Synapsin I Synchronizes GABA Release in Distinct Interneuron Subpopulations

2019 ◽  
Vol 30 (3) ◽  
pp. 1393-1406
Author(s):  
N Forte ◽  
F Binda ◽  
A Contestabile ◽  
F Benfenati ◽  
P Baldelli
Keyword(s):  
In Situ Hybridization ◽  
Patch Clamp ◽  
Action Potential ◽  
Hippocampal Slices ◽  
Gaba Release ◽  
Aminobutyric Acid ◽  
Synapsin I ◽  
Gamma Aminobutyric Acid ◽  
Asynchronous Release

Abstract Neurotransmitters can be released either synchronously or asynchronously with respect to action potential timing. Synapsins (Syns) are a family of synaptic vesicle (SV) phosphoproteins that assist gamma-aminobutyric acid (GABA) release and allow a physiological excitation/inhibition balance. Consistently, deletion of either or both Syn1 and Syn2 genes is epileptogenic. In this work, we have characterized the effect of SynI knockout (KO) in the regulation of GABA release dynamics. Using patch-clamp recordings in hippocampal slices, we demonstrate that the lack of SynI impairs synchronous GABA release via a reduction of the readily releasable SVs and, in parallel, increases asynchronous GABA release. The effects of SynI deletion on synchronous GABA release were occluded by ω-AgatoxinIVA, indicating the involvement of P/Q-type Ca2+channel-expressing neurons. Using in situ hybridization, we show that SynI is more expressed in parvalbumin (PV) interneurons, characterized by synchronous release, than in cholecystokinin or SOM interneurons, characterized by a more asynchronous release. Optogenetic activation of PV and SOM interneurons revealed a specific reduction of synchronous release in PV/SynIKO interneurons associated with an increased asynchronous release in SOM/SynIKO interneurons. The results demonstrate that SynI is differentially expressed in interneuron subpopulations, where it boosts synchronous and limits asynchronous GABA release.

GABA release in posterior hypothalamus across sleep-wake cycle

1996 ◽  
Vol 271 (6) ◽  
pp. R1707-R1712 ◽  
Author(s):  
D. Nitz ◽  
J. M. Siegel
Keyword(s):  
Receptor Agonist ◽  
High Performance ◽  
Slow Wave Sleep ◽  
Gaba Release ◽  
Posterior Hypothalamus ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Rapid Eye Movement Sleep ◽  
Unit Discharge ◽  
Selective Increase

The activity of neurons in the posterior hypothalamus (PH) is thought to contribute to the production of wakefulness and electroencephalograph desynchronization. Inactivation of neuronal activity in this area is known to induce sleep. Most PH neurons decrease unit discharge during slow-wave sleep (SWS) relative to wake and rapid eye movement sleep. In the present study, we sought to examine potential sources of inhibition or disfacilitation underlying the reduction of PH unit activity during SWS in the cat. We employed the microdialysis technique in conjunction with high-performance liquid chromatography methods for the quantification of glutamate, glycine, and gamma-aminobutyric acid (GABA) release. We found a selective increase in GABA release during SWS in the PH. Glutamate and glycine levels were unchanged across the sleep-wake cycle. microinjection of the GABAA-receptor agonist muscimol, into the same areas from which microdialysis samples were collected, increased SWS time. Our studies support the hypothesis that GABA release in the posterior hypothalamus mediates inhibition of posterior hypothalamic neurons, thereby facilitating SWS.

Expression of the Na(+)-K(+)-2Cl- cotransporter BSC2 in the nervous system

1997 ◽  
Vol 272 (1) ◽  
pp. C173-C183 ◽  
Author(s):  
M. D. Plotkin ◽  
M. R. Kaplan ◽  
L. N. Peterson ◽  
S. R. Gullans ◽  
S. C. Hebert ◽  
...  
Keyword(s):  
Nervous System ◽  
In Situ Hybridization ◽  
Polyclonal Antibodies ◽  
Neuronal Response ◽  
Primary Cultures ◽  
Apical Surface ◽  
Gamma Aminobutyric Acid ◽  
Confocal Immunofluorescence Microscopy ◽  
Apical Localization

We used in situ hybridization and immunocytochemistry with polyclonal antibodies against the mouse bumetanide-sensitive Na(+)-K(+)-2Cl- cotransporter (mBSC2) to determine the location of this cotransporter in rat brain. Northern blots and in situ hybridization showed the presence of cotransporter mRNA in the brain, with an especially high level of expression in the choroid plexus (CP). Affinity-purified anti-BSC2 antibody identified proteins of 145-155 kDa on Western blot analysis and immunoprecipitation of brain and CP membrane protein. Indirect immunofluorescence demonstrated that BSC2 protein is located on the apical surface of the CP and is heterogeneously distributed in cell bodies and dendrites of neurons in the central and peripheral nervous system. The apical localization of BSC2 in the CP was confirmed by 86Rb+ uptakes in primary cultures of CP cells grown on permeable filters and confocal immunofluorescence microscopy. The apical localization of the cotransporter in CP epithelium suggests a role for the cotransporter in cerebrospinal fluid K+ homeostasis. In neurons, the cotransporter may help regulate intracellular Cl- concentration and thereby affect neuronal response to gamma-aminobutyric acid.

