8. THE LATERAL LINE ORGAN MECHANORECEPTORS
257
body surrounded by vesicles with a diameter of 350 A (Fig. 14). These
vesicles are similar to presynaptic vesicles in motor end plates and at
other sites in the nervous system where neurochemical transmission
occurs. It is thus likely that sensory transmission is mediated by a transmitter substance of yet unknown pharmacology. A second type of nerve
endings also contact the hair cells, these are endings of efferent nerve
fibers and are characterized by the presence of synaptic vesicles inside
the nerve ending and by a subsynaptic sac inside the hair cell in apposition to the nerve ending. The transmitter has not been identified although
it is likely to be acetylcholine which has been demonstrated to occur in
the efferent system of the inner ear (Schuknecht et al., 1959).
The liberation of transmitter substance at a neurochemical synapse
results from depolarization of the presynaptic terminal caused by the
nerve action potential traveling down the axon into the terminal. That
the release mechanism is in fact governed by the presynaptic potentialand not a consequence of other changes occurring in the presynaptic
membrane when it is depolarized by the action potential-has recently
been demonstrated by Katz and Miledi (1967). They found, in muscle
end plates and in squid giant synapses where electrical excitability was
blocked by tetrodotoxin, that transmitter release could be evoked by
electric pulses delivered to the presynaptic terminal. It remains to be seen
whether the receptor potential in the hair cell may have a similar function
of governing the release of the transmitter at the afferent synapse. One
indication that potential change is causative in transmission is the fact
that efferent nerve endings inhibit afferent nerve impulses (Russell, 1968)
via their action on the hair cell. Efferents have been seen to terminate
on hair cells only (Hama, 1965; Flock, 1965); no synaptic contacts have
been seen between efferent nerve endings and afferent terminals, and so
inhibition is by presynaptic action on the hair cell. In similar situations
within the nervous system inhibition is brought about by a hyperpolarizing effect of the efferent synapse or by shunting of current which would
otherwise have excited the afferent synapse. Thus, here, it is by manipulation of the presynaptic potential that inhibition is brought about. On
the other hand, the receptor potential is quite small-even at high
intensities of stimulation it rarely exceeds 1 mV. Is it possible for such
a small potential change to have an effect on transmitter release?
Certain fishes are equipped with electroreceptor organs which derive
from the lateral line system. These organs are extremely sensitive to
external potential fields. In some types of electroreceptor organs the
afferent discharge rate is linearly related to graded stimuli (see Bennett,
1965, and this volume). Excitation of the afferent terminal is likely to be
by chemical transmission, the voltage across the presynaptic membrane
257
body surrounded by vesicles with a diameter of 350 A (Fig. 14). These
vesicles are similar to presynaptic vesicles in motor end plates and at
other sites in the nervous system where neurochemical transmission
occurs. It is thus likely that sensory transmission is mediated by a transmitter substance of yet unknown pharmacology. A second type of nerve
endings also contact the hair cells, these are endings of efferent nerve
fibers and are characterized by the presence of synaptic vesicles inside
the nerve ending and by a subsynaptic sac inside the hair cell in apposition to the nerve ending. The transmitter has not been identified although
it is likely to be acetylcholine which has been demonstrated to occur in
the efferent system of the inner ear (Schuknecht et al., 1959).
The liberation of transmitter substance at a neurochemical synapse
results from depolarization of the presynaptic terminal caused by the
nerve action potential traveling down the axon into the terminal. That
the release mechanism is in fact governed by the presynaptic potentialand not a consequence of other changes occurring in the presynaptic
membrane when it is depolarized by the action potential-has recently
been demonstrated by Katz and Miledi (1967). They found, in muscle
end plates and in squid giant synapses where electrical excitability was
blocked by tetrodotoxin, that transmitter release could be evoked by
electric pulses delivered to the presynaptic terminal. It remains to be seen
whether the receptor potential in the hair cell may have a similar function
of governing the release of the transmitter at the afferent synapse. One
indication that potential change is causative in transmission is the fact
that efferent nerve endings inhibit afferent nerve impulses (Russell, 1968)
via their action on the hair cell. Efferents have been seen to terminate
on hair cells only (Hama, 1965; Flock, 1965); no synaptic contacts have
been seen between efferent nerve endings and afferent terminals, and so
inhibition is by presynaptic action on the hair cell. In similar situations
within the nervous system inhibition is brought about by a hyperpolarizing effect of the efferent synapse or by shunting of current which would
otherwise have excited the afferent synapse. Thus, here, it is by manipulation of the presynaptic potential that inhibition is brought about. On
the other hand, the receptor potential is quite small-even at high
intensities of stimulation it rarely exceeds 1 mV. Is it possible for such
a small potential change to have an effect on transmitter release?
Certain fishes are equipped with electroreceptor organs which derive
from the lateral line system. These organs are extremely sensitive to
external potential fields. In some types of electroreceptor organs the
afferent discharge rate is linearly related to graded stimuli (see Bennett,
1965, and this volume). Excitation of the afferent terminal is likely to be
by chemical transmission, the voltage across the presynaptic membrane