Tagged: Biological Psychiatry
Altered ventral striatal (vST) activation to reward expectancy is a well-established intermediate phenotype for psychiatric disorders, specifically schizophrenia. Preclinical research suggests that striatal alterations are related to a reduced inhibition by the hippocampal formation but its role in human transdiagnostic reward-network dysfunctions is not well understood.
The understanding of the neural control of appetite sheds light into the pathogenesis of eating disorders, such as anorexia nervosa and obesity. Both diseases are a result of maladaptive eating behaviors (overeating or undereating) and associated with life-threatening health problems. The fine regulation of appetite involves genetic, physiological and environmental factors which are detected and integrated in the brain by specific neuronal populations. For centuries, the hypothalamus has been the center of attention in the scientific community as a key regulator of appetite.
Cornichon homolog-3 (CNIH3) is an AMPA receptor (AMPAR) auxiliary protein prominently expressed in the dorsal hippocampus (dHPC), a region that plays a critical role in spatial memory and synaptic plasticity. However, effects of CNIH3 on AMPAR-dependent synaptic function and behavior have not been investigated.
Anterior limb of the internal capsule (ALIC) deep brain stimulation (DBS) shows stable efficacy in refractory obsessive-compulsive disorder (OCD) (1). Recently, several DBS connectivity studies in OCD have investigated the effect of DBS on the structural and functional connectivity in the nucleus accumbens (NAc) and ALIC (2–5). For electrophysiological effects, we attempt to examine the local effects of effective DBS in the NAc/ALIC by long-term recording the local field potentials (LFPs) in a case of OCD.
There is a high co-occurrence of risky substance use among adults with traumatic brain injury (TBI), although it is unknown if the neurological sequelae of TBI can promote this behavior. We propose that to conclude TBI can cause risky substance use, it must be determined that TBI precedes risky substance use, that confounders with the potential to increase the likelihood of both TBI and risky substance use must be ruled out, and that there must be a plausible mechanism of action. In this review, we address these factors by providing an overview of key clinical and preclinical studies, and list...