Effect of exposure in vitro to ethanol and hypoxia on gamma-aminobutyric acid efflux in the hippocampus of the fetal and adult guinea-pig

1995 ◽  
Vol 7 (5) ◽  
pp. 1339 ◽  
Author(s):  
MC Catlin ◽  
DH Penning ◽  
JF Brien
Keyword(s):  
Guinea Pig ◽  
Hippocampal Slices ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Gaba System ◽  
Direct Exposure ◽  
Interface System ◽  
Near Term ◽  
Co2 Environment

The objective of this study was to determine the effects of acute direct exposure to ethanol, hypoxia or ethanol plus hypoxia on K+-stimulated gamma-aminobutyric acid (GABA) efflux (neuronal release minus uptake) in the hippocampus of the near-term fetal and adult guinea-pig. Transverse hippocampal slices were studied in a static-interface system. Exposure in vitro to ethanol or hypoxia involved 10-min incubation with 50 mM ethanol or 10-min incubation in a 95% N2/5% CO2 environment. GABA was quantitated by HPLC. Ethanol did not alter K+-stimulated GABA efflux; hypoxia augmented K+-stimulated GABA efflux three-fold in the near-term fetus and seven-fold in the adult; concurrent exposure to ethanol did not alter the effect of hypoxia. The data demonstrate that, for acute direct exposure to hypoxia and/or ethanol, only hypoxia increases K+-stimulated GABA efflux, the magnitude of which is dependent on the extent of development of the GABA system.

Uptake and release of gamma-aminobutyric acid in guinea pig gallbladder

1985 ◽  
Vol 249 (2) ◽  
pp. G192-G196 ◽  
Author(s):  
N. Saito ◽  
K. Taniyama ◽  
C. Tanaka
Keyword(s):  
Guinea Pig ◽  
Ganglion Cells ◽  
Regional Distribution ◽  
Gaba Release ◽  
Aminobutyric Acid ◽  
Transport Systems ◽  
Gamma Aminobutyric Acid ◽  
Beta Alanine ◽  
High Affinity ◽  
Uptake And Release

The presence of gamma-aminobutyric acid (GABA)-ergic neuron in guinea pig gallbladder was investigated by measuring GABA contents and glutamate decarboxylase (GAD) activity and by demonstrating the uptake and release of [3H]GABA. GABA and GAD are both present in the gallbladder, and a positive correlation in regional distribution was observed among GABA, GAD, and the number of ganglion cells. The uptake of [3H]GABA by the gallbladder showed two saturable components; a high-affinity component (Km = 23.3 microM, Vmax = 7.63 nmol X g-1 X 10 min-1) and a low-affinity component (Km = 515 microM, Vmax = 57.1 nmol X g-1 X 10 min-1). These high-affinity and low-affinity transport systems corresponded to those obtained in the presence of beta-alanine and L-2,4-diaminobutyric acid, respectively, thereby suggesting the presence of neuronal and nonneuronal GABA transport systems in this tissue. Electrical transmural stimulation produced an increase in [3H]-GABA release from the isolated gallbladder preloaded with [3H]GABA, in the presence of beta-alanine. The stimulation-evoked release of [3H]GABA was prevented by calcium-free medium containing 1 mM EGTA and tetrodotoxin, thereby indicating that the released GABA originates from the nerve terminals. These results provide evidence for the presence of GABA-ergic neurons in the guinea pig gallbladder.

gamma-Aminobutyric acid concentrations are maintained in anoxic turtle brain

1985 ◽  
Vol 249 (3) ◽  
pp. R372-R374 ◽  
Author(s):  
P. L. Lutz ◽  
R. Edwards ◽  
P. M. McMahon
Keyword(s):  
Initial Period ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Pseudemys Scripta

Changes in gamma-aminobutyric acid (GABA) concentrations in the turtle (Pseudemys scripta elegans) brain were studied in situ during prolonged anoxia. With the onset of anoxia, the well-documented rapid increases in GABA found in mammalian brains were not observed in the turtle brain. Although not statistically significant, mean GABA concentrations in the turtle brain were reduced from anesthetized control values during the first 30 min of anoxia. During this initial period brain glutamate content declined. Even after 2 h of nitrogen respiration, GABA in the turtle brain still did not rise above control levels. By the 4th h of anoxia, however, GABA had increased to 147% of control values.

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