Behavioral pharmacology of orofacial movement disorders.

Dysfunction in orofacial movement is evident in patients with schizophrenia, Parkinson's disease and Huntington's disease. In animal studies on orofacial dyskinesia, these neurological disorders have been considered as a starting point to examine the pathophysiology and mechanisms underlying the symptoms. There is circumstantial evidence that orofacial dyskinesia in humans might be the consequence of hyperfunctioning mesolimbic-pallidal circuitry, in which the mesolimbic region occupies a central role, in contrast to typical Parkinson-like symptoms which involve hypofunction in the nigrostriato-nigral circuity. Studies in animals suffer from technical difficulties concerning the assessment of orofacial behaviors. There are some experimental designs that provide detailed information on the amplitude and the frequency of the jaw movements. By using such methods, the involvement of neurotransmitter systems and functional neural connections within the basal ganglia has been studied in rat rhythmical jaw movements. Regarding neurotransmitter systems, dopaminergic, cholinergic, γ-aminobutyric acid (GABA)ergic and glutamaterigic systems have been shown to be involved in rat rhythmical jaw movements. The involved neural connections have also been investigated, focusing on the differential role between the dorsal and ventral part of the striatum, the shell and core of the nucleus accumbens and the output pathways from the striatum and the nucleus accumbens. Taking available clinical and experimental evidence, the orofacial dyskinesias are thought to arise when hierarchically lower order output stations of the mesolimbic region start to dysfunction as a consequence of the arrival of distorted information sent by the mesolimbic region. This review seeks to provide an overview of prior and recent findings across several orofacial movement disorders and interpret new insights in the context of the limitations of behavioral pharmacology and prior knowledge of the regulation of behavior by dopamine receptors and other related neuronal systems.