Abstract
The tritium overflow evoked by electrical stimulation of rabbit hippocampal slices labeled with [3H]noradrenaline was inhibited by omega-conotoxin GVIA, a peptide modulator of the N-type voltage-sensitive calcium channel (N-VSCC). The magnitude of this inhibition was unchanged in the presence of substances which interact with N- and/or L-VSCCs (cadmium, neomycin, (-)- and (+)-202-791), alpha 2-adrenoceptors (idazoxan, UK-14304), protein kinase C (4 beta-phorbol-12,13-dibutyrate) or potassium channels (4-aminopyridine). This finding suggests that the attenuation of calcium-dependent neurotransmitter release by omega-conotoxin GVIA is relatively insensitive to alterations of such release effected by other substances.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Aminopyridines / pharmacology
-
Animals
-
Brimonidine Tartrate
-
Cadmium / pharmacology
-
Calcium Channel Blockers / pharmacology*
-
Dioxanes / pharmacology
-
Hippocampus / drug effects
-
Hippocampus / metabolism*
-
Idazoxan
-
In Vitro Techniques
-
Mollusk Venoms / pharmacology*
-
Neomycin / pharmacology
-
Nicotinic Acids / pharmacology
-
Norepinephrine / metabolism*
-
Oxadiazoles*
-
Phorbol Esters / pharmacology
-
Quinoxalines / pharmacology
-
Rabbits
-
omega-Conotoxin GVIA
Substances
-
Aminopyridines
-
Calcium Channel Blockers
-
Dioxanes
-
Mollusk Venoms
-
Nicotinic Acids
-
Oxadiazoles
-
Phorbol Esters
-
Quinoxalines
-
Cadmium
-
PN 202-791
-
Brimonidine Tartrate
-
omega-Conotoxin GVIA
-
Neomycin
-
Norepinephrine
-
Idazoxan