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An animal model of tardive dyskinesia was used to evaluate the potential antidyskinetic properties of the neuropeptide L-prolyl-L-leucyl-glycinamide (PLG). In rats, PLG administered concurrently with the neuroleptic drug haloperidol or chlorpromazine antagonized the enhancement of specific [3H]spiroperidol binding in the striatum that is associated with(More)
The postnatal development of rat brain dopamine D4 receptor gene expression was studied in animals 1 day to 1 year old, using the polymerase chain reaction technique. The level of expression of the D4 mRNA was appreciable at birth (day 1), increased to maximum at day 3, and showed declines at day 28. D4 mRNA expression remained unchanged at the ages of 6(More)
The postnatal development of rat brain dopamine D2 receptor gene expression was investigated in animals 1 day to 1 year old. The level of expression of the striatal D2 mRNA was appreciable at birth (day 1), steadily increased to a maximum at day 28, and showed declines at ages 6 months and one year. The mRNA development profile was similar to that of(More)
The mechanism of action subserving the potential anti-Parkinsonian properties of L-prolyl-L-leucyl-glycinamide (PLG) was investigated in behavioural and neurochemical models of dopaminergic function in the rat. Acute administration of PLG (20 and 40 mg kg-1 SC) failed to alter appreciably the intensity of the cataleptic response elicited by haloperidol (3(More)
The typical antipsychotic drug haloperidol causes vacuous chewing movements (VCM) in rats, which are representative of early-Parkinsonian symptoms or later-onset extrapyramidal side effects of tardive dyskinesia (TD) in humans. Haloperidol (HP) has been hypothesized to potentiate increases in oxidative stress or free radical-mediated levels of toxic(More)
Positive alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor modulators include benzamide compounds that allosterically modulate AMPA glutamate receptors. These small molecules that cross the blood-brain barrier have been shown to act as a neuroprotectant by increasing the levels of endogenous brain-derived neurotrophic factor (BDNF).(More)
The intranigral administration of 6-hydroxydopamine resulted in the destruction of dopaminergic nerve terminals in the rat caudate nucleus and a 98% decrease in dopamine content. The time courses of the effects of this treatment on dopamine stimulated cyclic 3',5'-AMP accumulation in slices of caudate nucleus and on dopamine receptors in two behaviorally(More)
Recent studies on the phosphoprotein synapsin II have revealed reduced expression in postmortem medial prefrontal cortex tissues from subjects with schizophrenia, and chronic antipsychotic drug treatment has resulted in concurrent increases in synapsin II mRNA and protein levels. Collectively, this research suggests a role of synapsin II in the(More)
We previously demonstrated that chronic treatment with the dopamine-D2 receptor antagonist, haloperidol, increases mRNA and protein content of the phosphoprotein, synapsin II, in the rat striatum. Since dopamine-D2 receptor antagonism and dopamine-D1 receptor blockade can have opposing effects on gene expression, the present investigation compared the(More)