Effect of D1 agonists to reverse PCP-induced cognition in novel object recognition in Rats Essay

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Effect of D1 agonists to reverse PCP-induced cognition in novel object recognition in Rats

Background/Aims:
Animal models are a key feature in the development of novel therapies in the treatment of cognitive dysfunction and the negative symptoms of schizophrenia. In recent research, there has been a primary focus on targeting NMDA receptor antagonism as a therapy (Neill et. al., 2010). Dopamine D1 receptors (DRD1) have also been picked out as an aim for cognition enhancement in the treatment of mental disorders such as schizophrenia (Takahashi et. al., 2012). In laboratory work, it has been systematically demonstrated that the use of sub-chronic phencyclidine (PCP) doses in rats manufactures strong and durable cognition deficits in novel object recognition tests (McLean et. al., 2009). There have also been introductory investigations into the efficacy of antipsychotics to treat PCP-induces social interaction and cognition deficits in rats. Because of this, it is believed that positive inflections on NMDA and DRD1 receptors can reverse sub-chronic PCP-induced deficits in the novel object recognition task in rats (Snigdha and Neill, 2007).
Aim: To examine whether PCP-induced cognitive deficits in the novel object recognition (NOR) tasks could be resolved by the selective dopamine agonist, drug A.

Methods
In group 1, 10 female lister-hooded rats were tested to perform a novel object recognition task as described above (reference). The rats were originally treated with the vehicle drug (control solution of saline) and 1% Tween 80 orally (p.o.) for 60 minutes and tested in the NOR task. The rats were then treated with sub-chronic PCP and 1% Tween 80 p.o. and performed the NOR task again. The PCP-treated rats were then given treatment of either risperidone (0.16mg/kg, s.c.) or drug A (0.05mg/kg, 0.1mg/kg, 0.25mg/kg; p.o.) and were then re-tested in the NOR task. The basis of the NOR task includes an initial…