9. THE MAUTHNER CELL
341
(eyes, jaw, and operculi) require bilateral and symmetrical muscle
activity, and this results from the excitation of either Mauthner cell.
Only the collateral inhibition of both the Mauthner cells in the brain
can minimize the possibility of the circuits involved in these cranial
movements being reactivated before the peak response is passed; fortunately, this collateral inhibition acts both on the cell from which it
originates and on the opposite one.
Nevertheless, in view of the phenomenon of fatigue, it is not clear
exactly what the function of the collateral inhibition could be. If, however, reexcitation of the Mauthner cells is a possibility, then its prevention would clearly minimize the amount of fatigue which could be
caused; we have mentioned that even when the crossed inhibition is
acting in the spinal cord, the excitatory neural systems still fatigue (Section IX, A, 1, c above). There would thus be a gain in the prevention of the (useless) reactivation of the circuitry at such a time, consequently reducing the fatigue in the susceptible parts of this circuitry.
2. THE SOURCES OF REEXCITATION OF THE MAUTHNER CELLS
Is there a likelihood of stimuli occurring which could cause reexcitation of a Mauthner cell during the increasing, or peak, reflex response,
a situation which we suggest above is undesirable? A number of possibilities can be mentioned: ( a ) recxcitation, following a single startleresponse, by the mechanical disturbance of the tailflip itself; ( b ) multiple
excitations resulting from multiple reflections of a sound wave from
nearby structures or other fish; and ( c ) in a shoal of fish, repeated excitation by the mechanical disturbances deriving from startle-responses
or sudden movements of nearby fish. In this context one might speculate
as to the possibility that the first sudden movement of a fish could
excite a startle-response in nearby fish, possibly coupled with optical
stimuli leading to an orientated response, and that this could conceivably be the basis of the sudden changes of direction observed in
shoals of freely swimming fish.
It should be noted that the collateral inhibition of the Mauthner
cell will not prevent its excitation with the near certainty that the
crossing inhibition in the cord prevents the excitation of the primary
motoneuron. Furthermore, the collateral inhibition acting on the lateral
dendrite (and possibly on the VIIIth nerve excitatory system itself)
lasts longer than that acting on the Mauthner cell soma (see Furukawa,
1966). Possibly, inputs to the somatic region of the Mauthner cell can
initiate excitability changes even before the lateral dendrite is responsive again to the ipsilateral VIIIth nerve input. The crossed VIIIth
341
(eyes, jaw, and operculi) require bilateral and symmetrical muscle
activity, and this results from the excitation of either Mauthner cell.
Only the collateral inhibition of both the Mauthner cells in the brain
can minimize the possibility of the circuits involved in these cranial
movements being reactivated before the peak response is passed; fortunately, this collateral inhibition acts both on the cell from which it
originates and on the opposite one.
Nevertheless, in view of the phenomenon of fatigue, it is not clear
exactly what the function of the collateral inhibition could be. If, however, reexcitation of the Mauthner cells is a possibility, then its prevention would clearly minimize the amount of fatigue which could be
caused; we have mentioned that even when the crossed inhibition is
acting in the spinal cord, the excitatory neural systems still fatigue (Section IX, A, 1, c above). There would thus be a gain in the prevention of the (useless) reactivation of the circuitry at such a time, consequently reducing the fatigue in the susceptible parts of this circuitry.
2. THE SOURCES OF REEXCITATION OF THE MAUTHNER CELLS
Is there a likelihood of stimuli occurring which could cause reexcitation of a Mauthner cell during the increasing, or peak, reflex response,
a situation which we suggest above is undesirable? A number of possibilities can be mentioned: ( a ) recxcitation, following a single startleresponse, by the mechanical disturbance of the tailflip itself; ( b ) multiple
excitations resulting from multiple reflections of a sound wave from
nearby structures or other fish; and ( c ) in a shoal of fish, repeated excitation by the mechanical disturbances deriving from startle-responses
or sudden movements of nearby fish. In this context one might speculate
as to the possibility that the first sudden movement of a fish could
excite a startle-response in nearby fish, possibly coupled with optical
stimuli leading to an orientated response, and that this could conceivably be the basis of the sudden changes of direction observed in
shoals of freely swimming fish.
It should be noted that the collateral inhibition of the Mauthner
cell will not prevent its excitation with the near certainty that the
crossing inhibition in the cord prevents the excitation of the primary
motoneuron. Furthermore, the collateral inhibition acting on the lateral
dendrite (and possibly on the VIIIth nerve excitatory system itself)
lasts longer than that acting on the Mauthner cell soma (see Furukawa,
1966). Possibly, inputs to the somatic region of the Mauthner cell can
initiate excitability changes even before the lateral dendrite is responsive again to the ipsilateral VIIIth nerve input. The crossed VIIIth