H Haghdoost-Yazdi1, F Rajaei, M Janahmadi. 1. Department of Physiology and Cellular and Molecular Research Center, Qazvin University of Medical Sciences, Tehran, Iran. hhaghdoost@qums.ac.ir
Abstract
OBJECTIVE: Cerebellar Purkinje cells (PCs) fire burst of Na(+) spikes riding on a Ca(2+) spike which basically involves the same ionic channels and currents establishing the paroxysmal depolarization shift (PDS) discharges. METHODS: Intracellular recordings were taken from somata of PCs to explore effects of the epileptogenic drugs of pentylenetetrazol (PTZ), bicuculline methiodide (BCC) and 4-aminopyridine (4-AP) on the firing behavior of these cells. RESULTS: PCs showed spontaneous PDS-like events in presence of these drugs. Generally, PTZ and BCC-induced PDSs were similar in shape and properties but were remarkably different from 4-AP-induced PDSs. Blockade of glutamate transmission inhibited generation of PDSs by PTZ and BCC but it did not affect discharge of PDSs induced by 4-AP. Careful analysis of PDS discharges revealed that they have remarkable differences with normal and 4-AP-induced spontaneous activity. DISCUSSION: Data presented here indicate that PDS discharges in PCs are induced either by the imbalance between excitatory and inhibitory synaptic transmission or by the suppression of 4-AP-sensitive currents.
OBJECTIVE: Cerebellar Purkinje cells (PCs) fire burst of Na(+) spikes riding on a Ca(2+) spike which basically involves the same ionic channels and currents establishing the paroxysmal depolarization shift (PDS) discharges. METHODS: Intracellular recordings were taken from somata of PCs to explore effects of the epileptogenic drugs of pentylenetetrazol (PTZ), bicuculline methiodide (BCC) and 4-aminopyridine (4-AP) on the firing behavior of these cells. RESULTS: PCs showed spontaneous PDS-like events in presence of these drugs. Generally, PTZ and BCC-induced PDSs were similar in shape and properties but were remarkably different from 4-AP-induced PDSs. Blockade of glutamate transmission inhibited generation of PDSs by PTZ and BCC but it did not affect discharge of PDSs induced by 4-AP. Careful analysis of PDS discharges revealed that they have remarkable differences with normal and 4-AP-induced spontaneous activity. DISCUSSION: Data presented here indicate that PDS discharges in PCs are induced either by the imbalance between excitatory and inhibitory synaptic transmission or by the suppression of 4-AP-sensitive currents.