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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.
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