GABA, but Not Bestrophin-1, Is Localized in Astroglial Processes in the Mouse Hippocampus and the Cerebellum.

Front Mol Neurosci

Section of Anatomy, Department of Molecular Medicine, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.

Published: July 2020

GABA is proposed to act as a gliotransmitter in the brain. Differences in GABA release from astroglia are thought to underlie differences in tonic inhibition between the cerebellum and the CA1 hippocampus. Here we used quantitative immunogold cytochemistry to localize and compare the levels of GABA in astroglia in these brain regions. We found that the density of GABA immunogold particles was similar in delicate processes of Bergman glia in the cerebellum and astrocytes in the CA1 hippocampus. The astrocytic GABA release is proposed to be mediated by, among others, the Ca activated Cl channel bestrophin-1. The bestrophin-1 antibodies did not show any significant bestrophin-1 signal in the brain of wt mice, nor in bestrophin-1 knockout mice. The bestrophin-1 signal was low both on Western blots and immunofluorescence laser scanning microscopic images. These results suggest that GABA is localized in astroglia, but in similar concentrations in the cerebellum and CA1 hippocampus, and thus cannot account for differences in tonic inhibition between these brain regions. Furthermore, our data seem to suggest that the GABA release from astroglia previously observed in the hippocampus and cerebellum occurs via mechanisms other than bestrophin-1.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7399226PMC
http://dx.doi.org/10.3389/fnmol.2020.00135DOI Listing

Publication Analysis

Top Keywords

gaba release
12
ca1 hippocampus
12
gaba
8
hippocampus cerebellum
8
release astroglia
8
differences tonic
8
tonic inhibition
8
cerebellum ca1
8
brain regions
8
bestrophin-1 signal
8

Similar Publications

A creatine efflux transporter in oligodendrocytes.

FEBS J

January 2025

Department of Pharmacology, Faculty of Medicine and University Hospital Cologne, University of Cologne, Germany.

Creatine is essential for ATP regeneration in energy-demanding cells. Creatine deficiency results in severe neurodevelopmental impairments. In the brain, creatine is synthesized locally by oligodendrocytes to supply neighboring neurons.

View Article and Find Full Text PDF

In corticostriatal nerve terminals, glutamate release is stimulated by adenosine via A receptors (ARs) and simultaneously inhibited by endocannabinoids via CB receptors (CBRs). We previously identified presynaptic AR-CBR heterotetrameric complexes in corticostriatal nerve terminals. We now explored the possible functional interaction between ARs and CBRs in purified striatal GABAergic nerve terminals (synaptosomes) and compared these findings with those on the release of glutamate.

View Article and Find Full Text PDF

Purpose Of Review: Baclofen, a muscle relaxant that reduces the release of excitatory neurotransmitters in the pre-synaptic neurons stimulating inhibitory neuronal signals in post-synaptic neurons, has been around for over 5 decades. Baclofen is used primarily for spasticity and since 1982, has had a role as an intrathecal agent. In the present investigation, we review research trends and updates on safety and efficacy of intrathecal baclofen (ITB) pumps.

View Article and Find Full Text PDF

While hypothalamic kisspeptin (KP) neurons play well-established roles in the estrogen-dependent regulation of reproduction, little is known about extrahypothalamic KP-producing (KP) neurons of the lateral septum. As established previously, expression in this region is low and regulated by estrogen receptor- and GABA receptor-dependent mechanisms. Our present experiments on knock-in mice revealed that transgene expression in the LS begins at P33-36 in females and P40-45 in males and is stimulated by estrogen receptor signaling.

View Article and Find Full Text PDF

Terminal Schwann cells (TSCs) are capable of regulating acetylcholine (ACh) release at the neuromuscular junction (NMJ). We have identified GABA as a gliotransmitter at mouse NMJs. When ACh activates α7 nicotinic ACh receptor (nAChRs) on TSCs, GABA is released and activates GABA receptors on the nerve terminal that subsequently reduce ACh release.

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!