Acute Eticlopride Treatment Alleviates Cognitive Deficits Produced by Neonatal Quinpirole Treatment

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This study was designed to investigate the effects of acute eticlopride (0.02 mg/kg, D2 antagonist) treatment, given immediately before training, in rats neonatally treated with quinpirole, which has been shown to produce long-term D2 receptor supersensitization. Rats were given quinpirole (1mg/kg) or saline treatment from P1-21. Beginning on P22, rats were administered eticlopride or saline (i.p.) fifteen mins before each of seven days of training. Rats were tested on the Morris water task (MWT). For the first three consecutive days, rats were tested on the place version of the MWT with a stationary platform. Animals were given 24 training trials followed by a probe trial, and swim patterns were analyzed with platform removed. The next day, animals began testing on the match-to-place version for four consecutive days and two daily trials were given with the platform moved to a new location each day. On both the search time and target visit measures of the probe trial, animals neonatally treated with quinpirole demonstrated a deficit, and eticlopride eliminated this deficit. Interestingly, animals neonatally treated with saline but given eticlopride before training also demonstrated a deficit on both measures. On the match-to-place version, the difference in latency to locate the platform between the two daily trials served as the dependent measure. Similar to the MWT place version, eticlopride treatment eliminated deficits produced by neonatal quinpirole treatment on this task, and eticlopride produced a deficit in saline controls. This study demonstrates that in a model of dopamine D2 supersensitivity, it appears that the increased sensitivity of the D2 receptor is important for cognitive function.


Key West, FL

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