Nuclear calcium signaling evoked by cholinergic stimulation in hippocampal CA1 pyramidal neurons

Power, JM and Sah, P (2002) Nuclear calcium signaling evoked by cholinergic stimulation in hippocampal CA1 pyramidal neurons. Journal of Neuroscience, 22 9: 3454-3462.

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Author Power, JM
Sah, P
Title Nuclear calcium signaling evoked by cholinergic stimulation in hippocampal CA1 pyramidal neurons
Journal name Journal of Neuroscience   Check publisher's open access policy
ISSN 0270-6474
Publication date 2002-01-01
Sub-type Article (original research)
Open Access Status File (Publisher version)
Volume 22
Issue 9
Start page 3454
End page 3462
Total pages 9
Place of publication Washington
Publisher Soc Neuroscience
Language eng
Abstract The cholinergic system is thought to play an important role in hippocampal-dependent learning and memory. However, the mechanism of action of the cholinergic system in these actions in not well understood. Here we examined the effect of muscarinic receptor stimulation in hippocampal CA1 pyramidal neurons using whole-cell recordings in acute brain slices coupled with high-speed imaging of intracellular calcium. Activation of muscarinic acetylcholine receptors by synaptic stimulation of cholinergic afferents or application of muscarinic agonist in CA1 pyramidal neurons evoked a focal rise in free calcium in the apical dendrite that propagated as a wave into the soma and invaded the nucleus. The calcium rise to a single action potential was reduced during muscarinic stimulation. Conversely, the calcium rise during trains of action potentials was enhanced during muscarinic stimulation. The enhancement of free intracellular calcium was most pronounced in the soma and nuclear regions. In many cases, the calcium rise was distinguished by a clear inflection in the rising phase of the calcium transient, indicative of a regenerative response. Both calcium waves and the amplification of action potential-induced calcium transients were blocked the emptying of intracellular calcium stores or by antagonism of inositol 1,4,5-trisphosphate receptors with heparin or caffeine. Ryanodine receptors were not essential for the calcium waves or enhancement of calcium responses. Because rises in nuclear calcium are known to initiate the transcription of novel genes, we suggest that these actions of cholinergic stimulation may underlie its effects on learning and memory.
Keyword Neurosciences
Learning
Memory
Nucleus
Ip3
Acetylcholine
Ryanodine
Backpropagating Action-potentials
Acetylcholine-receptor Proteins
Gene-expression
Dendritic Spines
Rat Hippocampus
Inositol Trisphosphate
Creb Phosphorylation
Liver Nuclei
Ca2+ Release
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Unknown

Document type: Journal Article
Sub-type: Article (original research)
Collections: Excellence in Research Australia (ERA) - Collection
Queensland Brain Institute Publications
 
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Created: Mon, 13 Aug 2007, 22:56:29 EST