The medium spiny neurons (MSNs), which comprise the direct and indirect output pathways from the striatum, use gamma-aminobutyric acid (GABA) as their major fact-acting neurotransmitter. We generated mice carrying a conditional allele of the Gad1 gene, which encodes GAD67, one of the two enzymes responsible for GABA biosynthesis, and bred them to mice expressing Cre recombinase at the dopamine D1 receptor locus (Drd1a) to selectively reduce GABA synthesis in the direct output pathway from the striatum. We show that these mice are deficient in some types of motor skills, but normal for others, suggesting a differential role for GABA release from D1 receptor-containing neurons.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3360952 | PMC |
http://dx.doi.org/10.1002/dvg.20405 | DOI Listing |
J Integr Neurosci
October 2023
Chongqing Key Laboratory of Translational Medical Research in Cognitive Development and Learning and Memory Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Child Health and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Children's Hospital of Chongqing Medical University, 400015 Chongqing, China.
Background: Astrocytes are essential for synaptic transmission, and their dysfunction can result in neuropsychiatric disorders such as anxiety and depression. Many studies have shown that global knockout of Melatonin receptor 2 () is associated with the development of various mental disorders.
Aim: This study aimed to investigate the effects of astrocyte ablation of on cognitive function and anxiety-like behavior in mice, as well as the potential biological mechanisms.
Neurochem Int
October 2023
The School of Mental Health and Psychological Sciences, Anhui Medical University, Hefei, China; Research Center for Translational Medicine, The Second Hospital of Anhui Medical University, Hefei, China; Anhui Province Key Laboratory of Cognition and Neuropsychiatric Disorders, Hefei, China. Electronic address:
Autism spectrum disorder (ASD) is a series of highly inherited neurodevelopmental disorders. Loss-of-function (LOF) mutations in the CACNA2D3 gene are associated with ASD. However, the underlying mechanism is unknown.
View Article and Find Full Text PDFCommun Biol
May 2023
Department of Biomedical and Life Sciences, Lancaster University, Lancaster, LA1 4YW, UK.
Autism spectrum disorders are more common in males, and have a substantial genetic component. Chromosomal 16p11.2 deletions in particular carry strong genetic risk for autism, yet their neurobiological impact is poorly characterised, particularly at the integrated systems level.
View Article and Find Full Text PDFMol Cell Neurosci
September 2022
Center for Molecular Morphology, Section for Stereology and Microscopy, Department of Clinical Medicine, Aarhus University, Denmark; Department of Pathology, Aarhus University Hospital, Denmark. Electronic address:
The 22q11.2 hemizygous deletion confers high risk for multiple neurodevelopmental disorders. Inhibitory signaling, largely regulated through GABA receptors, is suggested to serve a multitude of brain functions that are disrupted in the 22q11.
View Article and Find Full Text PDFCereb Cortex
March 2023
Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Qingdao University, 308 Ningxia Rd, Qingdao, Shandong, 266071, China.
Growth hormone secretagogue receptor 1a (GHSR1a)-the receptor for orexigenic hormone ghrelin-is a G protein-coupled receptor that is widely distributed in the brain, including the hippocampus. Studies have demonstrated that genetic deletion of GHSR1a affects memory, suggesting the importance of ghrelin/GHSR1a signaling in cognitive control. However, current reports are controversial, and the mechanism underlying GHSR1a modulation of memory is uncertain.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!