Mescaline: excitatory effects on acoustic startle are blocked by serotonin2 antagonists
Psychopharmacology November 1, 1987 DOI: 10.1007/bf00187244 via OpenAlex
Summary
AI-generated from the abstractMescaline (20 mg/kg) consistently increases the amplitude of the acoustic startle reflex in rats. This excitatory effect is blocked in a dose-related manner by the serotonin2 (5-HT2) antagonist ritanserin (ED50 dose = 0.25 mg/kg IP), while even a high dose of ritanserin (2.0 mg/kg) does not block the excitatory effects of amphetamine on startle. Other 5-HT2 antagonists (ketanserin, cinanserin, LY 53857) also block mescaline's effect, but the 5-HT1 antagonist pindolol (5 mg/kg) does not. These findings support the hypothesis that hallucinogens' behavioral effects are mediated by agonist actions at 5-HT2 receptors.
Study at a glance
| Characteristics | Experimental study Peer reviewed |
|---|---|
| Population | Rats |
| Interventions | Mescaline Ritanserin Ketanserin Cinanserin LY 53857 Pindolol |
| Dose | 20 mg/kg mescaline, 0.25 mg/kg IP ritanserin (ED50), 2.0 mg/kg ritanserin, 5 mg/kg pindolol |
| Topics | Mescaline |
| Keywords | Excitatory postsynaptic potential Moro reflex Psychology Neuroscience |
| Citations | 23 |
| Key finding | Mescaline's excitatory effect on the acoustic startle reflex is blocked by 5-HT2 antagonists but not by a 5-HT1 antagonist, supporting the role of 5-HT2 receptors in hallucinogen action. |
Abstract
The ability of serotonin2 (5-HT2) antagonists to block the excitatory effects of mescaline on the acoustic startle reflex were analyzed. Mescaline (20 mg/kg) caused a consistent increase in the amplitude of the acoustic startle reflex. This effect was blocked in a dose-related fashion by the 5-HT2 antagonist ritanserin (ED50 dose = 0.25 mg/kg IP). In contrast, even a high dose of ritanserin (2.0 mg/kg) did not block the excitatory effects of amphetamine on startle. Other 5-HT2 antagonists (ketanserin, cinanserin, LY 53857) also blocked mescaline's effect, whereas the 5-HT1 antagonist pindolol (5 mg/kg) did not. These results support the hypothesis that the behavioral effects of hallucinogens are mediated by agonist actions at 5-HT2 receptors.