Experience-dependent plasticity acts via GluR1 and a novel neuronal nitric oxide synthase-dependent synaptic mechanism in adult cortex

Dachtler, James ORCID: https://orcid.org/0000-0001-6942-7844, Hardingham, Neil Robert, Glazewski, Stanislaw, Wright, Nicholas Fraser, Blain, Emma Jane ORCID: https://orcid.org/0000-0001-8944-4254 and Fox, Kevin Dyson ORCID: https://orcid.org/0000-0002-2563-112X 2011. Experience-dependent plasticity acts via GluR1 and a novel neuronal nitric oxide synthase-dependent synaptic mechanism in adult cortex. Journal of Neuroscience 31 (31) , pp. 11220-11230. 10.1523/JNEUROSCI.1590-11.2011

Preview

PDF - Published Version Download (1MB) | Preview

Abstract

Synaptic plasticity directs development of the nervous system and is thought to underlie memory storage in adult animals. A great deal of our current understanding of the role of AMPA receptors in synaptic plasticity comes from studies on developing cortex and cell cultures. In the present study, we instead focus on plasticity in mature neurons in the neocortex of adult animals. We find that the glutamate receptor 1 (GluR1) subunit of the AMPA receptor is involved in experience-dependent plasticity in adult cortex in vivo and that it acts in addition to neuronal nitric oxide synthase (αNOS1), an enzyme that produces the rapid synaptic signaling molecule nitric oxide (NO). Potentiation of the spared whisker response, following single whisker experience, is ∼33% less in GluR1-null mutants than in wild types. We found that the remaining plasticity depended on αNOS1. Potentiation was reduced by >42% in the single αNOS1-null mutants and completely abolished in GluR1/αNOS1 double-knock-out mice. However, potentiation in GluR1/NOS3 double knock-outs occurred at similar levels to that seen in GluR1 single knock-outs. Synaptic plasticity in the layer IV to II/III pathway in vitro mirrored the results in vivo, in that LTP was present in GluR1/NOS3 double-knock-out mice but not in the GluR1/αNOS1 animals. While basal levels of NO in cortical slices depended on both αNOS1 and NOS3, NMDA receptor-dependent NO release only depended on αNOS1 and not on NOS3. These findings demonstrate that αNOS1 acts in concert with GluR1 to produce experience-dependent plasticity in the neocortex.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Biosciences Psychology
Subjects:	Q Science > Q Science (General) R Medicine > RC Internal medicine > RC0321 Neuroscience. Biological psychiatry. Neuropsychiatry
Publisher:	Society for Neuroscience
ISSN:	0270-6474
Funders:	MRC
Date of First Compliant Deposit:	30 March 2016
Last Modified:	14 Jun 2023 22:10
URI:	https://orca.cardiff.ac.uk/id/eprint/24326

Citation Data

Cited 33 times in Scopus. View in Scopus. Powered By Scopus® Data

Actions (repository staff only)

Edit Item