Jingzhu Liao

Keywords placebo analgesia pain opioid conditioning PAG descending pathway photopharmacology neuropeptide Introduction Placebo analgesia is a form of cognitive pain modulation in which expectations and prior experience suppress pain in response to an inert treatment.1,2,3,4,5 In humans, placebo effects can be induced through conditioning, verbal suggestion, or contextual cues, and they contribute substantially to analgesic efficacy in both experimental and clinical settings.

Abstract Copy number variations in the ARHGAP10 gene encoding Rho GTPase–activating protein 10 are significantly associated with schizophrenia. ARHGAP10 negatively regulates RhoA/Rho-kinase (ROCK) signaling. We previously demonstrated that fasudil, a non-selective ROCK inhibitor, exhibited antipsychotic-like effects in several mouse models of schizophrenia. ROCK has two subtypes, ROCK1 and ROCK2. ROCK1 is mainly expressed in the thymus and blood, while ROCK2 is predominantly expressed in the brain.

Abstract In placebo analgesia, prior experience and expectations lead to pain suppression by the administration of an inert substance, but causal evidence for its neural basis is lacking. To identify the underlying neural circuits, we reverse-translated a conditioned placebo protocol from humans to mice. Surprisingly, the placebo effect suppresses both nociception and unconditioned emotional-motivational pain-related behavior.