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Brain Sciences
Special Issues
New Insights in GABA Signaling
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New Insights in GABA Signaling

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Molecular and Cellular Neuroscience".

Deadline for manuscript submissions: closed (1 January 2024) | Viewed by 3003

Special Issue Editors

Dr. Jorge A. Miranda-Barrientos

E-Mail Website
Guest Editor
Neural Plasticity Section, Lieber Institute for Brain Development, Baltimore, MD 21205, USA
Interests: motivated behaviors; electrophysiology; in vivo calcium imaging; inhibition; glutamate/GABA co-transmission; attention; neuronal circuits; plasticity
Prof. Dr. Janko Samardžić

E-Mail Website
Guest Editor
Institute of Pharmacology, Clinical Pharmacology and Toxicology, Faculty of Medicine, University of Belgrade, 11000 Belgrade, Serbia
Interests: neuropsychopharmacology; neuroscience; GABA; glutamate; pharmacogenetics; pharmacotherapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Gamma-aminobutyric acid (GABA) is the primary inhibitory neurotransmitter within the central nervous system, and neurons that synthesize and release GABA are widely distributed throughout the brain. GABAergic transmission, mediated by GABAergic neurons through local or long-range projections, has been shown to be crucial in sculpting neural networks, refining signal processing, preventing hyperexcitability, and maintaining homeostasis within neural circuits, thus playing a crucial role in the establishment of functional neural networks and the regulation of various neurophysiological and behavioral processes.

Alterations in GABAergic transmission have been implicated in several neurological and psychiatric disorders. Research into GABAergic signaling in postsynaptic neurons and mechanisms that regulate GABAergic neuron activity is crucial for a deeper understanding of brain function in health and disease, and the development of novel therapeutic strategies has aimed to restore and modulate synaptic transmission to improve brain function and treat a wide range of neuropsychiatric disorders. The GABAergic synapse is the site of action of several different classes of drugs that modulate inhibitory neurotransmission and is used in the pharmacotherapy of anxiety and sleep disorders, epilepsy, alcohol withdrawal, and the induction and maintenance of anesthesia.

This Special Issue aims to collate experts to share cutting-edge research on GABAergic transmission and GABAergic circuits. All kinds of physiology, pharmacology, and pathophysiology studies involving GABAergic circuits and behaviors regulated by GABAergic transmission are welcome.

Dr. Jorge A. Miranda-Barrientos
Prof. Dr. Janko Samardžić
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Brain Sciences is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • GABA
  • neurotransmission
  • signaling
  • physiology
  • pharmacology
  • behavior
  • neuroscience
  • neuropsychiatric disorders

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Published Papers (1 paper)

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Research

11 pages, 1558 KiB  
Article
Prolonged Zaleplon Treatment Increases the Expression of Proteins Involved in GABAergic and Glutamatergic Signaling in the Rat Hippocampus
by Jelena Martinovic, Janko Samardzic, Marina Zaric Kontic, Sanja Ivkovic, Sanja Dacic, Tamara Major, Milica Radosavljevic and Dubravka Svob Strac
Brain Sci. 2023, 13(12), 1707; https://doi.org/10.3390/brainsci13121707 - 12 Dec 2023
Cited by 1 | Viewed by 1864
Abstract
Zaleplon is a positive allosteric modulator of the γ-aminobutyric acid (GABA)A receptor approved for the short-term treatment of insomnia. Previous publications on zaleplon have not addressed the proteins involved in its mechanism of action but have mostly referred to behavioral or pharmacological [...] Read more.
Zaleplon is a positive allosteric modulator of the γ-aminobutyric acid (GABA)A receptor approved for the short-term treatment of insomnia. Previous publications on zaleplon have not addressed the proteins involved in its mechanism of action but have mostly referred to behavioral or pharmacological studies. Since both GABAergic and glutamatergic signaling have been shown to regulate wakefulness and sleep, we examined the effects of prolonged zaleplon treatment (0.625 mg/kg for 5 days) on these systems in the hippocampus of male Wistar rats. Western blot and immunohistochemical analyses showed that the upregulated components of GABAergic signaling (glutamate decarboxylase, vesicular GABA transporter, GABA, and α1 subunit of the GABAA receptor) were accompanied by increased protein levels in the glutamatergic system (vesicular glutamate transporter 1 and NR1, NR2A, and NR2B subunits of N-methyl-d-aspartate receptor). Our results, showing that zaleplon enhances GABA neurotransmission in the hippocampus, were not surprising. However, we found that treatment also increased glutamatergic signaling. This could be the result of the downregulation of adenosine A1 receptors, important modulators of the glutamatergic system. Further studies are needed to investigate the effects of the zaleplon-induced increase in hippocampal glutamatergic neurotransmission and the possible involvement of the adenosine system in zaleplon’s mechanism of action. Full article
(This article belongs to the Special Issue New Insights in GABA Signaling)
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