Acute effects of lithium chloride on noradrenergic neurons from rat cerebral cortex.
Acute effects of lithium chloride upon the parameters of central noradrenergic function were assessed at either a therapeutic dose (2 m-equiv/kg) or a toxic one (10 m-equiv/kg) on rats. Lithium chloride lacked a direct effect on tyrosine hydroxylase (TH), monoamine oxidase (MAO), or catechol-O-methyltransferase (COMT) in concentrations up to 2 mM. A single i.p. injection of both studied doses inhibited MAO a hr later. Endogenous NA levels in frontal cerebral cortex were increased by a therapeutic dose and slightly increased by a toxic dose. Uptake of [3H]NA was increased in pretreated tissues at a therapeutic level but decreased by a toxic dose. The unmetabolized [3H]NA was always increased over controls.
D000818:Animals; D002394:Catechol O-Methyltransferase / Q000096:biosynthesis*; D002540:Cerebral Cortex / Q000201:enzymology* / Q000378:metabolism; D002712:Chlorides / Q000494:pharmacology*; D004790:Enzyme Induction / Q000187:drug effects; D066298:In Vitro Techniques; D008094:Lithium / Q000494:pharmacology*; D018021:Lithium Chloride; D008297:Male; D008995:Monoamine Oxidase / Q000096:biosynthesis*; D009638:Norepinephrine / Q000378:metabolism*; D051381:Rats; D014446:Tyrosine 3-Monooxygenase / Q000096:biosynthesis*
D002712:Chlorides; D008094:Lithium; D014446:Tyrosine 3-Monooxygenase; D008995:Monoamine Oxidase; D002394:Catechol O-Methyltransferase; D018021:Lithium Chloride; D009638:Norepinephrine