
Biological Psychiatry, Journal Year: 2022, Volume and Issue: 93(5), P. 405 - 418
Published: Nov. 9, 2022
Language: Английский
Biological Psychiatry, Journal Year: 2022, Volume and Issue: 93(5), P. 405 - 418
Published: Nov. 9, 2022
Language: Английский
Journal of Psychopharmacology, Journal Year: 2020, Volume and Issue: 34(2), P. 167 - 180
Published: Jan. 16, 2020
Psilocybin has shown promise as a treatment for depression but its therapeutic mechanisms are not properly understood. In contrast to the presumed actions of antidepressants, we recently found increased amygdala responsiveness fearful faces one day after open-label with psilocybin (25 mg) in 19 patients treatment-resistant depression, which correlated efficacy.Aiming further unravel psilocybin, present study extends this basic activation analysis. We hypothesised changed functional connectivity, more precisely decreased amygdala-ventromedial prefrontal cortex during face processing psilocybin.Psychophysiological interaction analyses were conducted on magnetic resonance imaging data from classic face/emotion perception task, bilateral and ventromedial time-series physiological regressors. Average parameter estimates (beta weights) significant clusters clinical outcomes at week.Results showed cortex-right connectivity post- (versus pre-) treatment; decrease was associated levels rumination week. This effect driven by changes response neutral (but happy) faces. Independent whole-brain also revealed post-treatment increase between occipital-parietal cortices processing.These results consistent idea that therapy revives emotional neural psychological level, may be key mechanism psychedelic therapy. Future larger placebo-controlled studies needed examine replicability current findings.
Language: Английский
Citations
157Journal of Neuroinflammation, Journal Year: 2020, Volume and Issue: 17(1)
Published: June 8, 2020
Abstract Background Major depressive disorder (MDD) is a highly prevalent psychiatric disorder, and inflammation has been considered crucial components of the pathogenesis depression. NLRP1 inflammasome-driven inflammatory response believed to participate in many neurological disorders. However, it unclear whether inflammasome implicated development Methods Animal models depression were established by four different chronic stress stimuli including unpredictable mild (CUMS), restrain (CRS), social defeat (CSDS), repeat (RSDS). Depressive-like behaviors determined sucrose preference test (SPT), forced swim (FST), tail-suspension (TST), open-field (OFT), interaction (SIT), light-dark (LDT). The expression complexes, BDNF, CXCL1/CXCR2 tested western blot quantitative real-time PCR. levels cytokines enzyme-linked immunosorbent assay (ELISA) kits. Nlrp1a knockdown was performed an adeno-associated virus (AAV) vector containing Nlrp1a-shRNA-eGFP infusion. Results Chronic activated hippocampal promoted release pro-inflammatory IL-1β, IL-18, IL-6, TNF-α mice. Hippocampal prevented ameliorated stress-induced depressive-like behaviors. Also, caused increase low BDNF Interestingly, inhibited up-regulation restored hippocampus. Conclusions contributes induced mechanism may be related CXCL1/CXCR2/BDNF signaling pathway. Thus, could become potential antidepressant target.
Language: Английский
Citations
153American Journal of Psychiatry, Journal Year: 2020, Volume and Issue: 177(10), P. 902 - 916
Published: Oct. 1, 2020
Language: Английский
Citations
145Neuroscience & Biobehavioral Reviews, Journal Year: 2022, Volume and Issue: 135, P. 104583 - 104583
Published: Feb. 22, 2022
Language: Английский
Citations
123Biological Psychiatry, Journal Year: 2022, Volume and Issue: 93(5), P. 405 - 418
Published: Nov. 9, 2022
Language: Английский
Citations
117