Serotonergic mediation of cocaine seizures in mice.
We used genetically heterogeneous HS mice to investigate the effects of drugs that alter brain concentrations of serotonin on cocaine-induced convulsions and lethality. The racemer of fenfluramine, which increases synaptic serotonin, was coadministered with a dose (60 mg/kg, intraperitoneally) of cocaine that does not produce status epilepticus or death. This drug combination significantly increased the occurrence and decreased the time of onset of status epilepticus, but did not affect lethality. Likewise, 2.5 mg/kg of the D-isomer, of fenfluramine increased the occurrence of status epilepticus. Neither isomer effected lethality. When 2.5 mg/kg cinanserin, a drug that antagonizes postsynaptic serotonergic receptors, was coadministered with a higher (95 mg/kg) dose of cocaine, the time of onset of status epilepticus was significantly increased, whereas lethality was reduced. The results are discussed in light of the action of cocaine upon serotonin neurons and the relationship between seizurogenic activity and cocaine-induced lethality.[1]References
- Serotonergic mediation of cocaine seizures in mice. Schechter, M.D., Meehan, S.M. Pharmacol. Biochem. Behav. (1995) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
