title: Striatal information signaling and integration in globus pallidus: timing matters.
abstract: Advances in research on globus pallidus (GP) suggest that this 'long thought to be' relay in the 'indirect pathway' plays a unique and critical role in basal ganglia function. The traditional idea of parallel processing within the basal ganglia is also challenged by recent findings. It is now clear that axons of GP neurons form large, perisomatic baskets around target neurons in all major basal ganglia nuclei, thereby exerting a profound influence on the output of the entire basal ganglia. GP neurons are autonomously active both in vivo and in vitro. It is believed that temporal information carried along the corticostriatopallidal pathway is critical for proper motor execution. The importance of appropriately controlled discharge of GP neurons is highlighted by psychomotor disorders such as Parkinson's disease, in which alterations in the pattern and synchrony of discharge in GP neurons are thought to contribute to motor symptoms. Several lines of evidence suggest that the aberrant activity of GP neurons following dopamine depletion is caused by alteration in the synaptic input from both striatum and subthalamic nucleus. In normal subjects, the capability of striatal input in translating cortical input into precisely timed responses in GP neurons is mediated by (1) the expression of postsynaptic GABA(A) receptor composed of subunits with fast kinetic properties; (2) an effective GABA reuptake system in terminating the action of synaptically released GABA, and (3) the existence of dendritic HCN channels that actively abbreviate the time course of the inhibitory postsynaptic potentials and reset rhythmic discharge. Despite the rapid pace in uncovering the elements that shape the activity along the striatopallidosubthalamic pathway, the origin of rhythmic, synchronized bursting of GP neurons seen in parkinsonism has not been fully established experimentally. Further elucidation of the factors that control the information transfer in the striatopallidal synapses is thus critical to our understanding of basal ganglia function and establishing treatment for Parkinson's disease and other basal ganglia disorders.
authors.affiliation: Department of Physiology and Institute for Neuroscience, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
authors.forename: C Savio
authors.initials: CS
authors.lastname: Chan
authors.forename: D James
authors.initials: DJ
authors.lastname: Surmeier
authors.forename: Wing-Ho
authors.initials: WH
authors.lastname: Yung
mesh_terms: D000818:Animals; D001479:Basal Ganglia / Q000502:physiology; D005917:Globus Pallidus / Q000166:cytology / Q000502:physiology* / Q000503:physiopathology; D006801:Humans; D017072:Neostriatum / Q000166:cytology / Q000502:physiology*; D010300:Parkinson Disease / Q000503:physiopathology; D015398:Signal Transduction / Q000502:physiology*; D013569:Synapses / Q000502:physiology; D005680:gamma-Aminobutyric Acid / Q000502:physiology
chemical_list: D005680:gamma-Aminobutyric Acid