Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
April 1, 2023
Aeseul Kim, Sun Mi Gu, Haemiru Lee et al.
5 citations
Prenatal exposure to NMDA receptor antagonists like ketamine and methoxetamine in pregnant rats leads to psychosis-like behaviors in their offspring, including hyperactivity and reduced prepulse inhibition (PPI), a measure of sensorimotor gating. These effects are linked to increased expression of the arginine vasopressin receptor 1A (Avpr1a) in the striatum, and artificially overexpressing Avpr1a in the striatum also impairs PPI. Additionally, the treatments raise levels of glutamate decarboxylase 67 (GAD67) and GABA in the striatum, indicating that prenatal NMDA receptor blockade disrupts GABAergic neuron function and sensorimotor gating through Avpr1a regulation.
Pharmacology, biochemistry, and behavior
February 1, 2022
Jin Mook Kim, Boreum Han, Hyun Kyu Min et al.
4 citations
Deschloroketamine (10 mg/kg) and diphenidine (10-60 mg/kg) produced increased locomotor activation and stereotypy similar to ketamine (10 mg/kg) in mice. Both substances increased preference for the drug-paired compartment in conditioned place preference testing, indicating rewarding effects. In self-administration tests, deschloroketamine (1 mg/kg/infusion) increased active lever presses and infusions, suggesting reinforcing effects, whereas diphenidine (1, 2 mg/kg/infusion) did not alter these measures. Both compounds increased dopamine levels in PC-12 cells. The data suggest deschloroketamine may have both rewarding and reinforcing effects, while diphenidine only induced rewarding effects.
Journal of veterinary science
September 1, 2024
Sun Mi Gu, Eunchong Hong, Sowoon Seo et al.
1 citation
Reducing levels of the GABA-synthesis enzyme GAD67 in the dorsal striatum of mice increased depression-like behavior but decreased anxiety. The reduction also heightened the rewarding effect of ketamine, measured by conditioned place preference, but did not alter the reward behavior triggered by the cannabinoid agonist JWH-018. The findings suggest that lower striatal GAD67 weakens GABAergic signaling, which may make the brain more vulnerable to ketamine's reward effects by enhancing NMDA receptor inhibition.