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David C. Burr

Istituto di Scienza e Tecnologie dell'Informazione "Alessandro Faedo"

3 papers in the library · 325 citations · publishing 2004-2010

Papers

Using Psilocybin to Investigate the Relationship between Attention, Working Memory, and the Serotonin 1A and 2A Receptors

Journal of Cognitive Neuroscience October 1, 2005 Olivia Carter, David C. Burr, John D. Pettigrew et al. 236 citations

A hallucinogenic drug that activates serotonin receptors, psilocybin, impaired healthy volunteers' ability to track moving objects but did not affect their spatial working memory. Blocking the 5-HT2A receptor with ketanserin before psilocybin did not prevent this attentional deficit, pointing to the 5-HT1A receptor as the likely cause. The authors suggest the impairment may stem from a reduced ability to filter out distractions rather than a loss of attentional capacity. Eight participants completed both tasks under placebo, psilocybin, ketanserin, and the combination.

Psilocybin impairs high-level but not low-level motion perception

Neuroreport August 1, 2004 Olivia Carter, John D. Pettigrew, David C. Burr et al. 83 citations

The hallucinogenic drug psilocybin, which activates serotonin receptors, selectively impairs the ability to perceive coherent motion in random dot patterns, a task that relies on high-level global motion detectors, while leaving contrast sensitivity for drifting gratings, mediated by low-level detectors, unaffected. This pattern of visual processing deficits mirrors those seen in schizophrenia, suggesting psilocybin may serve as a pharmacological model for studying psychosis and the neural basis of visual perception.

Using psilocybin to investigate the relationship between attention, working memory and the serotonin 5-HT1A and 5-HT2A receptors

Journal of Vision March 17, 2010 Olivia Carter, David C. Burr, John D. Pettigrew et al. 6 citations

A hallucinogenic drug that activates serotonin receptors, psilocybin, impairs the ability to track multiple moving objects but does not affect spatial working memory, indicating a functional separation between these two cognitive processes. Blocking one type of serotonin receptor (5-HT2A) with ketanserin did not prevent this attentional deficit, pointing to the involvement of another receptor (5-HT1A) instead. The impairment may stem from difficulty ignoring distractions rather than a reduction in attentional capacity itself.