.DMA also facilitated social communication, as measured by a significant increase

in the “extroversion” subscale of the Adjective Mood Rating Scale. This increase correlated with CBF in the temporal cortex, amygdala, and orbitofrontal cortex. These brain regions are richly interconnected and together form the basolateral circuit which, according to current theories, is involved in the mediation of social communication.106,107 Inhibitors,research,lifescience,medical Lesions or disturbances of this circuit can lead to decreased social interaction, inadequate social behavior, or even the inability to decode social cues.108-108 The marked modulation of activity in the basolateral circuit produced by M.DMA and its association with increased click here extroversion provide further support for a critical role of the basolateral circuit in the processing of socially relevant information. The present findings suggest that an amygdala-centered network including ventral-frontal and temporal cortices underlies the cooccurrence of pleasurable emotion and enhanced social communication, providing a rationale for the interrclatcdness

Inhibitors,research,lifescience,medical of emotional and social processes. Thus, further research into the neurochemical mechanisms of MDMA could advance our understanding of the neuroanatomical regulation of mood Inhibitors,research,lifescience,medical and social interaction. Neurotransmitter systems involved in the effects of MDMA On the basis of mechanistic studies in animals, it Inhibitors,research,lifescience,medical has been widely assumed that the psychological effects of MDMA in humans might be mediated through its potent ability to release serotonin, and to a lesser extent DA.111 In addition, MDMA has moderate affinity for the serotonergic 5-HT2 and adrenergic α2 receptors.76 To elucidate the contribution of neurotransmitter and receptor systems Inhibitors,research,lifescience,medical in the action of MDMA, the blocking effects of specific receptor antagonists on MDMA-induced psychological and behavioral alterations were investigated. In these studies, we found that pretreatment with the selective serotonin-reuptake inhibitor (SSRI) citalopram markedly reduced all of the psychological effects

of MDMA in healthy volunteers, indicating that the effects of MDMA in humans are largely due to 5-HT transporter-mediated enhanced 5-HT release.112 The 5-HT2 antagonist ketanserin only because moderately attenuated the MDM’A experience, but significantly abolished the perceptual effects.113 This suggests that stimulation of 5-HT2 receptors mediates the mild hallucinogen-like action of MDMA in humans, such as intensification of colors. Finally, the D2 antagonist haloperidol only partly reduced the euphoric effects of MDMA suggesting that DA contributes little to the psychological effects of MDMA at the dose tested.114,115 Surprisingly, MDMA dose-dependently reduced sensorimotor gating, as indexed by the PPI of startle in rats, but increased PPI in healthy human subjects under comparable conditions.