Site of Origin and Propagation of Spike in the Giant Neuron of Aplysia

Abstract

A B S T R A C T The form and time sequence of spikes generated by orthodromic, antidromic, and direct stimulation and during spontaneous activity have been studied with intracellular electrodes simultaneously introduced in the soma and in different parts of the axon of the giant nerve cell of AiOlysla. Evidence was obtained that :under normal conditions of excitability, the spike originates at some distance from the soma in an axonal region with a higher excitability surpassing that of the surrounding membranes. Between the trigger zone and the soma is situated a region of transitional excitability where the conduction of the spike towards the soma may be blocked at a functionally determined and variable locus. The cell body is electrically excitable, but has the highest threshold of all parts of the neuron. The inactivation or even the removal of the cell body does not suppress synaptic transmission.The use of modern electrophysiological methods allowing intracellular and extremely localized extracellular recordings has provided recent evidence of the heterogeneity of membrane properties in different regions of a single neuron. Thus, it was shown that the site of spike initiation is not to be found in the part of the neuron in which the synaptic contacts are most dense, but in a special region in which the intrinsic membrane excitability is particularly high. Suggestions by Gesell (12) and Bishop (3) that the spike takes origin in the axon hillock region having no or few synapses, received a splendid confirmation with the work of Araki and Otani (1), Fuortes, Frank, and Becker (11), Coombs, Curtis, and Eccles (4, 5), and others on the vertebrate spinal motoneuron. In the crustacean stretch receptor Edwards and Ottoson (8) have localized the site of spike initiation in the axon relatively far from the cell body, and Diamond, Gray, and Sato (6) have concluded that the discharge of the Pacinian corpuscle originates in the first axonal node.The Aplysia giant neuron (GN) with its large cell body (300 to 800/~ in

Initiation of Sodium Spikelets in Basal Dendrites of Neocortical Pyramidal Neurons

“…Locally triggered basal spikelets on the other hand, not only lack the passive boost of the somatic AP, but even worse, their generator current is sucked up by an enormous nearby current sink -the cell body. That a sudden increase in diameter at a neurite-soma junction presents a serious obstacle for propagation of sodium spikes has been shown previously in computer simulations (Goldstein & Rall, 1974;Parnas, Hochstein & Parnas, 1976;Archie & Mel, 2000;Hossain et al, 2005), and, most importantly, in experimental measurements of action potential propagation from the neuronal process into the soma (Tauc, 1962;Ramon, Joyner & Moore, 1975;Golding & Spruston, 1998;Antic et al, 2000;Golding, Staff & Spruston, 2002). Therefore, the relatively low density of sodium channels in basal dendrites, in combination with the proximity of the cell body, might be responsible for the low incidence of basal spikelets in the somatic recordings (Fig.…”

Spike initiation by transmembrane current: a white‐noise analysis.

“…The Gaussian white noise was injected intrasomatically, though the locus of spike initiation (at least for cell R2) is approximately 1 mm from the soma (Tauc, 1962). It wa s therefore important to establish that influential components of the somatically SPIKE INITIATION BY WVHITE-NOISE CURRENT 283 injected noise were not altered significantly in the process of electrotonic propagation to the spike-initiation point.…”

“…It wa s therefore important to establish that influential components of the somatically SPIKE INITIATION BY WVHITE-NOISE CURRENT 283 injected noise were not altered significantly in the process of electrotonic propagation to the spike-initiation point. The attenuation of each applied frequency with distance along the cell was studied in R2, a cell that allows impalement of the soma with stimulating and recording electrodes and of the axon with a third electrode for recording (Tauc, 1962). The between-electrode distance (from soma to axon) underestimates the actual cellular distances which could not be measured.…”

Studies of antidromically identified neurosecretory cells of the hypothalamus by intracellular and extracellular recordings

“…In mammalian spinal motoneurones the IS and SD spikes are never completely separated; only a slight delay is observed in the rising phase of the antidromic action potential before complete block of the SD spike occurs. In aplysia ganglion cells, in which afferents synapse at the axon hillock, such separation between the A-and B-spikes occurs quite often (Tauc, 1962). If we assume in the case of the neurosecretory cell that the small spike originates from the axon hillock region and the large spike from soma-dendritic region, as occurs in spinal motoneurones, the observed difficulty of antidromic impulse invasion from axon hillock to soma-dendritic regions must be due to some morphological uniqueness of this cell.…”