Lithium, but not carbamazepine, potentiates hyperactivity induced by intra-accumbens cholera toxin

Ora Kofman, Peter P. Li, Jerry J. Warsh

Research output: Contribution to journalArticlepeer-review

16 Scopus citations


Elevated G protein abundance and/or function has been implicated in the pathophysiology and pharmacotherapy of bipolar affective disorder. To test the interactions between chronic lithium and carbamazepine on behavioral changes induced by cholera toxin (CTX), which catalyzes ADP-ribosylation and constitutively activates Gas/olf, rats were given chronic dietary lithium, carbamazepine (CBZ), or regular food (REG) and injected bilaterally in the nucleus accumbens (nACC) with CTX (400 ng/ml/side) or vehicle. Locomotor activity was tested daily for 2 weeks after the injection. CTX increased locomotor activity, but a significant interaction between drug treatment and CTX reflected a two- to threefold increase of CTX-induced hyperactivity in the lithium-treated group. In contrast, on day 1, the CBZ-CTX group was significantly more active than the the LI-CTX and REG-CTX groups, both of which had suppressed locomotor activity. There was a significant reduction in CTX-catalyzed ADP ribosylation of Gαs (52 kDa and 45 kDa) in the nucleus accumbens in all three CTX-treated groups. The potentiation of the behavioral effect of CTX by lithium supports the hypothesis that lithium interacts with G proteins; however, the mechanism of interaction appears to be more complex than direct attenuation of Gas function, as previously suggested.

Original languageEnglish
Pages (from-to)191-200
Number of pages10
JournalPharmacology Biochemistry and Behavior
Issue number1
StatePublished - 1 Jan 1998
Externally publishedYes


  • Bipolar affective disorder
  • Carbamazepine
  • Cholera toxin
  • G protein
  • Lithium
  • Locomotor activity nucleus accumbens

ASJC Scopus subject areas

  • Biochemistry
  • Toxicology
  • Pharmacology
  • Clinical Biochemistry
  • Biological Psychiatry
  • Behavioral Neuroscience


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