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GABAergic and Glycinergic Neurons
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GABAergic and Glycinergic Neurons

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (30 September 2022) | Viewed by 19594

Special Issue Editors

Prof. Dr. Yuchio Yanagawa

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Guest Editor
Department of Genetic and Behavioral Neuroscience, Gunma University Graduate School of Medicine, 3-39-22 Showa-machi, Maebashi 371-8511, Japan
Interests: molecular and cellular neurobiology; behavior; neuropsychiatric disorder; animal disease model; inhibitory neuron; transgenic rodent
Dr. Akiko Arata

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Guest Editor
Division of Physiome, Department of Physiology, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya 663-8501, Japan
Interests: respiratory physiology; perinatal physiology; system neuroscience; development of neuronal network; sensory-motor control; neonatal period

Special Issue Information

Dear Colleagues,

Neurons are typically classified into two groups, i.e., excitatory and inhibitory neurons. Inhibitory neurons play an important role in the regulation and stabilization of network activities and are essential for a number of brain functions, such as cognition, perception, movement, and respiration. Inhibitory neurons are composed of GABAergic and glycinergic neurons, which release GABA and glycine, respectively, as neurotransmitters. GABAergic neurons are widely spread in the CNS, whereas glycinergic neurons are largely restricted to the brainstem and spinal cord. GABAergic and glycinergic neurons are scattered in their locations and thus are difficult to identify in living brain preparations. However, the recent development of tools and technologies for characterizing these neurons, such as transgenic mice, viruses, optogenetics, and DREAD (Designer Receptors Exclusively Activated by Designer Drugs), has made it easier to study these neurons.

The goal of this Special Issue is to bring together experts studying GABAergic and/or glycinergic neurons. It will present studies on (1) the structure and function of GABAergic/glycinergic neurons, (2) the development of GABAergic/glycinergic networks that involve switching from excitatory neurons to inhibitory ones, (3) new mechanisms and roles of GABAergic/glycinergic neurons in behavior, (4) diseases related to GABAergic/glycinergic neurons, and (5) research tools for investigating GABAergic/glycinergic neurons. This Special Issue will welcome original research articles focusing on GABAergic and/or glycinergic neurons and review articles discussing our current knowledge of GABAergic and/or glycinergic neurons.

Prof. Dr. Yuchio Yanagawa
Dr. Akiko Arata
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • GABAergic neuron
  • glycinergic neuron
  • neurotransmitter
  • GABA
  • glycine
  • transporter
  • perception
  • sensation
  • movement
  • respiration
  • network switching
  • behavior
  • disease

Published Papers (6 papers)

