Ionotropic and metabotropic GABA and glutamate receptors in primate basal ganglia.

J Chem Neuroanat

Division of Neuroscience, Yerkes Regional Primate Research Center, Emory University, 954, Gatewood Rd NE, Atlanta, GA 30322, USA.

Published: July 2001

The functions of glutamate and GABA in the CNS are mediated by ionotropic and metabotropic, G protein-coupled, receptors. Both receptor families are widely expressed in basal ganglia structures in primates and nonprimates. The recent development of highly specific antibodies and/or cDNA probes allowed the better characterization of the cellular localization of various GABA and glutamate receptor subtypes in the primate basal ganglia. Furthermore, the use of high resolution immunogold techniques at the electron microscopic level led to major breakthroughs in our understanding of the subsynaptic and subcellular localization of these receptors in primates. In this review, we will provide a detailed account of the current knowledge of the localization of these receptors in the basal ganglia of humans and monkeys.

Download full-text PDF

Source
http://dx.doi.org/10.1016/s0891-0618(01)00098-9DOI Listing

Publication Analysis

Top Keywords

basal ganglia
16
ionotropic metabotropic
8
gaba glutamate
8
primate basal
8
localization receptors
8
metabotropic gaba
4
receptors
4
glutamate receptors
4
receptors primate
4
basal
4

Similar Publications

In this study, we analyzed the spatio-temporal pattern of expression of specific transcription factors (PITX2, FOXA1, BARHL1, FOXP1, FOXP2) in the human fetal subthalamic nucleus and its neighboring structures from 11 postconceptional weeks (PCW) to 3 postnatal months. We found that all analyzed transcription factors are expressed already during the early fetal period (at 11 PCW). Both FOXP1- and FOXP2-immunoreactive cells were found in the subthalamic nucleus as well as in the striatum, thalamus, reticular nucleus, but not in the zona incerta.

View Article and Find Full Text PDF

Movement disorders such as Parkinson's disease (PD) and cervical dystonia (CD) are associated with abnormal neuronal activity in the globus pallidus internus (GPi). Reduced firing rate and presence of spiking bursts are typical for CD, whereas PD is characterized by high frequency tonic activity. This research aims to identify the most important pallidal spiking parameters to classify these conditions.

View Article and Find Full Text PDF

Background: Obsessive-compulsive disorder (OCD) may develop following brain lesions, but lesion distribution and connectivity patterns are unknown.

Methods: OCD-associated lesions, identified from systematic literature search, were traced on common brain space and compared to control lesions (N=608). Topography was analyzed using brain atlases, and lesion location networks computed using normative functional connectivity (N=1000).

View Article and Find Full Text PDF

Neurobiological mechanism of music improving gait disorder in patients with Parkinson's disease: a mini review.

Front Neurol

January 2025

Department of Basic Medical Sciences, School of Medicine, Xiamen University, Xiamen, China.

Walking ability is essential for human survival and health. Its basic rhythm is mainly generated by the central pattern generator of the spinal cord. The rhythmic stimulation of music to the auditory center affects the cerebral cortex and other higher nerve centers, and acts on the central pattern generator.

View Article and Find Full Text PDF

Objective: Epilepsy is considered as a network disorder of interacting brain regions. The propagation of local epileptic activity from the seizure onset zone (SOZ) along neuronal networks determines the semiology of seizures. However, in highly interconnected brain regions such as the insula, the association between the SOZ and semiology is blurred necessitating invasive stereoelectroencephalography (SEEG).

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!