9. THE MAUTHNER CELL
337
entirely to do with a simple but powerful escape reflex, a mechanism
for avoidance of predators (see below).
If the excitatory cascade does exist (Section VI, E), it is still
possible for the primary motoneurons, and the subsequently activated
group B motoneurons, to be utilized for swimming; but the presumed
coordination required would be best achieved by controlling the motoneurons from non-Mauthner systems. That way the individual “cascades”
( i.e., those involving only one primary motoneuron) would provide
the minimum functional units. When the Mauthner axons are involved,
all the primary motoneurons and all the subsequently activated group
B cells together constitute the minimum unit. Of great relevance here
are the findings of Sims (1962) on the larvae of Xenopus laevis. After
section of their spinal cords the animals showed, not surprisingly, a
loss of locomotory movement below the level of the lesion and had
no startle-response. Subsequently their normal swimming ability returned. Histological examination showed that a great deal of regeneration had occurred in the spinal cords. However, below the level of spinal
section the Mauthner axons appeared to have degenerated irreversibly.
The startle-response, when it reappeared in the recovered animals, never
involved the part of the tail innervated from cord levels below that of
the original lesion but only that from above. This is telling support for
the rejection of the suggestion that Mauthner cells are involved in
swimming, and strengthens the conclusions reached in Section IX, C
below.
c. The Fatigue. It is of interest that the fatique in the collateral
inhibitory systems in the brain is also probably located in the Mauthner
collaterals rather than the interneurons which are almost certainly involved in the inhibitory pathways; recordings from such interneurons
(cf. Furukawa and Furshpan, 1963) show that their excitation ceases
during repetitive activation of the Mauthner cell, at frequencies which
cause fatigue of the collateral inhibition (cf. Fig. 40). We have observed that repetitive activation of both Mauthner axons synchronously
still causes fatigue in the neuronal circuit, even though there is no output
from the spinal cord (resulting from crossed inhibition). When, in the
train of stimuli, one is omitted on one side only, there is no motoneuron
discharge in response to the impulse in the opposite Mauthner axon,
the usual recovery period is required. This shows that the phenomenon is
not owing to a “Renshaw inhibition” initiated from excited motoneurons.
It seems possible that the phenomenon of fatigue in the various
Mauthner cell functions may reflect the relatively enormous integrative
and distributive function which is required of this single central neuron.
337
entirely to do with a simple but powerful escape reflex, a mechanism
for avoidance of predators (see below).
If the excitatory cascade does exist (Section VI, E), it is still
possible for the primary motoneurons, and the subsequently activated
group B motoneurons, to be utilized for swimming; but the presumed
coordination required would be best achieved by controlling the motoneurons from non-Mauthner systems. That way the individual “cascades”
( i.e., those involving only one primary motoneuron) would provide
the minimum functional units. When the Mauthner axons are involved,
all the primary motoneurons and all the subsequently activated group
B cells together constitute the minimum unit. Of great relevance here
are the findings of Sims (1962) on the larvae of Xenopus laevis. After
section of their spinal cords the animals showed, not surprisingly, a
loss of locomotory movement below the level of the lesion and had
no startle-response. Subsequently their normal swimming ability returned. Histological examination showed that a great deal of regeneration had occurred in the spinal cords. However, below the level of spinal
section the Mauthner axons appeared to have degenerated irreversibly.
The startle-response, when it reappeared in the recovered animals, never
involved the part of the tail innervated from cord levels below that of
the original lesion but only that from above. This is telling support for
the rejection of the suggestion that Mauthner cells are involved in
swimming, and strengthens the conclusions reached in Section IX, C
below.
c. The Fatigue. It is of interest that the fatique in the collateral
inhibitory systems in the brain is also probably located in the Mauthner
collaterals rather than the interneurons which are almost certainly involved in the inhibitory pathways; recordings from such interneurons
(cf. Furukawa and Furshpan, 1963) show that their excitation ceases
during repetitive activation of the Mauthner cell, at frequencies which
cause fatigue of the collateral inhibition (cf. Fig. 40). We have observed that repetitive activation of both Mauthner axons synchronously
still causes fatigue in the neuronal circuit, even though there is no output
from the spinal cord (resulting from crossed inhibition). When, in the
train of stimuli, one is omitted on one side only, there is no motoneuron
discharge in response to the impulse in the opposite Mauthner axon,
the usual recovery period is required. This shows that the phenomenon is
not owing to a “Renshaw inhibition” initiated from excited motoneurons.
It seems possible that the phenomenon of fatigue in the various
Mauthner cell functions may reflect the relatively enormous integrative
and distributive function which is required of this single central neuron.