Behavioral effects of non-viral mediated RNA interference of synapsin II in the medial prefrontal cortex of the rat.

Synapsin II is a synaptic vesicle-associated phosphoprotein that has been implicated in the pathophysiology of schizophrenia. Researchers have demonstrated reductions in synapsin II mRNA and protein in post-mortem prefrontal cortex and hippocampus samples from patients with schizophrenia. Synapsin II protein expression has been shown to be regulated by dopamine D(1) and D(2) receptor activation.

Alpha-phenyl-N-tert-butylnitrone prevents oxidative stress in a haloperidol-induced animal model of tardive dyskinesia: investigating the behavioural and biochemical changes.

Haloperidol (HP) is a widely prescribed antipsychotic drug used for the treatment of mental disorders. However, while providing therapeutic benefits, this drug also causes serious extrapyramidal side effects, such as tardive dyskinesia (TD). Upon chronic administration, HP causes behavioural supersensitivity to dopamine D2 receptor agonists, as well as the development of vacuous chewing movements (VCMs), in an animal model of human TD.

Curcumin prevents haloperidol-induced development of abnormal oro-facial movements: possible implications of Bcl-XL in its mechanism of action.

Curcumin (Curcuma Longa Linn), the active component of turmeric, has been shown to be effective in ameliorating several stress and drug-induced disorders in rats and humans. However, it is unclear whether short term curcumin administration can prevent the abnormal oro-facial movements (AOFM) which develop following blockade of dopamine D2 receptors by antagonist such as Haloperidol. The objective of this study is to determine whether short term treatment with curcumin along with Haloperidol can prevent the development of AOFM in rats.

PAOPA, a potent analogue of Pro-Leu-glycinamide and allosteric modulator of the dopamine D2 receptor, prevents NMDA receptor antagonist (MK-801)-induced deficits in social interaction in the rat: implications for the treatment of negative symptoms in schizophrenia.

The aim of this study was to investigate whether a potent analogue of the endogenous brain peptide l-prolyl-l-leucyl-glycinamide (PLG), (3(R)-[(2(S)-pyrrolidinylcarbonyl)amino]-2-oxo-1-pyrrolidineacetamide (PAOPA), can prevent the induction of social withdrawal caused by sub-chronic treatment with the non-competitive NMDA (N-methyl-l-aspartate) receptor antagonist, MK-801. Results indicate that MK-801 (0.5 mg/kg) significantly decreased social interaction following sub-chronic treatment (7 days).