324
J. DIAMOND
the postsynaptic membrane of the Mauthner cell (Fig. 36). It begins
some few tenths of a millisecond after a single VIIIth nerve volley is
initiated on the opposite side and may last 10-30 msec or even longer.
The earliest phase of this inhibition probably involves a direct VIIIth
nerve pathway, the latency of its action allowing only for the synaptic
delay at the Mauthner cell itself (unless an electrically excited interneuron were interposed en route) ( Furshpan and Furukawa, 1962).
Obviously only this particularly early inhibitory action is relevant to
the present discussion, and the probable role of the later components
is considered in Section IX, D. We are especially concerned with very
small fractions of 1 msec. Exactly how soon can this crossing inhibition
become effective?
The fibers responsible for the crossed inhibition probably include
those ending as “unmyelinated club endings” at the axon hillock region
(see Fig. 4 legend). Suppose these conduct even as fast as 5-10 meters/
sec (which we may also accept for the conduction velocity in those
ipsilateral VIIIth nerve excitatory fibers which transmit chemically).
The crossed inhibitory pathway is about 1 mm longer than the ipsilateral
excitatory pathway in a moderate-sized goldfish. The inhibitory volley
would therefore arrive at the contralateral cell some 0.1-0.2 msec after
that cell received the excitatory volley in its own VIIIth nerve “chemical”
fibers, and it can be estimated from Furshpan’s data (1964), some 0.3-0.4
msec after the excitatory volley in the VIIIth nerve electrically transmitting fibers. Since the electrically transmitted e.p.s.p. is capable of
initiating a spike within about 0.2-0.3 msec of its onset, there seems
no conceivable way in which its effects could be interfered with by
this crossing inhibition.
We must remember that we are dealing with the asymmetrical situation, and therefore the inhibitory volley will arrive fractionally earlier
at the contralateral Mauthner cell than the calculation allows, and the
excitatory volley fractionally later. Moreover, in a small fish the crossed
inhibitory pathway is less than 1 mm longer than the ipsilateral excitatory one. Thus, particularly in small fish, we have the possible result
that just before the electrically transmitted e.p.s.p. fires the spike in
the contralateral Mauthner cell (the vibrational stimulus is taken to
be more effective on the ipsilateral side), the crossed inhibitory volley
arrives there from the ipsilateral vestibular apparatus. But there uill
be a minimum synaptic delay of about 0.4 msec before this inhibitory
input becomas dective. Our conclusion must be therefore that the
crossed, chemically transmitted inhibition almost certainly cannot interfere with the electrical excitation of a Mauthner cell by its own VIIIth
nerve input, wen in the asymmetrical situation.
J. DIAMOND
the postsynaptic membrane of the Mauthner cell (Fig. 36). It begins
some few tenths of a millisecond after a single VIIIth nerve volley is
initiated on the opposite side and may last 10-30 msec or even longer.
The earliest phase of this inhibition probably involves a direct VIIIth
nerve pathway, the latency of its action allowing only for the synaptic
delay at the Mauthner cell itself (unless an electrically excited interneuron were interposed en route) ( Furshpan and Furukawa, 1962).
Obviously only this particularly early inhibitory action is relevant to
the present discussion, and the probable role of the later components
is considered in Section IX, D. We are especially concerned with very
small fractions of 1 msec. Exactly how soon can this crossing inhibition
become effective?
The fibers responsible for the crossed inhibition probably include
those ending as “unmyelinated club endings” at the axon hillock region
(see Fig. 4 legend). Suppose these conduct even as fast as 5-10 meters/
sec (which we may also accept for the conduction velocity in those
ipsilateral VIIIth nerve excitatory fibers which transmit chemically).
The crossed inhibitory pathway is about 1 mm longer than the ipsilateral
excitatory pathway in a moderate-sized goldfish. The inhibitory volley
would therefore arrive at the contralateral cell some 0.1-0.2 msec after
that cell received the excitatory volley in its own VIIIth nerve “chemical”
fibers, and it can be estimated from Furshpan’s data (1964), some 0.3-0.4
msec after the excitatory volley in the VIIIth nerve electrically transmitting fibers. Since the electrically transmitted e.p.s.p. is capable of
initiating a spike within about 0.2-0.3 msec of its onset, there seems
no conceivable way in which its effects could be interfered with by
this crossing inhibition.
We must remember that we are dealing with the asymmetrical situation, and therefore the inhibitory volley will arrive fractionally earlier
at the contralateral Mauthner cell than the calculation allows, and the
excitatory volley fractionally later. Moreover, in a small fish the crossed
inhibitory pathway is less than 1 mm longer than the ipsilateral excitatory one. Thus, particularly in small fish, we have the possible result
that just before the electrically transmitted e.p.s.p. fires the spike in
the contralateral Mauthner cell (the vibrational stimulus is taken to
be more effective on the ipsilateral side), the crossed inhibitory volley
arrives there from the ipsilateral vestibular apparatus. But there uill
be a minimum synaptic delay of about 0.4 msec before this inhibitory
input becomas dective. Our conclusion must be therefore that the
crossed, chemically transmitted inhibition almost certainly cannot interfere with the electrical excitation of a Mauthner cell by its own VIIIth
nerve input, wen in the asymmetrical situation.