Abstract:
:Carbon monoxide (CO) induces a long-lasting alteration in cerebellar alpha 3-Na,K-ATPase independent of [Na+] but linked to cGMP synthesis and localized to Purkinje neurons. The action of CO is absent in Purkinje neuron-deficient mice, mimicked by 8-Br-cGMP, and blocked by inhibition of PKG. Glutamate (Glu) and metabotropic agonists mimic the action of CO, an effect that requires PKC and is associated with CO synthesis. These data suggest that CO regulates Na,K-ATPase through cGMP and PKG, and that Glu regulates CO through mGluRs. This system is also modulated by NMDA agonists and nitric oxide, possibly via Glu release, as well as by free radicals. These findings offer a mechanism by which CO, Glu, and free radicals can exert specific effects on synaptic transmission (relevant to long-term changes in cell excitability), as well as more general actions on energy metabolism (relevant to the pathophysiology of excitotoxicity).
journal_name
Neuronjournal_title
Neuronauthors
Nathanson JA,Scavone C,Scanlon C,McKee Mdoi
10.1016/0896-6273(95)90222-8subject
Has Abstractpub_date
1995-04-01 00:00:00pages
781-94issue
4eissn
0896-6273issn
1097-4199pii
0896-6273(95)90222-8journal_volume
14pub_type
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