Mescaline: Its effects on learning rate and dopamine metabolism in goldfish (Carassius auratus)
E. A. Zeller, Gregory S. Couper, Shankar V. Huprikar, Alan M. Mellow, Rebecca Moody
Cellular and Molecular Life Sciences November 1, 1976 DOI: 10.1007/bf01937429 via OpenAlex
Summary
AI-generated from the abstractMescaline initially boosted learning rates in goldfish given high doses, but smaller doses over three days impaired their ability to avoid electric shocks. Apomorphine and L-dopa produced similar short-term improvements, while fluphenazine reduced avoidance. The authors suggest mescaline triggers dopamine release that stimulates central dopaminergic systems; then monoamine oxidase destroys the liberated dopamine, and the resulting dopamine deficit likely causes the behavioral changes seen in the chronic experiment.
Study at a glance
| Characteristics | Experimental study Peer reviewed |
|---|---|
| Population | Goldfish (Carassius auratus) |
| Interventions | mescaline apomorphine L-dopa fluphenazine |
| Duration | Short term (high doses) and 3 days (smaller doses) |
| Topics | Mescaline |
| Keywords | Carassius auratus Dopamine Chemistry Pharmacology |
| Citations | 1 |
| Key finding | High mescaline doses increase learning rates in goldfish, but prolonged exposure to smaller doses reduces shock-avoidance behavior, likely due to a dopamine deficit after MAO breakdown. |
Abstract
The pharmacological action of mescaline on goldfish was studied with the Bitterman-Agranoff shock-avoidance test. In short term experiments with high mescaline doses an increase in learning rates was observed. Similar results were obtained with apomorphine and L-dopa. However, when the fish were exposed to smaller mescaline doses (or to fluphenazine) for 3 days, their ability to avoid electric shock was reduced. Apparently, mescaline induced a release of dopamine which stimulated central dopaminergic systems. Subsequently, MAO destroys the liberated dopamine. Thus, the ensuing dopamine deficit appears to be responsible for the marked changes in behavior in the chronic experiment.