EFFECT OF INACTIVATION OF D2 DOPAMINERGIC RECEPTORS AND OF THE MANIPULATION OF THE SUBTALAMIC CORE ON BEHAVIOR MOTOR IN HEMIPARKINSONISM MODELS IN RODENTS

Abstract

Parkinson's disease (PD) is clinically characterized by: tremor at rest, muscle stiffness, decrease in the number of voluntary movements (hypokinesia), as well as reduction in the speed and amplitude of these (bradykinesia). Currently, PD is considered a central nervous system disorder that affects the basal ganglia, a term coined from use to refer to the gray nuclei at the base of the brain. These cores make up a complex unit that has multiple afferent and efferent connections with regions of the cerebral cortex, cerebellum, motor thalamus, and various subcortical structures. The cardinal signs of PD derive from striatal dopamine deficiency and constitute the main objective of all the therapeutic approaches that currently exist. So the current treatment of PD is based on the use of drugs that attempt to compensate for the nigrostriatal dopaminergic deficit. Levodopa constitutes the more effective symptomatic treatment, however, with prolonged use of this drug complications appear motor such as involuntary movements (dyskinesias) and fluctuations in motor response. Consequently after 5 years of treatment the beneficial effects of levodopa diminish and motor complications appear difficult to treat. All these facts have contributed to the emphasis of pathophysiological investigations with therapeutic intentions in PD, has focused in recent years on understanding the origin of dyskinesias and on seek new therapeutic alternatives for the disease.