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Research

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10 pages, 2138 KiB  
Article
Analyses of the Mode of Action of an Alpha-Adrenoceptor Blocker in Substantia Gelatinosa Neurons in Rats
by Daisuke Uta, Tsuyoshi Hattori and Megumu Yoshimura
Int. J. Mol. Sci. 2021, 22(17), 9636; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22179636 - 06 Sep 2021
Viewed by 1857
Abstract
To elucidate why naftopidil increases the frequency of spontaneous synaptic currents in only some substantia gelatinosa (SG) neurons, post-hoc analyses were performed. Blind patch-clamp recording was performed using slice preparations of SG neurons from the spinal cords of adult rats. Spontaneous inhibitory and [...] Read more.
To elucidate why naftopidil increases the frequency of spontaneous synaptic currents in only some substantia gelatinosa (SG) neurons, post-hoc analyses were performed. Blind patch-clamp recording was performed using slice preparations of SG neurons from the spinal cords of adult rats. Spontaneous inhibitory and excitatory postsynaptic currents (sIPSCs and sEPSCs, respectively) were recorded. The ratios of the frequency and amplitude of the sIPSCs and sEPSCs following the introduction of naftopidil compared with baseline, and after the application of naftopidil, serotonin (5-HT), and prazosin, compared with noradrenaline (NA) were evaluated. First, the sIPSC analysis indicated that SG neurons reached their full response ratio for NA at 50 μM. Second, they responded to 5-HT (50 μM) with a response ratio similar to that for NA, but prazosin (10 μM) did not change the sEPSCs and sIPSCs. Third, the highest concentration of naftopidil (100 μM) led to two types of response in the SG neurons, which corresponded with the reactions to 5-HT and prazosin. These results indicate that not all neurons were necessarily activated by naftopidil, and that the micturition reflex may be regulated in a sophisticated manner by inhibitory mechanisms in these interneurons. Full article
(This article belongs to the Special Issue GABAergic and Glycinergic Neurons)
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12 pages, 12979 KiB  
Article
Reelin Affects Signaling Pathways of a Group of Inhibitory Neurons and the Development of Inhibitory Synapses in Primary Neurons
by Seong-Eun Lee and Gum Hwa Lee
Int. J. Mol. Sci. 2021, 22(14), 7510; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22147510 - 13 Jul 2021
Cited by 1 | Viewed by 2257
Abstract
Reelin is a secretory protein involved in a variety of processes in forebrain development and function, including neuronal migration, dendrite growth, spine formation, and synaptic plasticity. Most of the function of Reelin is focused on excitatory neurons; however, little is known about its [...] Read more.
Reelin is a secretory protein involved in a variety of processes in forebrain development and function, including neuronal migration, dendrite growth, spine formation, and synaptic plasticity. Most of the function of Reelin is focused on excitatory neurons; however, little is known about its effects on inhibitory neurons and inhibitory synapses. In this study, we investigated the phosphatidylinositol 3-kinase/Akt pathway of Reelin in primary cortical and hippocampal neurons. Individual neurons were visualized using immunofluorescence to distinguish inhibitory neurons from excitatory neurons. Reelin-rich protein supplementation significantly induced the phosphorylation of Akt and ribosomal S6 protein in excitatory neurons, but not in most inhibitory neurons. In somatostatin-expressing inhibitory neurons, one of major subtypes of inhibitory neurons, Reelin-rich protein supplementation induced the phosphorylation of S6. Subsequently, we investigated whether or not Reelin-rich protein supplementation affected dendrite development in cultured inhibitory neurons. Reelin-rich protein supplementation did not change the total length of dendrites in inhibitory neurons in vitro. Finally, we examined the development of inhibitory synapses in primary hippocampal neurons and found that Reelin-rich protein supplementation significantly reduced the density of gephyrin–VGAT-positive clusters in the dendritic regions without changing the expression levels of several inhibitory synapse-related proteins. These findings indicate a new role for Reelin in specific groups of inhibitory neurons and the development of inhibitory synapses, which may contribute to the underlying cellular mechanisms of RELN-associated neurological disorders. Full article
(This article belongs to the Special Issue GABAergic and Glycinergic Neurons)
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11 pages, 2998 KiB  
Article
Inspiratory Off-Switch Mediated by Optogenetic Activation of Inhibitory Neurons in the preBötzinger Complex In Vivo
by Swen Hülsmann, Liya Hagos, Volker Eulenburg and Johannes Hirrlinger
Int. J. Mol. Sci. 2021, 22(4), 2019; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22042019 - 18 Feb 2021
Cited by 9 | Viewed by 3631
Abstract
The role of inhibitory neurons in the respiratory network is a matter of ongoing debate. Conflicting and contradicting results are manifold and the question whether inhibitory neurons are essential for the generation of the respiratory rhythm as such is controversial. Inhibitory neurons are [...] Read more.
The role of inhibitory neurons in the respiratory network is a matter of ongoing debate. Conflicting and contradicting results are manifold and the question whether inhibitory neurons are essential for the generation of the respiratory rhythm as such is controversial. Inhibitory neurons are required in pulmonary reflexes for adapting the activity of the central respiratory network to the status of the lung and it is hypothesized that glycinergic neurons mediate the inspiratory off-switch. Over the years, optogenetic tools have been developed that allow for cell-specific activation of subsets of neurons in vitro and in vivo. In this study, we aimed to identify the effect of activation of inhibitory neurons in vivo. Here, we used a conditional transgenic mouse line that expresses Channelrhodopsin 2 in inhibitory neurons. A 200 µm multimode optical fiber ferrule was implanted in adult mice using stereotaxic surgery, allowing us to stimulate inhibitory, respiratory neurons within the core excitatory network in the preBötzinger complex of the ventrolateral medulla. We show that, in anesthetized mice, activation of inhibitory neurons by blue light (470 nm) continuously or with stimulation frequencies above 10 Hz results in a significant reduction of the respiratory rate, in some cases leading to complete cessation of breathing. However, a lower stimulation frequency (4–5 Hz) could induce a significant increase in the respiratory rate. This phenomenon can be explained by the resetting of the respiratory cycle, since stimulation during inspiration shortened the associated breath and thereby increased the respiratory rate, while stimulation during the expiratory interval reduced the respiratory rate. Taken together, these results support the concept that activation of inhibitory neurons mediates phase-switching by inhibiting excitatory rhythmogenic neurons in the preBötzinger complex. Full article
(This article belongs to the Special Issue GABAergic and Glycinergic Neurons)
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Review

