Do Motor‐nerve Terminals Have Γ‐aminobutyric Acid Receptors?

Smart, Trevor G.

doi:10.1111/j.1476-5381.1980.tb10937.x

Cited by 9 publications

(8 citation statements)

References 32 publications

(56 reference statements)

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“…Similarly, the frequency of the spontaneously occurring MEPPs did not change following GABA treatment at the same concentration (control: 0.78 ± 0.16 s −1 ; GABA: 0.90 ± 0.20 s −1 , paired t ‐test, t 3 = 1.94, p = 0.15). These results are consistent with those of the study conducted by Smart () on mouse neuromuscular junctions, indicating that, in the rat synapse, GABA did not change either the sensitivity of the postsynaptic nicotinic receptors to ACh nor the intensity of the spontaneous quantal mediator release. The decrease in the H‐effect under the influence of GABA revealed in our studies thus actually reflects the reduction in the intensity of the non‐quantal ACh release from the motor nerve terminal.…”

Section: Resultssupporting

confidence: 92%

“…Despite the fact that many studies have investigated the putative involvement of GABA in the functioning of the neuromuscular junction, the action of this amino acid or the existence of specific GABA receptors in these synapses remains unclear (Hofmann et al . ; Smart ; Chiou and Chang ). It should be noted that the authors of these studies (Smart ; Chiou and Chang ) investigated only the possibility of GABA's impact on processes of vesicular (quantal) ACh release.…”

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confidence: 99%

“…; Smart ; Chiou and Chang ). It should be noted that the authors of these studies (Smart ; Chiou and Chang ) investigated only the possibility of GABA's impact on processes of vesicular (quantal) ACh release. To date, it has been established that, in the absence of nerve impulses, ACh release from motor nerve endings mostly occurs non‐quantally and that this type of release can perform an important neurotrophic function in maintaining the morphological and functional properties of the skeletal muscles (Vyskocil et al .…”

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confidence: 99%

“…Moreover, it has been shown that GABA reduces acetylcholine (ACh) release from the preganglionic fibers in the rat cervical ganglion (Brown and Higgins 1979) and in the bullfrog sympathetic ganglion (Kato and Kuba 1980). Despite the fact that many studies have investigated the putative involvement of GABA in the functioning of the neuromuscular junction, the action of this amino acid or the existence of specific GABA receptors in these synapses remains unclear (Hofmann et al 1962;Smart 1980;Chiou and Chang 1994). It should be noted that the authors of these studies (Smart 1980;Chiou and Chang 1994) investigated only the possibility of GABA's impact on processes of vesicular (quantal) ACh release.…”

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confidence: 99%

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Metabotropic GABA_B receptors mediate GABA inhibition of acetylcholine release in the rat neuromuscular junction

Malomouzh

Петров

Нуруллин

et al. 2015

Journal of Neurochemistry

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Gamma-aminobutyric acid (GABA) is an amino acid which acts as a neurotransmitter in the central nervous system. Here, we studied the effects of GABA on non-quantal, spontaneous, and evoked quantal acetylcholine (ACh) release from motor nerve endings. We found that while the application of 10 lM of GABA had no effect on spontaneous quantal ACh release, as detected by the frequency of miniature endplate potentials, GABA reduced the non-quantal ACh release by 57%, as determined by the H-effect value. Finally, the evoked quantal ACh release, estimated by calculating the quantal content of full-sized endplate potentials (EPPs), was reduced by 34%. GABA's inhibitory effect remained unchanged after pre-incubation with picrotoxin, an ionotropic GABA A receptor blocker, but was attenuated following application of the GABA B receptor blocker CGP 55845, which itself had no effect on ACh release. An inhibitor of phospholipase C, U73122, completely prevented the GABA-induced decrease in ACh release. Immunofluorescence demonstrated the presence of both subunits of the GABA B receptor (GABA B R1 and GABA B R2) in the neuromuscular junction. These findings suggest that metabotropic GABA B receptors are expressed in the mammalian neuromuscular synapse and their activation results in a phospholipase C-mediated reduction in the intensity of non-quantal and evoked quantal ACh release. Keywords: GABA receptors, phospholipase C, quantal and non-quantal acetylcholine release. A compound called c-aminobutyric acid (GABA), which is synthesized by the enzyme L-glutamate decarboxylase (GAD; EC 4.1.1.15), is the basic inhibitory neurotransmitter in the synapses of the central nervous system (CNS). It plays a key role in the development, maturation, and functioning of the adult brain by modulating neuronal activity (Watanabe et al. 2002;Obata 2013). The synaptic action of GABA occurs via the activation of ionotropic GABA A receptors and metabotropic GABA B receptors (Bowery et al. 2002;Olsen and Sieghart 2008). The physiological role of GABA in the CNS is studied largely because GABAergic signaling dysfunction underlies the development of a broad spectrum of neurological and psychiatric diseases, including anxiety, sleep disorder, muscle rigidity, Parkinson's disease, Huntington's disease, epilepsy, and schizophrenia (Obata 2013; Smith-Hicks 2013).

