Effect of subchronic phencyclidine administration on sucrose preference and hippocampal parvalbumin immunoreactivity in the rat

• Published in: Neuroscience letters 2010-03, Vol.471 (3), p.144-147
• Main Authors: Jenkins, Trisha A., Harte, Michael K., Reynolds, Gavin P.
• Format: Article
• Language: English
• Subjects: Affective Symptoms - psychology; Anhedonia; Animals; Biological and medical sciences; Choice Behavior; Disease Models, Animal; Dose-Response Relationship, Drug; Drinking; Drinking Behavior - drug effects; Fundamental and applied biological sciences. Psychology; Hippocampus; Hippocampus - drug effects; Hippocampus - metabolism; Immunohistochemistry; Male; Neurons - drug effects; Neurons - metabolism; Parvalbumin; Parvalbumins - metabolism; Phencyclidine; Phencyclidine - administration & dosage; Pleasure; Rat; Rats; Receptors, N-Methyl-D-Aspartate - antagonists & inhibitors; Schizophrenia - metabolism; Schizophrenia - pathology; Schizophrenic Psychology; Sucrose; Taste; Vertebrates: nervous system and sense organs
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/j.neulet.2010.01.028

Persistent blockade of NMDA receptor function by repeated phencyclidine dosing produces pathophysiological changes that model deficits observed in schizophrenia. The present study investigates the effects of subchronic phencyclidine administration (PCP; 2 or 5 mg/kg bi-daily for 7 days followed by a drug-free period) on sucrose choice, a measure of anhedonia. Sucrose preference in a two-bottle sucrose–water choice test was assessed 1 and 2 weeks after PCP. Results showed no differences in sucrose intake between PCP rats and controls, nor a difference in water intake or total volume of liquid consumed at either time-point. Six weeks post-PCP, analysis of brains showed a reduction in expression of parvalbumin immunoreactive neurons in the hippocampus with significant reductions localised to the CA1 and CA2/3 regions. These results demonstrate that while subchronic PCP may not be a valid model for the negative symptom of anhedonia observed in schizophrenia, it induces pathology in the brain in hippocampal subregions that are reminiscent of changes observed in schizophrenia.