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      Deficits in parvalbumin and calbindin immunoreactive cells in the hippocampus of isolation reared rats.

      Journal of Neural Transmission
      Animals, Biological Markers, chemistry, metabolism, Calbindin 2, Calbindins, Cell Count, Female, Hippocampus, pathology, Housing, Animal, Interneurons, Parvalbumins, biosynthesis, deficiency, Rats, Rats, Sprague-Dawley, Reflex, Startle, physiology, S100 Calcium Binding Protein G, Social Isolation, psychology, gamma-Aminobutyric Acid

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          Abstract

          Post-mortem studies have provided evidence for abnormalities of the gamma-aminobutyric acid (GABA)-ergic system in schizophrenia. The calcium-binding proteins (CBPs), parvalbumin (PV), calbindin (CB) and calretinin (CR) can be used as markers for specific subpopulations of GABAergic neurons in the brain. Isolation rearing of rats is a non-pharmacological, non-lesion manipulation that leads to deficits in prepulse inhibition of the startle reflex (PPI) and other behavioural and neurochemical alterations reminiscent of schizophrenia. Female rats were reared in social housing (groups of three) or singly for 11 weeks post weaning and PPI was measured. Brains were removed and hippocampal CBP- containing neurons determined following immunocytochemical staining. Compared to socially housed rats, isolated rats exhibited PPI deficits and reductions in PV and CB-immunoreactive cells in the hippocampus, with no significant change in CR. These findings demonstrate selective abnormalities of sub-populations of GABAergic interneurons in the hippocampus of isolation reared rats, which resemble the neuronal deficits seen in this region in schizophrenia.

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