Methysergide potentiates the hyperactivity produced by MDMA in rats.
Pharmacology, biochemistry, and behavior March 1988 DOI: 10.1016/0091-3057(88)90034-2 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Controlled experimental animal study Peer reviewed |
|---|---|
| Population | Rats |
| Interventions | Methysergide Amphetamine MDMA |
| Dose | Methysergide 0, 2.5, 5, 10 mg/kg; amphetamine 0.5 mg/kg; MDMA 10 mg/kg |
| Duration | Locomotor activity measured for 120 minutes after injection |
| Measures | Locomotor activity measured in photocell cages |
| Topics | MDMA |
| Key findings | Methysergide (2.5, 5, and 10 mg/kg), which had no effect alone, significantly potentiated MDMA-induced locomotor hyperactivity but not amphetamine-induced hyperactivity. The authors propose that MDMA's intrinsic serotonergic agonist properties may counteract the indirect sympathomimetic effects thought to underlie its locomotor hyperactivity. |
Abstract
Although some substituted amphetamines, like MDA, produce a combination of sympathomimetic stimulation and perceptual alterations, the psychoactive qualities of MDMA are less distinctive. MDMA binds to serotonergic receptors and has been shown to potently deplete brain serotonin concentrations. Biochemical and behavioral evidence suggests that MDMA may also act on the dopamine system. The present study explored the effects of blocking serotonin receptors on MDMA and amphetamine induced locomotor hyperactivity in rats. Locomotor activity was measured in photocell cages for 120 minutes following injection of methysergide (0, 2.5, 5, 10 mg/kg) or methysergide in combination with amphetamine (0.5 mg/kg) or MDMA (10 mg/kg). Methysergide, which had no effect on its own, significantly potentiated the locomotor hyperactivity produced by MDMA but not amphetamine. Thus, the intrinsic serotonergic agonist properties of MDMA may actually counteract the indirect sympathomimetic effects thought to be responsible for the locomotor hyperactivity MDMA produces.