GABAA receptors mediate inhibition of T cell responses

  title={GABAA receptors mediate inhibition of T cell responses},
  author={Jide Tian and Cindy Chau and Tim G. Hales and Daniel L. Kaufman},
  journal={Journal of Neuroimmunology},
Activation of GABA(A) receptors inhibits T cell proliferation
It is concluded that activation of GABA(A)Rs provides immunosuppression by inhibiting T cell proliferation by inhibition of benzodiazepines or the neurosteroid allopregnanolone.
γ-Aminobutyric Acid Inhibits T Cell Autoimmunity and the Development of Inflammatory Responses in a Mouse Type 1 Diabetes Model1
GA at relatively low concentrations down-regulated effector T cell responses to β cell Ags ex vivo, and administration of GABA retarded the adoptive transfer of type 1 diabetes (T1D) in NOD/scid mice.
The immunological function of GABAergic system.
Results may indicate that GABAergic components provide a new therapeutic approach for inflammatory and autoimmune diseases, such as experimental autoimmune encephalomyelitis, multiple sclerosis, and inflammatory bowel diseases.
Anaesthetic Impairment of Immune Function Is Mediated via GABAA Receptors
The functional data provide a possible explanation as to why chronic propofol and thiopental administration can increase the risk of infection in critically ill patients: their action on GABAA receptors inhibits normal monocyte behaviour.
Homotaurine, a safe blood-brain barrier permeable GABAA-R-specific agonist, ameliorates disease in mouse models of multiple sclerosis
The potential of BBB-permeable GABAA-R agonists as a new class of treatment to enhance CD8+ and CD4+ Treg responses and limit Th17 and Th1-medaited inflammation in the CNS is demonstrated.
Clinically applicable GABA receptor positive allosteric modulators promote ß-cell replication
It is shown that clinically applicable GABAA-R PAMs can increase significantly INS-1 ß-cell replication, which is enhanced by exogenous GABA application, and this suggests that Pams may potentiate the actions of GABA secreted by islet €cells on GabAA-Rs and provide a new class of drugs for diabetes treatment.
GABAergic signaling by cells of the immune system: more the rule than the exception.
The data raised the assumption of conserved GABA signaling in a broad range of mammalian cells and diversification of function in the immune system and, as an interspecies signaling molecule in host-microbe interactions.
GABAA‐receptor expression in glioma cells is triggered by contact with neuronal cells
It is shown that contact with neurons induces the expression of functional GABAA‐receptors, and with this form of interaction, neurons can influence tumour behaviour in the brain.
γ-Aninobutyric acid (GABA) suppresses antigen-specific immune responses in ovalbumin γ(OVA)-immunized BALB/c mice
The results suggest that the suppressive effect of GABA on Ag-specific immune responses contributes to the reduction of antigen-presenting function on CD11c+ dendritic cells.


GABAA receptor channels.
This chapter discusses the gamma-aminobutyric acid (GABA) receptor channels, which are the most abundant inhibitory neurotransmitter in the CNS. Following release from presynaptic vesicles, GABA
Recruitment of functional GABAA receptors to postsynaptic domains by insulin
Modification of synaptic strength in the mammalian central nervous system (CNS) occurs at both pre- and postsynaptic sites,. However, because postsynaptic receptors are likely to be saturated by
GABAB receptor pharmacology.
  • N. Bowery
  • Biology
    Annual review of pharmacology and toxicology
  • 1993
The discovery that GABAB antagonism can suppress absence seizures in rats has provided an important therapeutic target and the emergence of brain-penetrating GABAB antagonists being discovered makes future studies an exciting prospect.
Molecular biology of GABAA receptors
  • R. Olsen, A. Tobin
  • Biology, Chemistry
    FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • 1990
Subpopulations of GABAA receptors with different cellular and regional locations show differential sensitivity to GABA, to modulators like steroids, to physiological regulation, to disease processes, and to pharmacological manipulation by drugs such as benzodiazepines.
In vitro inhibition of cellular immune responses by benzodiazepines and PK 11195. Effects on mitogen- and alloantigen-driven lymphocyte proliferation and on IL-1, IL-2 synthesis and IL-2 receptor expression.
The most susceptible stage of mitogen-triggered T and B lymphocyte proliferation was found to be at incipience, and Cytotoxicity could not be made responsible for drug effects.
Modulation of T lymphocyte function by neuropeptides. Evidence for their role as local immunoregulatory elements.
It was concluded that the three study neuropeptides, over a broad range of concentrations, have profound stimulatory (and occasionally inhibitory) effects upon the function of a cloned T lymphocyte hybrid cell responding to specific Ag and that these events may reflect those of Ag-driven mucosal T lymphocytes exposed to neuropePTides in vivo.
Peripheral-type benzodiazepine receptors.