Topic: phencyclidine

Background: Hippocampal memory deficit is an important symptom in patients with schizophrenia that responds poorly to antipsychotic treatment. Here, we investigated deficits in hippocampal long-term potentiation/depotentiation changes in the sub-chronic phencyclidine (scPCP) rat model for schizophrenia and how chronic exercise as a non-pharmacological treatment may produce hippocampal synaptic and cognitive improvements.Methods: 60 Female Lister Hooded rats (50 for acute recording and 10 for chronic recording) were dosed with either saline or PCP (2 mg/kg, i.p.) twice daily for seven days foll

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

Cognitive deficits and negative symptoms associated with schizophrenia are poorly managed by current antipsychotics. In order to develop effective treatments, refining animal models of schizophrenia is essential. To address its multifactorial etiology, we developed a new 3-hit mouse model. This model was mostly concealing the glutamatergic deficit hypothesis of the pathology (underlying cognitive and negative deficits). Thus, a genetic susceptibility (serine racemase deletion) was associated to environmental stress (24h maternal separation at 9-day of age) and pharmacological treatment (phency

Cognitive impairments associated with schizophrenia (CIAS) are modelled in rodents using sub-chronic administration of phencyclidine (scPCP). Changes to inflammatory markers have been associated with CIAS in patients, while exercise can improve cognition clinically and pre-clinically. This study aimed to investigate the effect of exercise on cognition and inflammation in the scPCP mouse.Adult female c57 mice were dosed with vehicle (0.9% saline, n=28) or PCP (10mg/kg, n=28) once daily for 10 days and divided into sedentary or exercised groups. Exercised mice had running-wheel access for 1h dai

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

Social withdrawal in the sub-chronic phencyclidine (PCP) rat model, a behavioral correlate of the negative symptoms of schizophrenia, is probably the most well-studied; yet, little is known about the altered psychological processes underlying this behavioral deficit. Despite the complex nature of social behavior, social interaction is indeed often simplified to a single readout parameter (e.g., total time spent in social interaction) that has limited explanatory power. Therefore, we developed a comprehensive ethogram of the social, as well as non-social (i.e., self-oriented behaviors and arena

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