308
J. DIAMOND
supplying them. (Indeed, we know that such collaterals must subserve
the crossing inhibition. ) But there is another possibility worth considering, namely, that the Mauthner reflex involves an “excitatory cascade,”
in which the primary motoneurons are responsible for passing on the
excitation to other motoneurons and/ or interneurons. It is interesting
to note that where the comparison was possible the effects of the crossing inhibition lasted longer on later firing motoneurons than on earlier
ones; this would be necessary (if the suggested excitatory cascade were
involved) for the production of the variable muscle response observed
to occur toward the end of the inhibitory period. [The variable muscle
response and ventral root output (Fig. 28) which occurs at short
separation times between Mauthner impulses would, of course, depend
upon the crossing inhibition arriving in time to prevent the firing of
group B motoneurons but too late to prevent that of the primary motoneurons.] Another relevant finding was that the crossed excitation is
always associated with the ipsilateral excitation, which it follows by 1-3
msec; when the latter is reduced or abolished by inhibition or fatigue
(Fig. 44) so is the former, and to a roughly corresponding extent.
We may speculate further on the nature of an excitatory cascade
with regard to the fractionation of the response in the primary motoneuron. Figure 29 shows records of the activity in the cell body of such
a motoneuron, orthodromically and antidromically excited, during the
crossed inhibition evoked by excitation of the contralateral Mauthner
axon. The various components of the electrical response of this cell were
easily distinguishable because of its deterioration as a consequence of
the microelectrode impalement. However, that these components are
not experimental artifacts is indicated by the ease with which they could
always be revealed by the activation of the crossing inhibition. There
were four components comprising the orthodromic response in this
example but only two comprising antidromic. As we have seen, the
two extra components in the orthodromic records seem to be contributed
by the A1 unit. As the crossing inhibition, which followed the ipsilateral
excitation, was initiated progressively earlier ( Figs. 29c-e and g-i) the
excitatory response was broken up in both the orthodromic and the
antidromic records until first one major component disappeared (records
in Figs. 29d and h ) and subsequently a second (records in Figs. 29e and
i). A consideration of the antidromic responses indicates that the first
response to disappear must be attributed to the cell body-initial segment
region of the motoneuron and the second to the ventral dendrite. (Recordings made from a ventral dendrite itself often had only a “hump”
on the falling phase to indicate the “cell body”response.) In Fig. 29e
is seen the A l response as recorded in the primary motoneuron; bringing
the inhibition still earlier eliminated this also (not illustrated-note the
J. DIAMOND
supplying them. (Indeed, we know that such collaterals must subserve
the crossing inhibition. ) But there is another possibility worth considering, namely, that the Mauthner reflex involves an “excitatory cascade,”
in which the primary motoneurons are responsible for passing on the
excitation to other motoneurons and/ or interneurons. It is interesting
to note that where the comparison was possible the effects of the crossing inhibition lasted longer on later firing motoneurons than on earlier
ones; this would be necessary (if the suggested excitatory cascade were
involved) for the production of the variable muscle response observed
to occur toward the end of the inhibitory period. [The variable muscle
response and ventral root output (Fig. 28) which occurs at short
separation times between Mauthner impulses would, of course, depend
upon the crossing inhibition arriving in time to prevent the firing of
group B motoneurons but too late to prevent that of the primary motoneurons.] Another relevant finding was that the crossed excitation is
always associated with the ipsilateral excitation, which it follows by 1-3
msec; when the latter is reduced or abolished by inhibition or fatigue
(Fig. 44) so is the former, and to a roughly corresponding extent.
We may speculate further on the nature of an excitatory cascade
with regard to the fractionation of the response in the primary motoneuron. Figure 29 shows records of the activity in the cell body of such
a motoneuron, orthodromically and antidromically excited, during the
crossed inhibition evoked by excitation of the contralateral Mauthner
axon. The various components of the electrical response of this cell were
easily distinguishable because of its deterioration as a consequence of
the microelectrode impalement. However, that these components are
not experimental artifacts is indicated by the ease with which they could
always be revealed by the activation of the crossing inhibition. There
were four components comprising the orthodromic response in this
example but only two comprising antidromic. As we have seen, the
two extra components in the orthodromic records seem to be contributed
by the A1 unit. As the crossing inhibition, which followed the ipsilateral
excitation, was initiated progressively earlier ( Figs. 29c-e and g-i) the
excitatory response was broken up in both the orthodromic and the
antidromic records until first one major component disappeared (records
in Figs. 29d and h ) and subsequently a second (records in Figs. 29e and
i). A consideration of the antidromic responses indicates that the first
response to disappear must be attributed to the cell body-initial segment
region of the motoneuron and the second to the ventral dendrite. (Recordings made from a ventral dendrite itself often had only a “hump”
on the falling phase to indicate the “cell body”response.) In Fig. 29e
is seen the A l response as recorded in the primary motoneuron; bringing
the inhibition still earlier eliminated this also (not illustrated-note the