In:
Journal of Neurophysiology, American Physiological Society, Vol. 81, No. 2 ( 1999-02-01), p. 494-497
Kurzfassung:
Impairment of neocortical long-term potentiation in mice deficient of endothelial nitric oxide synthase. The role of the possible retrograde messenger nitric oxide (NO) in the induction of long-term potentiation (LTP) was studied in supragranular layers of somatosensory cortical slices obtained from adult mice. High-frequency stimulation produced a slowly rising, long-lasting (50 min) and significant ( P 〈 0.001) increase in the extracellular synaptic response by 23%. The induction of LTP was independent from activation of N-methyl-d-aspartate (NMDA) receptors, but prevented by bath application of N G -nitro-l-arginine methyl ester (l-NAME), indicating that one or several of the different NO synthases (NOS) produced NO within the postsynaptic neuron. No LTP could be induced in knockout mice lacking the endothelial NOS (eNOS) isoform. These data suggest that eNOS is involved in an NMDA receptor–independent form of LTP in the rodent cerebral cortex.
Materialart:
Online-Ressource
ISSN:
0022-3077
,
1522-1598
DOI:
10.1152/jn.1999.81.2.494
RVK:
XA 10000 ; XA 552555
Sprache:
Englisch
Verlag:
American Physiological Society
Publikationsdatum:
1999
ZDB Id:
80161-6
ZDB Id:
1467889-5