Abstract
Primary polydipsia, excessive drinking without known medical cause, is especially associated with a diagnosis of schizophrenia. We used animal models of schizophrenia-like symptoms to examine the effects on schedule-induced polydipsia: post-weaning social isolation rearing, subchronic MK-801 treatment (an NMDA-receptor antagonist) or the two combined. Male, Sprague-Dawley rats reared in groups or in isolation beginning at postnatal day 21 were further divided to receive subchronic MK-801 (0.5 mg/kg twice daily) or saline for 7 days beginning on postnatal day 62. Following a 4-day withdrawal period, all groups were trained on a schedule-induced polydipsia paradigm. Under food-restriction, animals reared in isolation and receiving food pellets at 1-min intervals developed significantly more drinking behavior than those reared with others. The addition of subchronic MK-801 treatment did not significantly augment the amount of water consumed. These findings suggest a predisposition to polydipsia is a schizophrenia-like behavioral effect of post-weaning social isolation.
Highlights
Primary polydipsia, the clinical term for ‘excessive water drinking’, is commonly associated with chronic psychiatric illness, reportedly occurring in a large subset of hospitalized patients with schizophrenia [1]
Quantified as the total duration of time spent at the drinking spout, the significantly greater drinking of the isolation rearing (IR) animals (Fig. 1A) took place in the 15– 20 s following consumption of the pellet further illustrating that more schedule-induced polydipsia (SIP) was achieved in the IR group
Animals exposed to an excessive drinking (SIP) paradigm following post-weaning social isolation, subchronic MK-801 or the two together (‘double-hit’) revealed that rearing animals in isolation significantly augmented drinking behavior
Summary
The clinical term for ‘excessive water drinking’, is commonly associated with chronic psychiatric illness, reportedly occurring in a large subset of hospitalized patients with schizophrenia [1]. The development of novel therapeutics is often aided by understanding the neuropathology of a behavior or disease, yet little is known about the neuronal mechanisms associated with polydipsia in schizophrenia. Because the hippocampus plays a modulatory role in vasopressin regulation, some hypothalamic-pituitary-adrenal responses to stress, and glucocorticoid feedback [7,8,9], these findings may suggest a hippocampal deficit in this population. Dysfunction of hippocampal neurons is a signature pathological feature of schizophrenia [11,12] suggesting a role for the pathology of schizophrenia in the development of polydipsia. Whether or not hippocampal neuropathology is causative of polydipsia associated with schizophrenia has yet to be determined
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