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\nNeuroscience"}],["$","meta","2",{"name":"publisher","content":"National Institutes of Health"}],["$","meta","3",{"property":"og:title","content":"NIH VideoCast - Striatal Synaptic and Dendritic Plasticity in Parkinson's Disease – It is Not Just About Dopamine"}],["$","meta","4",{"property":"og:description","content":"Research in Dr. Surmeier's lab revolves around the question of how neuromodulators shape excitability of basal ganglia neurons. Basal ganglia is a richly interconnected set of nuclei that regulate motor and cognitive behaviors. Disorders in basal ganglia function underlie a wide variety of psychomotor disorders including Parkinson's disease, dystonia, Huntington's disease, schizophrenia and Tourette's syndrome. In many of these diseases, the principal defect appears to involve an alteration in dopaminergic signaling. The symptoms of Parkinson's disease are a consequence of the death of dopaminergic neurons that innervate one of the basal ganglia nuclei, the striatum. Major goals have been to determine how dopamine modulates the excitability of striatal neurons. Unlike classical neurotransmitters, neuromodulators like dopamine influence neuronal activity by altering the properties of voltage-dependent and ligand-gated membrane channels. \n
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