Cholinergic-Mediated IP3-Receptor Activation Induces Long-Lasting Synaptic Enhancement in CA1 Pyramidal Neurons

Cholinergic-glutamatergic interactions influence forms of synaptic plasticity that are thought to mediate memory and learning. We tested in vitro the induction of long-lasting synaptic enhancement at Schaffer collaterals by acetylcholine (ACh) at the apical dendrite of CA1 pyramidal neurons and in v...

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Published inThe Journal of neuroscience Vol. 28; no. 6; pp. 1469 - 1478
Main Authors de Sevilla, David Fernandez, Nunez, Angel, Borde, Michel, Malinow, Roberto, Buno, Washington
Format Journal Article
LanguageEnglish
Published United States Soc Neuroscience 06.02.2008
Society for Neuroscience
Subjects
Acetylcholine - pharmacology
Acetylcholine - physiology
Animals
Calcium - metabolism
Cholinergic Agents - pharmacology
Female
Inositol 1,4,5-Trisphosphate Receptors - agonists
Inositol 1,4,5-Trisphosphate Receptors - metabolism
Long-Term Potentiation - drug effects
Long-Term Potentiation - physiology
Male
Neurons - drug effects
Neurons - metabolism
Pyramidal Cells - drug effects
Pyramidal Cells - metabolism
Rats
Rats, Wistar
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Summary:Cholinergic-glutamatergic interactions influence forms of synaptic plasticity that are thought to mediate memory and learning. We tested in vitro the induction of long-lasting synaptic enhancement at Schaffer collaterals by acetylcholine (ACh) at the apical dendrite of CA1 pyramidal neurons and in vivo by stimulation of cholinergic afferents. In vitro ACh induced a Ca2+ wave and synaptic enhancement mediated by insertion of AMPA receptors in spines. Activation of muscarinic ACh receptors (mAChRs) and Ca2+ release from inositol 1,4,5-trisphosphate (IP3)-sensitive stores were required for this synaptic enhancement that was insensitive to blockade of NMDA receptors and also triggered by IP3 uncaging. Activation of cholinergic afferents in vivo induced an analogous atropine-sensitive synaptic enhancement. We describe a novel form of synaptic enhancement (LTP(IP3)) that is induced in vitro and in vivo by activation of mAChRs. We conclude that Ca2+ released from postsynaptic endoplasmic reticulum stores is the critical event in the induction of this unique form of long-lasting synaptic enhancement.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
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ISSN:0270-6474
1529-2401
1529-2401
DOI:10.1523/JNEUROSCI.2723-07.2008