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Modulation of Calcium Entry and Glutamate Release in Cultured Cerebellar Granule Cells by Palytoxin by Carmen Vale; Amparo Alfonso; Cristina Suñol; Mercedes R. Vieytes; Luis M. Botana is a scholarly article available to read on EtoBox.

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## Abstract A channel open on the membrane can be formed by palytoxin (PTX). Ten nanomolar PTX caused an irreversible increase in the cytosolic calcium concentration ([Ca^2+^]~c~), which was abolished in the absence of external calcium. The increase was eliminated by saxitoxin (STX) and nifedipine (NIF). Calcium rise is secondary to the membrane depolarization. PTX effect on calcium was dependent on extracellular Na^+^. Li^+^ decreased the PTX‐evoked rise in [Ca^2+^]~c~; replacement of Na^+^ by N‐methyl‐D‐glucamine (NMDG) abolished PTX‐induced calcium increase. [Ca^2+^]~c~ increase by PTX was strongly reduced after inhibition of the reverse operation of the Na^+^/Ca^2+^ exchanger, in the presence of antagonists of excitatory amino acid (EAA) receptors, and by inhibition of neurotransmitter release. PTX did not modify calcium extrusion by the plasma membrane Ca^2+^‐ATPase (PMCA), because blockade of the calcium pump increased rather than decreased the PTX‐induced calcium influx. Extracellular levels of glutamate and aspartate were measured by HPLC and exocytotic neurotransmitter release by determination of synaptic vesicle exocytosis using total internal reflection fluorescence micr

Author

Carmen Vale; Amparo Alfonso; Cristina Suñol; Mercedes R. Vieytes; Luis M. Botana

Publisher

John Wiley and Sons; Wiley (John Wiley & Sons); John Wiley & Sons Inc.; Wiley (ISSN 0360-4012)

Published

2006

Language

EN