Tetrodotoxin-resistant dendritic spikes in avian Purkinje cells.

Abstract

Comparative studies of cerebellar electrophysiology indicated that surface stimulation of the cerebellar cortex evokes a sharp, superficial, positive-negative wave produced by direct stimulation of the parallel fibers, followed by a secondary negativity (cf. ref. 4). In most vertebrates this latter negativity, which is produced by the activation of the parallel fiber-Purkinje cell junction, reverses to a positive wave at 100 gm depth and remains positive throughout the depth of the molecular layer. The above comparative study further determined that in pigeons, as in alligators (2), the superficial negativity does not reverse in depth. This particular distribution of the late negative wave has been found to be correlated with the active current sinks which characterize dendritic electroresponsiveness in the cerebellar cortex (2, 3).The Fig. 1A. Analysis of the laminar field potential confirmed the presence of large negative potentials attributable to inward ionic transmembrane current in the molecular layer between 100 and 300 ,m from the surface. Characteristically, this negative field demonstrated a shift in latency with depth, as indicated by the second broken line in the figure. This delay has been interpreted as the conduction time of dendritic current sinks from their site of origin to the somatic level (2).Following Loc stimulation it is possible to obtain, at 400 ,m depth, intrasomatically recorded spikes from Purkinje cells which are identified by their antidromic invasion (3, 5). These intracellular records are characterized by a resting potential of -60 to -65 mV and by the generation of increasing numbers of action potentials as the Loc stimulus intensity is increased (Fig. 1B) (Fig. 1G). As reported for the alligator, hyperpolarizing current pulses injected through the recording pipette uncovered several distinct all-or-nothing components, indicating that these action potentials had more than one site of spike initiation (Fig. 1). As in other Purkinje cells (3), the dendritic spikes thus appear to be conducted to the soma in a noncontinuous manner and produce, at that level, the prolonged after-depolarization seen in Fig. 1B

Morphological and electrophysiological characteristics of rat cerebellar slices maintained in vitro.

“…The rapid inactivation of the initial somatic spike with depolarizing current and its resistance to hyperpolarization accord with properties expected from sodium-mediated, fast, low-threshold spikes (Hodgkin & Huxley, 1952;Llinas & Hess, 1976;Wong et al 1979), whereas in the dendrites, the suppression of the successive slow spikes of the response by small hyperpolarizing currents confirms their high threshold and, therefore, their probable different generating mechanism. The unusual increase in amplitude of these active dendritic …”

“…However, the initial spike recorded in the dendrites might also be generated locally by a high-threshold, slow regenerative process, therefore having an additional delay with respect to the underlying e.p.s.p. This would explain both the timing of the response and the resemblance between the initial spike of the dendritic climbing fibre response and active slow dendritic spikes previously recorded in vivo and in vitro (Llinas & Nicholson, 1971;Llinas & Hess, 1976;Llina's & Sugimori, 1979;Wong et al 1979). In keeping with this interpretation and with experiments in vivo by Martinez et al (1971), the long duration of the subsequent partial spikes of the burst response in dendritic as, in most cases, in somatic climbing fibre responses, suggests that they might also be actively generated in the dendrites, rather than in the initial segment as proposed by Pellionisz & Llinas (1977).…”

Sodium-dependent regenerative responses in dendrites of axotomized motoneurons in the cat.

“…Aithough dendritic Ca2+ spikes have been reported in a number of neurons (36)(37)(38)(39)(40)(41)(42)(43), claims of dendritic spiking produced by Na+ are rather rare (44) and have only been reported in a cell that is also known to have predominant Ca2' dendritic spikes (37,38). The dendritic Na+ spike found in axotomized motoneurons and described here appears to be the result of dynamic changes in neuronal function induced by pathology.…”

Initiation and spread of action potentials in granule cells maintained in vitro in slices of guinea‐pig hippocampus.

“…The dendritic spikes described here appear to be due to regenerative sodium channels of the type commonly found in axons, and not to the (? )Ca channels described by Llinas & Hess (1976) and Schwartzkroin & Slawsky (1977). They could be present by chance and have no role in the neurones' activity, however, several possibilities exist.…”