The effect of the blockade of the gamma-aminobutyric acid (GABA) uptake system on the amplitude of glutamatergic synaptic potentials was studied by using a corticostriatal slice preparation. Nipecotic acid (0.1-1 mM), a GABA uptake blocker, produced a dose-dependent decrease of the amplitude of kynurenate-sensitive excitatory synaptic potentials recorded in the neostriatum following cortical stimulation. Nipecotic acid did not affect the postsynaptic responses to exogenously applied glutamate. The presynaptic effect of endogenous GABA was bicuculline-resistant and was mimicked by baclofen (0.3-3 microM). This effect was not blocked by phaclofen (0.5-1 mM). These findings show that phaclofen-insensitive GABAB receptors, activated by endogenous GABA, mediate presynaptic inhibition of cortical glutamatergic inputs in the neostriatum.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/0304-3940(90)90258-b | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
bFGF-Chitosan "brain glue" promotes functional recovery after cortical ischemic stroke.
Bioact Mater
April 2025
Beijing Key Laboratory for Biomaterials and Neural Regeneration, Beijing Advanced Innovation Center for Biomedical Engineering, School of Biological Science and Medical Engineering, Beihang University, Beijing 100083, China.
The mammalian brain has an extremely limited ability to regenerate lost neurons and to recover function following ischemic stroke. A biomaterial strategy of slowly-releasing various regeneration-promoting factors to activate endogenous neurogenesis represents a safe and practical neuronal replacement therapy. In this study, basic fibroblast growth factor (bFGF)-Chitosan gel is injected into the stroke cavity.
View Article and Find Full Text PDFOpioidergic activation of the descending pain inhibitory system underlies placebo analgesia.
Sci Adv
January 2025
Laboratory for Biofunction Dynamics Imaging, RIKEN Center for Biosystems Dynamics Research, 6-7-3 Minatojima-Minamimachi, Chuo-ku, Kobe, Hyogo 650-0047, Japan.
Placebo analgesia is caused by inactive treatment, implicating endogenous brain function involvement. However, the neurobiological basis remains unclear. In this study, we found that μ-opioid signals in the medial prefrontal cortex (mPFC) activate the descending pain inhibitory system to initiate placebo analgesia in neuropathic pain rats.
View Article and Find Full Text PDFDesign, Synthesis, and Pharmacological Evaluation of Nonsteroidal Tricyclic Ligands as Modulators of GABA Receptors.
J Med Chem
January 2025
Department of Drug Design and Pharmacology, Faculty of Health and Medical Sciences, University of Copenhagen, Universitetsparken 2, Copenhagen DK-2100, Denmark.
GABA receptors (GABARs) are the major elements of inhibitory neurotransmission in the central nervous system (CNS). They are established targets for regulation by endogenous brain neuroactive steroids (NASs) such as pregnanolone. However, the complexity of de novo synthesis of NAS derivatives has hindered attempts to circumvent the principal limitations of using endogenous NASs, including selectivity and limited oral bioavailability.
View Article and Find Full Text PDFNeurosteroids and neurological disorders.
Korean J Physiol Pharmacol
January 2025
Department of Pharmacology, Catholic Kwandong University College of Medicine, Gangneung 25601, Korea.
Neurosteroids play an important role as endogenous neuromodulators that are locally produced in the central nervous system and rapidly change the excitability of neurons and the activation of microglial cells and astrocytes. Here we review the mechanisms of synthesis, metabolism, and actions of neurosteroids in the central nervous system. Neurosteroids are able to play a variety of roles in the central nervous system under physiological conditions by binding to membrane ion channels and receptors such as gamma-aminobutyric acid type A receptors, Nmethyl- D-aspartate receptors, L- and T-type calcium channels, and sigma-1 receptors.
View Article and Find Full Text PDFEfficacy of GABA aminotransferase inactivator OV329 in models of neuropathic and inflammatory pain without tolerance or addiction.
Proc Natl Acad Sci U S A
January 2025
Department of Psychological and Brain Sciences, Indiana University, Bloomington, IN 47405.
Dysregulation of GABAergic inhibition is associated with pathological pain. Consequently, enhancement of GABAergic transmission represents a potential analgesic strategy. However, therapeutic potential of current GABA agonists and modulators is limited by unwanted side effects.
View Article and Find Full Text PDFWant 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!