Regulation of orofacial movement: amino acid mechanisms and mutant models

Abstract

Generation and regulation of orofacial movements involve complex mechanisms that include primary roles not only for dopamine but also the amino acid neurotransmitters γ-aminobutyric acid (GABA) and glutamate. However, the roles of individual GABA and glutamate receptor subtypes, subunits and associated processes are unclear. Here we outline studies of motor function in mutant mice with "knockout" of GABA and glutamate receptor subtypes. We then review systematic studies of orofacial movements in mutants with (i) "Knockout" of phospholipase C-related catalytically inactive protein (PRIP), which regulates cell surface expression of GABA(A) receptors containing a γ2 subunit, and: (ii) Heterozygous deletion of neuregulin-1 which, inter alia, regulates glutamate receptor-mediated processes. Each of GABAergic and glutamatergic sytems regulate specific topographies of orofacial movement both individually and via interactions with dopaminergic processes.