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The Journal of Neurophysiology Vol. 81 No. 2 February 1999, pp. 494-497
Copyright ©1999 by the American Physiological Society
1Institute of Neurophysiology, 2Institute of Cardiovascular Physiology, and 3Center for Biological and Medical Research, University of Düsseldorf, D-40001 Dusseldorf, Germany
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
NG-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.
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