocation Translocation

Budding Endosome fusion

Docking Priming Fusion/

exocytosis Endocytosis

4 Ca2+

H+

Ca2+?

Plasma

membrane

Synaptic

cleft

Ca2+

FIGURE 6–5
Main proteins that interact to produce synaptic
vesicle docking and fusion in nerve endings.
(Reproduced with
permission from Ferro-Novick S, John R: Vesicle fusion from yeast to man. Nature
1994;370:191. Copyright by Macmillan Magazines.)

NSF

rab3

GTP

munc18/

rbSec1

α/γ

SNAPs

Syntaxin

Synaptobrevin

SNAP-

25

Synaptic vesicle Plasma membrane

Neuron: