» Articles » PMID: 24055402

The Parvalbumin-positive Interneurons in the Mouse Dentate Gyrus Express GABAA Receptor Subunits α1, β2, and δ Along Their Extrasynaptic Cell Membrane

Overview
Journal Neuroscience
Specialty Neurology
Date 2013 Sep 24
PMID 24055402
Citations 35
Authors
Affiliations
Soon will be listed here.
Abstract

Neuronal circuitries in the hippocampus are involved in navigation and memory and are controlled by major networks of GABAergic interneurons. Parvalbumin (PV)-expressing interneurons in the dentate gyrus (DG) are identified as fast-spiking cells, playing a crucial role in network oscillation and synchrony. The inhibitory modulation of these interneurons is thought to be mediated mainly through GABAA receptors, the major inhibitory neurotransmitter receptors in the brain. Here we show that all PV-positive interneurons in the granular/subgranular layer (GL/SGL) of the mouse DG express high levels of the GABAA receptor δ subunit. PV-containing interneurons in the hilus and the molecular layer, however, express the δ subunit to a lower extent. Only 8% of the somatostatin-containing interneurons express the δ subunit, whereas calbindin- or calretinin-containing interneurons in the DG seem not to express the GABAA receptor δ subunit at all. Hence, these cells receive a GABAergic control different from that of PV-containing interneurons in the GL/SGL. Experiments investigating a possible co-expression of GABAA receptor α1, α2, α3, α4, α5, β1, β2, β3, or γ2 subunits with PV and δ subunits indicated that α1 and β2 subunits are co-expressed with δ subunits along the extrasynaptic membranes of PV-interneurons. These results suggest a robust tonic GABAergic control of PV-containing interneurons in the GL/SGL of the DG via δ subunit-containing receptors. Our data are important for better understanding of the neuronal circuitries in the DG and the role of specific cell types under pathological conditions.

Citing Articles

Parvalbumin interneurons regulate rehabilitation-induced functional recovery after stroke and identify a rehabilitation drug.

Okabe N, Wei X, Abumeri F, Batac J, Hovanesyan M, Dai W Nat Commun. 2025; 16(1):2556.

PMID: 40089466 DOI: 10.1038/s41467-025-57860-0.


A therapeutic small molecule enhances γ-oscillations and improves cognition/memory in Alzheimer's disease model mice.

Wei X, Campagna J, Jagodzinska B, Wi D, Cohn W, Lee J Proc Natl Acad Sci U S A. 2024; 121(33):e2400420121.

PMID: 39106304 PMC: 11331084. DOI: 10.1073/pnas.2400420121.


Region and layer-specific expression of GABA receptor isoforms and KCC2 in developing cortex.

Zavalin K, Hassan A, Zhang Y, Khera Z, Lagrange A Front Cell Neurosci. 2024; 18:1390742.

PMID: 38894703 PMC: 11184147. DOI: 10.3389/fncel.2024.1390742.


Enhancing GABAergic Tonic Inhibition Reduces Seizure-Like Activity in the Neonatal Mouse Hippocampus and Neocortex.

Liddiard G, Suryavanshi P, Glykys J J Neurosci. 2024; 44(7).

PMID: 38176909 PMC: 10869160. DOI: 10.1523/JNEUROSCI.1342-23.2023.


Mesenchymal-derived extracellular vesicles enhance microglia-mediated synapse remodeling after cortical injury in aging Rhesus monkeys.

Zhou Y, Bhatt H, Mojica C, Xin H, Pessina M, Rosene D J Neuroinflammation. 2023; 20(1):201.

PMID: 37660145 PMC: 10475204. DOI: 10.1186/s12974-023-02880-0.