Brain mechanisms of hallucinogens and entactogens
Dialogues in Clinical Neuroscience – December 31, 2001
Source: OpenAlex
Summary
Neuroscience reveals a surprising shared pathway in Psychology: classic hallucinogens like Psilocybin and Mescaline, alongside psychotomimetic anesthetics, disrupt sensory gating. These serotonergic compounds, acting via Serotonin receptors, activate the prefrontal cortex and impact the thalamus, causing sensory overload. This Neurotransmitter Receptor Influence on Behavior contrasts sharply with MDMA. These Psychedelics and Drug Studies show MDMA fosters positive mood by activating prefrontolimbic areas while deactivating the amygdala and thalamus, impacting perception and potentially Memory and Neural Mechanisms.
Abstract
This review focuses on recent brain imaging and behavioral studies of sensory gating functions, which assess similarities between the effects of classic hallucinogens (eg, psilocybin), dissociative anesthetics (eg, ketamine), and entactogens (eg, 3,4-methylenedioxymethamphetamine [MDMA]) in humans. Serotonergic hallucinogens and psychotomimetic anesthetics produce overlapping psychotic syndromes associated with a marked activation of the prefrontal cortex (hyperfrontality) and other overlapping changes in temporoparietal, striatal, and thalamic regions, suggesting that both classes of drugs act upon a common final pathway. Together with the observation that both hallucinogens and N-methyl-oaspartate (NMDA) antagonists disrupt sensory gating in rats by acting on 5-hydroxytryptamine (serotonin) 5-HT(2) receptors located in cortico-striato-thalamic circuitry these findings suggest that disruption of cortico-subcortical processing leading to sensory overload of the cortex is a communality of these psychoses. In contrast to hallucinogens, the entactogen MDMA produces an emotional state of positive mood, concomitant with an activation of prefrontolimbiclparalimbic structures and a deactivation of amygdala and thalamus.