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Mechanisms for Synchronous Calcium Oscillations in Cultured Rat Cerebellar Neurons
Author(s) -
Nuñez Lucia,
Sanchez Ana,
Fonteriz Rosalba I.,
GarciaSancho Javier
Publication year - 1996
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.1996.tb01180.x
Subject(s) - nmda receptor , chemistry , biophysics , glutamatergic , neuroscience , calcium , glutamate receptor , cnqx , ampa receptor , tetrodotoxin , voltage dependent calcium channel , biology , receptor , biochemistry , organic chemistry
Removal of Mg 2+ caused oscillations of the cytosolic Ca 2+ concentration ([Ca 2+ ] i ) and the membrane potential in cultured cerebellar granule neurons. Oscillations of [Ca 2+ ] i were synchronous in all the cells, and were restricted to the neurons (immunocytochemically identified) that responded to exogenous N ‐methyl‐D‐aspartate (NMDA). Oscillations were blocked by Ca 2+ removal, nickel, NMDA receptor antagonists, ω‐agatoxin IVA, tetrodotoxin, sodium removal and γ‐aminobutyric acid, but not by dihydropyridines, ω‐conotoxin M VIIA or by emptying the intracellular Ca 2+ stores with thapsigargin or ionomycin. The upstroke of the [Ca 2+ ] i oscillations coincided in time with an increase in manganese permeability of the plasma membrane. Propagation of the [Ca 2+ ] i wave followed more than one pathway and the spatiotemporal pattern changed with time. Membrane potential oscillations consisted of transient slow depolarizations of ˜20 mV with faster phasic activity superimposed. We propose that the synchronous [Ca 2+ ] i oscillations are the expression of irradiation of random excitation through a neuronal network requiring generation of action potentials and functional glutamatergic synapses. Oscillations of [Ca 2+ ] i are due to cyclic Ca 2+ entry through NMDA receptor channels activated by synaptic release of glutamate, which requires Ca 2+ entry through P‐type Ca 2+ channels activated by action potentials at the presynaptic terminal.