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18 pages, 660 KiB  
Review
Investigating the Role of GABA in Neural Development and Disease Using Mice Lacking GAD67 or VGAT Genes
by Erika Bolneo, Pak Yan S. Chau, Peter G. Noakes and Mark C. Bellingham
Int. J. Mol. Sci. 2022, 23(14), 7965; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23147965 - 19 Jul 2022
Cited by 10 | Viewed by 5174
Abstract
Normal development and function of the central nervous system involves a balance between excitatory and inhibitory neurotransmission. Activity of both excitatory and inhibitory neurons is modulated by inhibitory signalling of the GABAergic and glycinergic systems. Mechanisms that regulate formation, maturation, refinement, and maintenance [...] Read more.
Normal development and function of the central nervous system involves a balance between excitatory and inhibitory neurotransmission. Activity of both excitatory and inhibitory neurons is modulated by inhibitory signalling of the GABAergic and glycinergic systems. Mechanisms that regulate formation, maturation, refinement, and maintenance of inhibitory synapses are established in early life. Deviations from ideal excitatory and inhibitory balance, such as down-regulated inhibition, are linked with many neurological diseases, including epilepsy, schizophrenia, anxiety, and autism spectrum disorders. In the mammalian forebrain, GABA is the primary inhibitory neurotransmitter, binding to GABA receptors, opening chloride channels and hyperpolarizing the cell. We review the involvement of down-regulated inhibitory signalling in neurological disorders, possible mechanisms for disease progression, and targets for therapeutic intervention. We conclude that transgenic models of disrupted inhibitory signalling—in GAD67+/− and VGAT−/− mice—are useful for investigating the effects of down-regulated inhibitory signalling in a range of neurological diseases. Full article
(This article belongs to the Special Issue GABAergic and Glycinergic Neurons)
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13 pages, 1094 KiB  
Review
Synergistic Control of Transmitter Turnover at Glycinergic Synapses by GlyT1, GlyT2, and ASC-1
by Volker Eulenburg and Swen Hülsmann
Int. J. Mol. Sci. 2022, 23(5), 2561; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23052561 - 25 Feb 2022
Cited by 12 | Viewed by 2380
Abstract
In addition to being involved in protein biosynthesis and metabolism, the amino acid glycine is the most important inhibitory neurotransmitter in caudal regions of the brain. These functions require a tight regulation of glycine concentration not only in the synaptic cleft, but also [...] Read more.
In addition to being involved in protein biosynthesis and metabolism, the amino acid glycine is the most important inhibitory neurotransmitter in caudal regions of the brain. These functions require a tight regulation of glycine concentration not only in the synaptic cleft, but also in various intracellular and extracellular compartments. This is achieved not only by confining the synthesis and degradation of glycine predominantly to the mitochondria, but also by the action of high-affinity large-capacity glycine transporters that mediate the transport of glycine across the membranes of presynaptic terminals or glial cells surrounding the synapses. Although most cells at glycine-dependent synapses express more than one transporter with high affinity for glycine, their synergistic functional interaction is only poorly understood. In this review, we summarize our current knowledge of the two high-affinity transporters for glycine, the sodium-dependent glycine transporters 1 (GlyT1; SLC6A9) and 2 (GlyT2; SLC6A5) and the alanine–serine–cysteine-1 transporter (Asc-1; SLC7A10). Full article
(This article belongs to the Special Issue GABAergic and Glycinergic Neurons)
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22 pages, 4914 KiB  
Review
Developmental Formation of the GABAergic and Glycinergic Networks in the Mouse Spinal Cord
by Chigusa Shimizu-Okabe, Shiori Kobayashi, Jeongtae Kim, Yoshinori Kosaka, Masanobu Sunagawa, Akihito Okabe and Chitoshi Takayama
Int. J. Mol. Sci. 2022, 23(2), 834; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23020834 - 13 Jan 2022
Cited by 9 | Viewed by 2937
Abstract
Gamma-aminobutyric acid (GABA) and glycine act as inhibitory neurotransmitters. Three types of inhibitory neurons and terminals, GABAergic, GABA/glycine coreleasing, and glycinergic, are orchestrated in the spinal cord neural circuits and play critical roles in regulating pain, locomotive movement, and respiratory rhythms. In this [...] Read more.
Gamma-aminobutyric acid (GABA) and glycine act as inhibitory neurotransmitters. Three types of inhibitory neurons and terminals, GABAergic, GABA/glycine coreleasing, and glycinergic, are orchestrated in the spinal cord neural circuits and play critical roles in regulating pain, locomotive movement, and respiratory rhythms. In this study, we first describe GABAergic and glycinergic transmission and inhibitory networks, consisting of three types of terminals in the mature mouse spinal cord. Second, we describe the developmental formation of GABAergic and glycinergic networks, with a specific focus on the differentiation of neurons, formation of synapses, maturation of removal systems, and changes in their action. GABAergic and glycinergic neurons are derived from the same domains of the ventricular zone. Initially, GABAergic neurons are differentiated, and their axons form synapses. Some of these neurons remain GABAergic in lamina I and II. Many GABAergic neurons convert to a coreleasing state. The coreleasing neurons and terminals remain in the dorsal horn, whereas many ultimately become glycinergic in the ventral horn. During the development of terminals and the transformation from radial glia to astrocytes, GABA and glycine receptor subunit compositions markedly change, removal systems mature, and GABAergic and glycinergic action shifts from excitatory to inhibitory. Full article
(This article belongs to the Special Issue GABAergic and Glycinergic Neurons)
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