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Publication : Impairment of neocortical long-term potentiation in mice deficient of endothelial nitric oxide synthase.

First Author  Haul S Year  1999
Journal  J Neurophysiol Volume  81
Issue  2 Pages  494-7
PubMed ID  10036253 Mgi Jnum  J:103986
Mgi Id  MGI:3610942 Doi  10.1152/jn.1999.81.2.494
Citation  Haul S, et al. (1999) Impairment of neocortical long-term potentiation in mice deficient of endothelial nitric oxide synthase. J Neurophysiol 81(2):494-7
abstractText  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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