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

Power, J. M. and Sah, P. (2005) Intracellular calcium store filling by an L-type calcium current in the basolateral amygdala at subthreshold membrane potentials. Journal of Physiology, 562 2: 439-453. doi:10.1113/jphysiol.2004.076711


Author Power, J. M.
Sah, P.
Title Intracellular calcium store filling by an L-type calcium current in the basolateral amygdala at subthreshold membrane potentials
Journal name Journal of Physiology   Check publisher's open access policy
ISSN 0022-3751
Publication date 2005
Sub-type Article (original research)
DOI 10.1113/jphysiol.2004.076711
Volume 562
Issue 2
Start page 439
End page 453
Total pages 15
Editor Steward O. Sage
Place of publication Oxford UK
Publisher The Physiological Society & Blackwell Publishing
Collection year 2005
Language eng
Subject 320702 Central Nervous System
C1
730104 Nervous system and disorders
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.
Keyword Algorithms
Amygdala/drug effects/metabolism/ physiology
Animals
Calcium/ metabolism
Calcium Channel Blockers/pharmacology
Calcium Channels, L-Type/drug effects/ metabolism
Inositol 1,4,5-Trisphosphate/physiology
Kinetics
Membrane Potentials/drug effects/physiology
Microscopy, Confocal
Microscopy, Fluorescence
Neuronal Plasticity/drug effects/physiology
Rats
Synapses/drug effects/physiology
omega-Conotoxin GVIA/pharmacology
Q-Index Code C1

 
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Created: Wed, 19 Mar 2008, 09:51:40 EST