Impulsivity is inherent to behavioral disorders such as substance abuse and binge eating. While the role of dopamine in impulse behavior is well established, γ-aminobutyric acid (GABA) therapies have promise for the treatment of maladaptive behaviors. In Parkinson disease (PD), dopaminergic therapies can result in the development of impulsive and compulsive behaviors, and this clinical syndrome shares similar pathophysiology to that seen in addiction, substance abuse, and binge-eating disorders. We hypothesized that impulsive PD patients have a reduced thalamic GABAergic response to dopamine therapy. To test this hypothesis, we employed GABA magnetic resonance spectroscopy, D2-like receptor PET imaging, and clinical and quantitative measures of impulsivity in PD patients (n = 33), before and after dopamine agonist administration. We find a blunted thalamic GABA response to dopamine agonists in patients with elevated impulsivity (p = 0.027). These results emphasize how dopamine treatment differentially augments thalamic GABA concentrations, which may modify behavioral impulsivity.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8983736 | PMC |
http://dx.doi.org/10.1038/s41531-022-00298-8 | DOI Listing |
J Neuroimaging
January 2025
Neurobiology Research Unit, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
Background And Purpose: This study aims to investigate the longitudinal changes in translocator protein (TSPO) following stroke in different brain regions and potential associations with chronic brain infarction.
Methods: Twelve patients underwent SPECT using the TSPO tracer 6-Chloro-2-(4'-123I-Iodophenyl)-3-(N,N-Diethyl)-Imidazo[1,2-a]Pyridine-3-Acetamide, as well as structural MRI, at 10, 41, and 128 days (median) after ischemic infarction in the middle cerebral artery. TSPO expression was measured in lesional (MRI lesion and SPECT lesion), connected (pons and ipsilesional thalamus), and nonconnected (ipsilesional cerebellum and contralesional occipital cortex) regions.
J Integr Neurosci
December 2024
Federal State Budgetary Educational Institution, Institute of Theoretical and Experimental Biophysics, 142290 Pushchino, Russia.
Background: Long-term use of levodopa, a metabolic precursor of dopamine (DA) for alleviation of motor symptoms in Parkinson's disease (PD), can cause a serious side effect known as levodopa-induced dyskinesia (LID). With the development of LID, high-frequency gamma oscillations (~100 Hz) are registered in the motor cortex (MCx) in patients with PD and rats with experimental PD. Studying alterations in the activity within major components of motor networks during transition from levodopa-off state to dyskinesia can provide useful information about their contribution to the development of abnormal gamma oscillations and LID.
View Article and Find Full Text PDFBrain Dev
December 2024
Division of Neurology, Saitama Children's Medical Center, 1-2 Chuo-ku Saitama-shi, Saitama 330-8777, Japan.
Purpose: This study aimed to elucidate the distribution of intracranial gamma-aminobutyric acid (GABA) receptors in patients with infantile epileptic spasms syndrome (IESS) of normal brain MRI findings using I-iomazenil single-photon emission computed tomography (IMZ-SPECT).
Methods: This retrospective study compared IMZ-SPECT images from 20 patients with IESS of unknown etiology with normal brain MRI (unknown IESS group) and 23 patients with developmentally normal epilepsy of the same age (developmentally normal group). A three-dimensional stereotactic region of interest (ROI) template was used to divide the brain into 24 segments (left and right callosomarginal, precentral, central, parietal, angular, temporal, posterior cerebral, pericallosal, lenticular nucleus, thalamus, hippocampus, and cerebellum), and the mean accumulation of I-iomazenil in each ROI was calculated.
J Comput Neurosci
December 2024
Department of Applied Mathematics, and Centre for Theoretical Neuroscience, University of Waterloo, 200 University Avenue W, Waterloo, N2L 3G1, ON, Canada.
Cell Rep
December 2024
Rehab Neural Engineering Labs, University of Pittsburgh, Pittsburgh, PA, USA; Department of Bioengineering, University of Pittsburgh, Pittsburgh, PA, USA; Center for Neural Basis of Cognition, Pittsburgh, PA, USA; Department of Neurological Surgery, University of Pittsburgh, Pittsburgh, PA, USA; Department of Neurobiology, University of Pittsburgh, Pittsburgh, PA, USA. Electronic address:
A century of research established that GABA inhibits proprioceptive inputs presynaptically to sculpt spinal neural inputs into skilled motor output. Recent results in mice challenged this theory by showing that GABA can also facilitate action potential conduction in proprioceptive afferents. Here, we tackle this controversy in monkeys, the most human-relevant animal model, and show that GABA receptors (GABARs) indeed facilitate sensory inputs to spinal motoneurons and interneurons and that this mechanism also influences sensory transmission to supraspinal centers.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!