Iontophoresis of Li+ antagonizes noradrenergic synaptic inhibition of rat cerebellar Purkinje cells.

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Abstract
Li salts provide effective therapy for manic-depressive psychosis, but the site and mechanism of this effect are unknown. The ability of Li applied by microiontophoresis to modify the responsiveness of cerebellar Purkinje neurons to iontophoretic applications of norepinephrine and .gamma.-aminobutyrate and to the inhibition produced by stimulation of the noradrenegic ceruleo-cerebellar pathway was tested. As in the rat hippocampal neurons acute exposure to Li produces selective, reversible antagonism of norepinephrine and noradrenergic pathway effects but does not affect .gamma.-aminobutyrate inhibitory action. Collectively these selective antagonisms of noradrenergic synaptic inhibitions in the cerebellum and hippocampus may show a general effect of Li suitable for extended observations in rats exposed to Li for the chronic periods needed to achieve therapeutic effects in man.