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J Physiol. 2005 Jan 15;562(Pt 2):439-53. Epub 2004 Nov 18.

Intracellular calcium store filling by an L-type calcium current in the basolateral amygdala at subthreshold membrane potentials.

Author information

1
Queensland Brain Institute, School of Biomedical Sciences, St Lucia, Queensland 4072, Australia.

Abstract

The long-term changes that underlie learning and memory are activated by rises in intracellular Ca2+ that activate a number of signalling pathways and trigger changes in gene transcription. Ca2+ rises due to influx via L-type voltage-dependent Ca2+ channels (L-VDCCs) and release from intracellular Ca2+ stores have been consistently implicated in the biochemical cascades that underlie the final changes in memory formation. Here, we show that pyramidal neurones in the basolateral amygdala express an L-VDCC that is active at resting membrane potentials. Subthreshold depolarization of neurones either by current injection or summating synaptic potentials led to a sustained rise in cytosolic Ca2+ that was blocked by the dihydropyridine nicardipine. Activation of metabotropic receptors released Ca2+ from intracellular Ca2+ stores. At hyperpolarized potentials, metabotropic-evoked store release ran down with repeated stimulation. Depolarization of cells to -50 mV, or maintaining them at the resting membrane potential, restored release from intracellular Ca2+ stores, an effect that was blocked by nicardipine. These results show that Ca2+ influx via a low-voltage-activated L-type Ca2+ current refills inositol 1,4,5-trisphosphate (IP(3))-sensitive intracellular Ca2+ stores, and maintains Ca2+ release and wave generation by metabotropic receptor activation.

PMID:
15550460
PMCID:
PMC1665498
DOI:
10.1113/jphysiol.2004.076711
[Indexed for MEDLINE]
Free PMC Article

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