Sensory deprivation unmasks a PKA-dependent synaptic plasticity that operates in parallel with CaMKII

Hardingham, Neil Robert, Wright, Nicholas Fraser, Dachtler, James ORCID: https://orcid.org/0000-0001-6942-7844 and Fox, Kevin Dyson ORCID: https://orcid.org/0000-0002-2563-112X 2008. Sensory deprivation unmasks a PKA-dependent synaptic plasticity that operates in parallel with CaMKII. Neuron 60 (5) , pp. 861-874. 10.1016/j.neuron.2008.10.018

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Abstract

Calcium/calmodulin kinase II (CaMKII) is required for LTP and experience-dependent potentiation in the barrel cortex. Here, we find that whisker deprivation increases LTP in the layer IV to II/III pathway and that PKA antagonists block the additional LTP. No LTP was seen in undeprived CaMKII-T286A mice, but whisker deprivation again unmasked PKA-sensitive LTP. Infusion of a PKA agonist potentiated EPSPs in deprived wild-types and deprived CaMKII-T286A point mutants but not in undeprived animals of either genotype. The PKA-dependent potentiation mechanism was not present in GluR1 knockouts. Infusion of a PKA antagonist caused depression of EPSPs in undeprived but not deprived cortex. LTD was occluded by whisker deprivation and blocked by PKA manipulation, but not blocked by cannabinoid antagonists. NMDA receptor currents were unaffected by sensory deprivation. These results suggest that sensory deprivation causes synaptic depression by reversing a PKA-dependent process that may act via GluR1.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Biosciences Psychology
Subjects:	R Medicine > RC Internal medicine > RC0321 Neuroscience. Biological psychiatry. Neuropsychiatry
Publisher:	Elsevier
ISSN:	0896-6273
Last Modified:	02 Dec 2022 11:58
URI:	https://orca.cardiff.ac.uk/id/eprint/9137

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