ArticleThe European journal of neuroscience2011
Non-neuronal, slow GABA signalling in the ventrobasal thalamus targets δ-subunit-containing GABA(A) receptors.
Article in The European journal of neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 45 citations in OpenAlex.
- Brainstem Neuroadaptations in Rodent Models of Parkinson's Disease.The European journal of neuroscience · 2025Article
- The GABA and GABA-Receptor System in Inflammation, Anti-Tumor Immune Responses, and COVID-19.Biomedicines · 2023Review
- Calcium signaling in astrocytes and gliotransmitter release.Frontiers in synaptic neuroscience · 2023Review
- GABAergic Regulation of Astroglial Gliotransmission through Cx43 Hemichannels.International journal of molecular sciences · 2022Article
- The Potential Role of Polyamines in Epilepsy and Epilepsy-Related Pathophysiological Changes.Biomolecules · 2022Review
- The ethanol inhibition of basolateral amygdala neuron spiking is mediated by a γ-aminobutyric acid type A-mediated tonic current.Alcoholism, clinical and experimental research · 2022Article
- Astrocytes contribute to pain gating in the spinal cord.Science advances · 2021Article
- Oligodendroglial GABAergic Signaling: More Than Inhibition!Neuroscience bulletin · 2021Review
- From Physiology to Pathology of Cortico-Thalamo-Cortical Oscillations: Astroglia as a Target for Further Research.Frontiers in neurology · 2021Review
- Expression and Function of GABA Receptors in Myelinating Cells.Frontiers in cellular neuroscience · 2020Article
- Astrocytes as Guardians of Neuronal Excitability: Mechanisms Underlying Epileptogenesis.Frontiers in neurology · 2020Review
- The Paradox of Astroglial CaFrontiers in cellular neuroscience · 2020Review
- GABA, but Not Bestrophin-1, Is Localized in Astroglial Processes in the Mouse Hippocampus and the Cerebellum.Frontiers in molecular neuroscience · 2020Article
- Involvement of extrasynaptic glutamate in physiological and pathophysiological changes of neuronal excitability.Cellular and molecular life sciences : CMLS · 2018Review
- Glia and gliotransmitters on carbon nanotubes.Nano reviews & experiments · 2017Article
- Tonic GABAA Receptors as Potential Target for the Treatment of Temporal Lobe Epilepsy.Molecular neurobiology · 2016Review
- Novel astrocyte targets: new avenues for the therapeutic treatment of epilepsy.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2015Review
- Astrocyte and Neuronal Plasticity in the Somatosensory System.Neural plasticity · 2015Review
- Astrocytic Actions on Extrasynaptic Neuronal Currents.Frontiers in cellular neuroscience · 2015Review
- Direct bidirectional μ-opioid control of midbrain dopamine neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The rodent ventrobasal (VB) thalamus contains a relatively uniform population of thalamocortical (TC) neurons that receive glutamatergic input from the vibrissae and the somatosensory cortex, and inhibitory input from the nucleus reticularis thalami (nRT). In this study we describe γ-aminobutyric acid (GABA)(A) receptor-dependent slow outward currents (SOCs) in TC neurons that are distinct from fast inhibitory postsynaptic currents (IPSCs) and tonic currents. SOCs occurred spontaneously or could be evoked by hypo-osmotic stimulus, and were not blocked by tetrodotoxin, removal of extracellular Ca(2+) or bafilomycin A1, indicating a non-synaptic, non-vesicular GABA origin. SOCs were more common in TC neurons of the VB compared with the dorsal lateral geniculate nucleus, and were rarely observed in nRT neurons, whilst SOC frequency in the VB increased with age. Application of THIP, a selective agonist at δ-subunit-containing GABA(A) receptors, occluded SOCs, whereas the benzodiazepine site inverse agonist β-CCB had no effect, but did inhibit spontaneous and evoked IPSCs. In addition, the occurrence of SOCs was reduced in mice lacking the δ-subunit, and their kinetics were also altered. The anti-epileptic drug vigabatrin increased SOC frequency in a time-dependent manner, but this effect was not due to reversal of GABA transporters. Together, these data indicate that SOCs in TC neurons arise from astrocytic GABA release, and are mediated by δ-subunit-containing GABA(A) receptors. Furthermore, these findings suggest that the therapeutic action of vigabatrin may occur through the augmentation of this astrocyte-neuron interaction, and highlight the importance of glial cells in CNS (patho) physiology.
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Registered trials
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