In vitro release of [3H]5-hydroxytryptamine from fetal and maternal brain by drugs of abuse.
K Kramer, E C Azmitia, P M Whitaker-Azmitia
Brain research. Developmental brain research March 18, 1994 DOI: 10.1016/0165-3806(94)90019-1 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | In vitro experimental study Peer reviewed |
|---|---|
| Population | Cortical synaptosomes from pregnant rats (gestational day 17) and rat fetuses (embryonic day 17) |
| Interventions | Cocaine Fenfluramine MDMA |
| Key findings | Cocaine and fenfluramine evoked high-affinity serotonin release (apparent at 10^-9 M) from fetal synaptosomes but not from maternal synaptosomes, whereas MDMA released similar amounts of serotonin in both. The authors suggest this fetal serotonin release may be one mechanism by which cocaine and fenfluramine cause teratogenic effects in utero. |
Abstract
Cortical synaptosomes were prepared from pregnant dams (GD-17) and rat fetuses (ED-17), loaded with [3H]5-HT and assayed to evaluate release mediated by cocaine (COC), fenfluramine (FEN) and 3,4-methylenedioxymethamphetamine (MDMA). COC and FEN elicited a high-affinity (10(-9) M) release response in fetal tissue which was not apparent in the dam. MDMA-induced release was similar in magnitude in both tissue types. Consequently, the release of 5-HT from developing neurons may be one mechanism by which COC and FEN elicit their teratogenetic effects in utero.
Citations in the library
Cited by 2
Cites 2
- The molecular mechanism of "ecstasy" [3,4-methylenedioxy-methamphetamine (MDMA)]: serotonin transporters are targets for MDMA-induced serotonin release. Proceedings of the National Academy of Sciences March 1, 1992
- The substituted amphetamines 3,4-methylenedioxymethamphetamine, methamphetamine, p-chloroamphetamine and fenfluramine induce 5-hydroxytryptamine release via a common mechanism blocked by fluoxetine and cocaine European Journal of Pharmacology May 1, 1992