9. THE MAUTHNER CELL
31 1
will be constant and highly predictable. The timing of the arrival of
these impulses, since their route to the special synaptic region is so
short and direct, depends entirely upon the timing of the excitation of
the Mauthner cells, and this is discussed later. However, the ability
of the impulses in the two Mauthner axons to cause an excitatory and
inhibitory interaction of such repeatable precision is largely dependent
on this special feature, a postsynaptic region both protected from the
usual influences which cause “synaptic noise” (see below) and isolated
in order to exclude the possibility of interaction there between the effects
of Mauthner inputs and those of other (non-Mauthner) inputs to the
spinal motoneuron.
Signals set up on either side of the proposed high resistance transitional region between the A l unit (the dendritic spine or intermediate
cell) and the A2 unit (actually the ventral dendrite of the primary
motoneuron) attenuate as they cross it. We have seen evidence of this
in the reduction in size of the A1 e.p.s.p. and action potential when they
are recorded in the ventral dendrite (Fig. 15). Their attenuation, however, is not so great as to prevent the initiation of spikes in the dendrite.
What is the evidence that signals actually generated in the cell body
and dendrites of the motoneuron will not cause any important effects
in the A1 unit? First (Fig. 17d), even an antidromic spike in the main
dendrite may not cause more than a few millivolts’ change in the A1
unit. Second, and much more significant, is the fact that in our experiments synaptic noise was never recorded in an A1 unit. Synaptic noise
is the occurrence of small transient fluctuations in membrane potential
believed to result usually from the sporadic arrival of impulses at
nerve endings synapsing on the cell (but see Katz and Miledi, 1963).
Such subthreshold synaptic activity however was recorded in the
motoneuron cell body and even in the main ventral dendrite, and often
this was “spontaneous.”
Figure 30A shows characteristic responses caused by producing
sounds in the vicinity of the fish, which presumably activated vestibular
neurons in the brain. Such neurons, then, can affect the primary motoneuron in the spinal cord independently of the Mauthner cells. We have
also been able to cause excitatory potentials in the primary motoneurons
by stimulating axons in the spinal cord other than the Mauthner axons
themselves (Fig. 30B). But no such effects were ever seen in the A1
unit itself. It seems that only the Mauthner axon collaterals make
contacts on these units (and naturally there are no spontaneous impulses
in such collaterals) and that signals generated by synaptic activity in the
parent motoneuron attenuate to negligible levels during their electrotonic conduction across the junction into the A1 unit. Furthermore,
31 1
will be constant and highly predictable. The timing of the arrival of
these impulses, since their route to the special synaptic region is so
short and direct, depends entirely upon the timing of the excitation of
the Mauthner cells, and this is discussed later. However, the ability
of the impulses in the two Mauthner axons to cause an excitatory and
inhibitory interaction of such repeatable precision is largely dependent
on this special feature, a postsynaptic region both protected from the
usual influences which cause “synaptic noise” (see below) and isolated
in order to exclude the possibility of interaction there between the effects
of Mauthner inputs and those of other (non-Mauthner) inputs to the
spinal motoneuron.
Signals set up on either side of the proposed high resistance transitional region between the A l unit (the dendritic spine or intermediate
cell) and the A2 unit (actually the ventral dendrite of the primary
motoneuron) attenuate as they cross it. We have seen evidence of this
in the reduction in size of the A1 e.p.s.p. and action potential when they
are recorded in the ventral dendrite (Fig. 15). Their attenuation, however, is not so great as to prevent the initiation of spikes in the dendrite.
What is the evidence that signals actually generated in the cell body
and dendrites of the motoneuron will not cause any important effects
in the A1 unit? First (Fig. 17d), even an antidromic spike in the main
dendrite may not cause more than a few millivolts’ change in the A1
unit. Second, and much more significant, is the fact that in our experiments synaptic noise was never recorded in an A1 unit. Synaptic noise
is the occurrence of small transient fluctuations in membrane potential
believed to result usually from the sporadic arrival of impulses at
nerve endings synapsing on the cell (but see Katz and Miledi, 1963).
Such subthreshold synaptic activity however was recorded in the
motoneuron cell body and even in the main ventral dendrite, and often
this was “spontaneous.”
Figure 30A shows characteristic responses caused by producing
sounds in the vicinity of the fish, which presumably activated vestibular
neurons in the brain. Such neurons, then, can affect the primary motoneuron in the spinal cord independently of the Mauthner cells. We have
also been able to cause excitatory potentials in the primary motoneurons
by stimulating axons in the spinal cord other than the Mauthner axons
themselves (Fig. 30B). But no such effects were ever seen in the A1
unit itself. It seems that only the Mauthner axon collaterals make
contacts on these units (and naturally there are no spontaneous impulses
in such collaterals) and that signals generated by synaptic activity in the
parent motoneuron attenuate to negligible levels during their electrotonic conduction across the junction into the A1 unit. Furthermore,