The Site of Impulse Initiation in Bipolar Receptor Neurons of Callinectes Sapidus

In the multipolar abdominal stretch receptors of the crayfish and lobster, action potentials are initiated in a segment of the axon central to the cell body (Case, Edwards, Gesteland & Ottoson, 1957; Edwards & Ottoson, 1958; Eyzaguirre & Kuffler, 1955). Since the soma lies at the periphery, close to the receptor region in the dendrites, the initial excitation set up by the mechanical stimulus must traverse the cell body to reach the spike trigger zone in the axon. A microelectrode placed in the soma of this cell detects the depolarization produced by the generator current flowing from dendrites to axon. This depolarization—the generator potential—is subsequently wiped out in the soma by the peripherally travelling action potential, only to be re-established if the excitation continues. In an earlier paper (Mendelson, 1963) on the movement-sensitive, bipolar receptor cells of the P.D. organ of Pachygrapsus crassipes, I reported that a microelectrode in the soma does not detect a potential change that may be attributed to the flow of generator current from the mechanically excited region. Action potentials in response to adequate stimuli rise abruptly from the resting (potential) base-line without preliminary slow depolarization, nor is there a steady maintained depolarization during a prolonged stimulus that elicits a train of impulses. I therefore proposed that in the bipolar movement-receptor neuron the impulse is initiated far distal to the soma and that appreciable generator currents do not ordinarily flow through the soma. Subsequently, Mellon & Kennedy (1964) presented quite strong evidence that in the bipolar neurons of the hair-pit receptors on the crayfish branchiostegite the action potential is initiated in the distal process of the cell; the spike then traverses the soma into the central axon. The hair-pit bipolars—like the P.D. bipolars—exhibit soma action potentials, in response to mechanical stimuli, that rise sharply out of the base-line without preliminary depolarization. Mellon & Kennedy also found that when an antidromic spike left the soma refractory, an electrical stimulus to the distal process produced a small partial spike in the soma; probably the orthodromic spike was blocked in the distal process. It was not possible with the experimental arrangement they used to demonstrate that there was no action potential in the central axon at the time of the blocked spike. This leaves a slight uncertainty. This paper presents further, decisive evidence