PMID: 6410443Jan 1, 1983Paper

Lithium-induced polydipsia: dependence on nigrostriatal dopamine pathway and relationship to changes in the renin-angiotensin system

Psychopharmacology
R B Mailman

Abstract

The dependence of lithium-induced polydipsia (LIP) on central monoamine pathways was investigated using several pharmacological manipulations. Intracisternal administration of 6-hydroxydopamine (6-OHDA) in combination with pargyline or desipramine was used to deplete dopamine (DA), norepinephrine, or both catecholamines. Significant decreases in LIP were seen after treatments that depleted brain DA, whereas depletion of norepinephrine alone did not affect LIP. Site-specific injection of 6-OHDA into the substantia nigra or caudate nucleus, but not the nucleus accumbens or noradrenergic dorsal bundle, also caused a decrease in LIP. Depletion of serotonin by intracisternal administration of 5,7-dihydroxytryptamine also had no effect on LIP. Consistent with these findings, the DA receptor blocker haloperidol attenuated LIP. Thus, LIP appears to be dependent on intact nigrostriatal DA fibers, but not on other monoaminergic systems in the brain. Lithium also increased plasma renin activity (PRA) and angiotensin I and II immunoreactivity in plasma, though the time course of LIP onset did not directly parallel these latter changes in the renin-angiotensin axis. Neither the PRA or angiotensin II immunoreactivity in lithium-treated anima...Continue Reading

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Citations

Jan 1, 1983·Progress in Neuro-psychopharmacology & Biological Psychiatry·C T Dourish
Jul 23, 2003·Pharmacology, Biochemistry, and Behavior·Christopher C BarneyJustin L Grobe
Nov 1, 1990·Environmental Health Perspectives·M A Verity
Feb 1, 1984·British Journal of Pharmacology·D Mailman
Sep 1, 2000·American Journal of Physiology. Renal Physiology·T H KwonS Nielsen

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