Functional connectivity and integrative properties of globus pallidus neurons

• Type of Material: Article
• Authors: Dieter Jaeger, Emory University; Hitoshi Kita, University Tennessee
• Language: English
• Date: 2011-12-15
• Publisher: Elsevier: 12 months
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © 2011 IBRO. Published by Elsevier Ltd. All rights reserved
• License: Creative Commons Attribution-NonCommerical-NoDerivs 3.0 Unported
• Final Published Version (URL): http://dx.doi.org/10.1016/j.neuroscience.2011.07.050
• Title of Journal or Parent Work: Neuroscience
• ISSN: 0306-4522
• Volume: 198
• Start Page: 44
• End Page: 53
• Grant/Funding Information: Supported by NIH/ NINDS Grants NS-57236 (HK) and NS1P50NS071669-01 (DJ)
• Keywords: spontaneous firing; Pallidum; GABA; basal ganglia; glutamate; modeling
• Research Categories: Biology, Neuroscience

Abstract

The globus pallidus consists of the external (GPe) and the internal (GPi) segments. The GPe and GPi have different functional roles. The GPe is located centrally within multiple basal ganglia feedforward and feedback connections. The GPi is an output nucleus of the basal ganglia. A complex interplay between intrinsic pacemaking conductances and the balance of glutamatergic and GABAergic input largely determines the rate and pattern of firing of pallidal neurons. The initial part of this article introduces recent findings made in vivo that are related to the roles of glutamatergic and GABAergic inputs in the control of pallidal activity. The latter part describes the roles of intrinsic mechanisms of GPe neurons in the integration of the synaptic inputs. The presence of dendritic voltage-gated sodium channels may allow the initiation of dendritic spikes, giving distal inputs on the long and thin GPe dendrites an opportunity to strongly shape spiking activity. Basal ganglia disorders including Parkinson's disease, hemiballismus, and dystonias are accompanied by increased irregularity and synchronized bursts of pallidal activity. These changes may be in part due to changes in the GABA release in the GPe and GPi, but also involve intrinsic cellular changes in pallidal neurons.