Intracellular studies on the effects of systemic administration of serotonin agonists on rat facial motoneurons.
C P Vandermaelen, G K Aghajanian
European journal of pharmacology February 26, 1982 DOI: 10.1016/0014-2999(82)90242-4 via PubMed
Summary
AI-generated from the abstractIn anesthetized rats, drugs that produce the behavioral serotonin syndrome—5-methoxy-N,N-dimethyltryptamine and p-chloroamphetamine—slowly depolarized facial motoneurons, increased their input resistance, and heightened their excitability. These effects match those seen when serotonin is applied directly to the same neurons, suggesting that such cellular changes contribute to some features of the serotonin syndrome.
Study at a glance
| Characteristics | Experimental study Peer reviewed |
|---|---|
| Population | Facial motoneurons of anesthetized rats |
| Interventions | 5-MeODMT PCA |
| Citations | 37 |
| Key finding | Systemic administration of 5-MeODMT and PCA causes slow depolarization, increased input resistance, and increased excitability of facial motoneurons, identical to the effects of direct serotonin application. |
Abstract
Intracellular recordings were made from facial motoneurons of anesthetized rats during systemic administration of 5-methoxy-N,-N-dimethyltryptamine (5-MeODMT) and p-chloroamphetamine (PCA), drugs which elicit the behavioral serotonin syndrome. Both drugs caused a slow depolarization, increased input resistance, and increased excitability of facial motoneurons. These changes are identical to those caused by direct microiontophoretic application of serotonin to these neurons, and probably underlie some of the components of the behavioral serotonin syndrome.