Topic: NMDA receptor hypofunction

As evidence for the NMDA receptor hypofunction theory of schizophrenia grows, more attention is being paid to restoring correct glutamatergic signalling as a therapy option leading to development of novel antipsychotics. The ESCRT proteins groups are involved in sorting ubiquitinated membrane receptors to lysosomes, which is a key method for reducing cell surface receptor signalling. The research illustrates the effect of knocking down and overexpression of TSG101 and VPS4a genes on the function of ESCRTs machinery and the expression of NMDA receptors. The average number of NMDA receptors on t

N-methyl-D-aspartate receptor (NMDA) antagonists, such as phencyclidine (PCP), sub-chronically (sc) administrated to rodents, can lead to robust and prolonged deficits in cognitive functions and mimic neurobiological deficits found in schizophrenia. Glycogen synthase kinase-3β (GSK-3β) inhibition has been identified as an important treatment for cognitive impairment in diverse neuropsychiatric diseases. However, whether GSK-3β inhibition rescues the cognitive deficits in a model of NMDA receptor hypofunction is unknown. This study examined the acute and sub-chronic effects of GSK-3β inhibition

Aberrant beta-gamma (20-80 Hz) frequency oscillations and impaired cognitive function are reported in schizophrenia patients. Impaired oscillations could be caused by changes in interneuron populations and increased neuroinflammation, as reported in post-mortem studies. Cognitive and network dysfunction can be modelled in rodents using the N-methyl-D-aspartate acid (NMDA) receptor antagonist phencyclidine (PCP). In vivo studies suggest sigma-1 receptor (σ1R) activation may reverse these deficits. We investigated the effect of acute PCP application and σ1R activation on glia and interneurons in