Elsevier

Brain Research

Volume 497, Issue 1, 11 September 1989, Pages 72-79
Brain Research

Chronic carbamazepine inhibits the development of local anesthetic seizures kindled by cocaine and lidocaine

https://doi.org/10.1016/0006-8993(89)90971-2Get rights and content

Abstract

The effects of carbamazepine (CBZ) treatment on local anesthetic-kindled seizures and lethality were evaluated in different stages of the kindling process and under different methods of CBZ administration. Chronic oral CBZ inhibited the development of both lidocaine- and cocaine-inducedseizures, but had little effect on the fully developed local anesthetic seizures. Chronic CBZ also decreased the incidence of seizure-related mortality in the cocaine-injected rats. Acute CBZ over a range of doses (15–50 mg/kg) had no effect on completed lidocaine-kindled or acute cocaine-induced seizures. Repeated i.p. injection of CBZ (15 mg/kg) also was without effect on the development of lidocaine- or cocaine-kindled seizures. The differential effects of CBZ depending upon stage of seizure development suggest that distinct mechanisms underlie the development versus maintenance of local anesthetic-kindled seizures. The effectiveness of chronic but not repeated, intermittent injections of CBZ sugests that different biochemical consequences result from the different treatment regimens. The possible utility of chronic CBZ in preventing the development of toxic side effects in human cocaine users is suggested by these data, but remains to be directly evaluated.

Reference (44)

  • AlbrightP.S. et al.

    Effects of carbamazepine and its epoxide metabolite on amygdala-induced seizures in rats

    Neurology

    (1984)
  • AlbrightP.S. et al.

    Development of a new pharmacological seizure model: effects of anticonvulsants on cortical- and amygdala-kindled seizures in the rat

    Epilepsia

    (1980)
  • AshtonD. et al.

    Behavioral analysis of the effects of 15 anticonvulsants in the amygdaloid kindled rat

    Psychopharmacology

    (1979)
  • BallebgerJ.C. et al.

    Carbamazepine (Tegretol) in manic-depressive illness: a new treatment

    Am. J. Psychiatry

    (1980)
  • BertilssonL.

    Clinical pharmacokinetics of carbamazepine

    Clin. Pharmacokinet.

    (1978)
  • BonduelleM.

    Current approaches to the treatment of trigeminal neuralgia

  • CallaghanN. et al.

    Withdrawal of anticonvulsant drugs in patients free of seizures for two years. A prospective study

    N. Engl. J. Med.

    (1988)
  • CereghinoJ.J. et al.

    Carbamazepine for epilepsy: a controlled prospective evaluation

    Neurology

    (1974)
  • ChuN.S.

    Carbamazepine: prevention of alcohol withdrawal seizures

    Neurology

    (1979)
  • GoodmanL.S. et al.

    The Pharmacological Basis of Therapeutics

    (1970)
  • JulienR.M. et al.

    Carbamazepine: mechanisms of action

  • MacdonaldR.L. et al.

    Anticonvulsant drug mechanisms of action

  • Cited by (39)

    • Chemical Kindling

      2006, Models of Seizures and Epilepsy
    • Characterization of the distribution of the cocaine priming threshold and the effect of SCH23390

      2002, Brain Research
      Citation Excerpt :

      Repeated measurement of the cocaine priming threshold is similar to the repeated measurement of the cocaine-induced seizure threshold. However, with repeated measurement the seizure threshold progressively declined [19,27]. This was interpreted as the development of sensitization to cocaine-induced seizures.

    • Pyriform cortex β-waves: Odor-specific sensitization following repeated olfactory stimulation

      2001, Brain Research
      Citation Excerpt :

      The results obtained in the chlorpromazine-treated rats also demonstrate that blockade of dopaminergic and α-adrenergic receptors by chlorpromazine [2] does not prevent β-wave sensitization. Although the olfactory sensitization demonstrated here is similar in certain respects to electrically-induced kindling [13], long-term potentiation [3,4] and sensitization to drugs [9,23,27,28,30,34] it also differs from these phenomena in several ways. First, odor-induced sensitization is perhaps a more physiological phenomenon than electrically or chemically induced-kindling or sensitization to drugs.

    View all citing articles on Scopus
    View full text