Abstract:
:cGMP has long been suspected to play a role in synaptic plasticity, but the inaccessibility of nerve terminals to electrical recording has impeded tests of this hypothesis. In posterior pituitary nerve terminals, nitric oxide enhanced Ca(2+)-activated K+ channel activity by activating guanylate cyclase and PKG. This enhancement occurred only at depolarized potentials, so the spike threshold remained unaltered but the afterhyperpolarization became larger. During spike trains, the enhanced afterhyperpolarization promoted Na+ channel recovery from inactivation, thus reducing action potential failures and allowing more Ca(2+) to enter. Activating guanylate cyclase, either with applied nitric oxide, or with physiological stimulation to activate nitric oxide synthase, increased action potential firing. Thus, the cGMP/nitric oxide cascade generates a short-term, use-dependent enhancement of release.
journal_name
Neuronjournal_title
Neuronauthors
Klyachko VA,Ahern GP,Jackson MBdoi
10.1016/s0896-6273(01)00449-4subject
Has Abstractpub_date
2001-09-27 00:00:00pages
1015-25issue
6eissn
0896-6273issn
1097-4199pii
S0896-6273(01)00449-4journal_volume
31pub_type
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