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

Abstract
Li salts provide effective therapy for manic-depressive psychosis, but the site and mechanism of this effect are not known. We have tested the ability of Li, applied by microiontophoresis, to modify the responsiveness of rat cerebellar Purkinje neurons to iontophoretic applications of norepinephrine and gamma-aminobutyrate and to the inhibition produced by stimulation of the noradrenergic ceruleo-cerebellar pathway. As previously reported for rat hippocampal neurons, acute exposure to Li produces selective, reversible antagonism of the effects of norepinephrine and the noradrenergic pathway but does not affect inhibitory actions of gamma-aminobutyrate. Collectively, these selective antagonisms of noradrenergic sympatic inhibitions in the cerebellum and hippocampus may indicate 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.
AuthorsG R Siggins, S J Henriksen, F Bloom
JournalProceedings of the National Academy of Sciences of the United States of America (Proc Natl Acad Sci U S A) Vol. 76 Issue 6 Pg. 3015-8 (Jun 1979) ISSN: 0027-8424 [Print] United States
PMID288083 (Publication Type: Journal Article)
Chemical References
  • gamma-Aminobutyric Acid
  • Lithium
  • Norepinephrine
Topics
  • Animals
  • Cerebellum (metabolism)
  • Iontophoresis
  • Lithium (pharmacology)
  • Male
  • Norepinephrine (pharmacology)
  • Purkinje Cells (drug effects, metabolism)
  • Rats
  • gamma-Aminobutyric Acid (pharmacology)

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