9. THE MAUTHNER CELL
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tinct sorts of unit, both apparently monosynaptically activated from
the Mauthner axon, which could help to explain some of the most important characteristics of the Mauthner reflex. There may be interesting
implications here for other neural systems, too; thus, the situation will
be dealt with in some detail.
The first point of interest becomes apparent when records of the
activity of an A1 and A2 unit from the same side of a given spinal
segment are aligned one above the other (with the two records of the
simultaneously recorded Mauthner axon spikes made coincident) ( Fig.
15). It can then be seen that the first and second phases of activity of
the two units occur at virtually the same time. But in the A2 unit their
amplitude is greatly reduced (Fig. 15b). These time coincidences and
other relevant findings presented below have suggested an interesting
possibility. It is as though an electrical junction exists between the two
units, thus allowing the electrical activity of the A1 unit to be detected
in the A2 unit also. On this basis, the electrically transmitted A1 response
would seem to be the immediate stimulus to the A2 unit, and the excitatory action of the Mauthner axon would be exerted directly on the
A1 unit. This hypothesis will be considered further.
3. THE IDENTITY OF GROUP A AND GROUP B CELLS
The A2 and B cells are certainly motoneurons since they can be
excited antidromically by stimulating appropriate ventral roots ( Figs.
l6b and 17b). However, when the antidromic and orthodromic records
from the same A2 cell are compared, it is seen that the first two components of the orthodromic response are absent in the antidromic record
(Fig. 16). These two components then do appear to comprise the excitatory potential immediately responsible for triggering the spike in the
A2 record, which is consistent with the hypothesis described above,
that they in fact represent the electrically transmitted activity of the A1
unit.
What is the identity of the A1 unit? It seems to be that first fired
off, apparently monosynaptically, by the Mauthner axon; and there
are reasons for assuming that it is excited via the release of a chemical
transmitter. Moreover, it appears to cause electrical excitation of the
A2 unit, an undoubted motoneuron. On the few occasions when it was
possible to make the test, A1 units could not be excited antidromically,
and only a small subthreshold depolarization was recorded in them
(Fig. 17d). Of course, this failure of antidromic invasion may have
resulted from damage, but it is also possible that the suggested electrical
coupling of A1 to A2 units involves a less effective current flow in the
287
tinct sorts of unit, both apparently monosynaptically activated from
the Mauthner axon, which could help to explain some of the most important characteristics of the Mauthner reflex. There may be interesting
implications here for other neural systems, too; thus, the situation will
be dealt with in some detail.
The first point of interest becomes apparent when records of the
activity of an A1 and A2 unit from the same side of a given spinal
segment are aligned one above the other (with the two records of the
simultaneously recorded Mauthner axon spikes made coincident) ( Fig.
15). It can then be seen that the first and second phases of activity of
the two units occur at virtually the same time. But in the A2 unit their
amplitude is greatly reduced (Fig. 15b). These time coincidences and
other relevant findings presented below have suggested an interesting
possibility. It is as though an electrical junction exists between the two
units, thus allowing the electrical activity of the A1 unit to be detected
in the A2 unit also. On this basis, the electrically transmitted A1 response
would seem to be the immediate stimulus to the A2 unit, and the excitatory action of the Mauthner axon would be exerted directly on the
A1 unit. This hypothesis will be considered further.
3. THE IDENTITY OF GROUP A AND GROUP B CELLS
The A2 and B cells are certainly motoneurons since they can be
excited antidromically by stimulating appropriate ventral roots ( Figs.
l6b and 17b). However, when the antidromic and orthodromic records
from the same A2 cell are compared, it is seen that the first two components of the orthodromic response are absent in the antidromic record
(Fig. 16). These two components then do appear to comprise the excitatory potential immediately responsible for triggering the spike in the
A2 record, which is consistent with the hypothesis described above,
that they in fact represent the electrically transmitted activity of the A1
unit.
What is the identity of the A1 unit? It seems to be that first fired
off, apparently monosynaptically, by the Mauthner axon; and there
are reasons for assuming that it is excited via the release of a chemical
transmitter. Moreover, it appears to cause electrical excitation of the
A2 unit, an undoubted motoneuron. On the few occasions when it was
possible to make the test, A1 units could not be excited antidromically,
and only a small subthreshold depolarization was recorded in them
(Fig. 17d). Of course, this failure of antidromic invasion may have
resulted from damage, but it is also possible that the suggested electrical
coupling of A1 to A2 units involves a less effective current flow in the