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Section: Resultssupporting

confidence: 92%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Metabotropic GABA_B receptors mediate GABA inhibition of acetylcholine release in the rat neuromuscular junction

Malomouzh

Петров

Нуруллин

et al. 2015

Journal of Neurochemistry

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“…In the majority of cases, it has been proved that the cause of pathology associated with the implementation and control of locomotion is localized in the CNS (Gazulla et al., ). Nevertheless, today no one can unambiguously deny or confirm the presence of elements of GABAergic signalling at the neuromuscular junction or its ability to affect cholinergic synaptic transmission, although numerous studies have been conducted on this subject (Chiou & Chang, ; Glavinović, ; Smart, ).…”

Section: Introductionmentioning

confidence: 99%

Enhancement of mouse diaphragm contractility in the presence of antagonists of GABA_A and GABA_B receptors

Lenina

Петров

Kovyazina

et al. 2019

Experimental Physiology

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New Findings What is the central question of this study?Do GABA receptors play any role at the neuromuscular junction? What is the main finding and its importance?In the presence of either ionotropic or metabotropic GABA receptor antagonists, diaphragm muscle force production elicited by stimulating the motor nerve at ≥50 Hz was increased. Our data indicate the presence of GABAergic signalling at the neuromuscular junction. Abstract Despite the signalling role of GABA in the brain and spinal cord, the role of this molecule in the peripheral nervous system and, in particular, at the neuromuscular junction remains practically unexplored. In the present work, the force of mouse diaphragm contractions was measured in the presence of blockers of metabotropic GABAB receptors (CGP 55845) and ionotropic GABAA receptors (picrotoxin) with various patterns of indirect and direct stimulation of muscle by trains of 40 pulses delivered at 10, 20, 50 and 70 Hz. It was found that neither blocker affected the diaphragm contractility caused by indirect stimulation through the motor nerve at 10 and 20 Hz. However, when the stimulation frequency was increased to 50 or 70 Hz, the force of subsequent contractions in the train (when compared with the amplitude of contraction in response to the first pulse) was increased by both CGP 55845 and picrotoxin. With direct stimulation of the diaphragm, no significant changes in the contraction force were detected at any frequency used. The results obtained support the following conclusions: (i) pharmacological inhibition of GABA receptors increases the contractile activity of skeletal muscle; and (ii) frequency‐dependent enhancement of GABA receptor activation takes place in the region of the neuromuscular junction.

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Transient GABA immunoreactivity in cranial nerves of the chick embryo

Bartheld

Rubel

1989

J of Comparative Neurology

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The distribution and time course of gamma-aminobutyric acid (GABA) immunoreactivity was investigated in the cranium of the chick embryo from 2 to 16 days of incubation (E2-16). A fraction of nerve fibers transiently stains GABA-positive in all cranial motor nerves and in the vestibular nerve. Cranial motor nerves stain GABA-positive from E4 to E11, including neuromuscular junctions at E8-11; labeled fibers are most frequent in the motor trigeminal root (E6-9.5). Substantial GABA staining is present from E4 to E10 in a subpopulation (1-2%) of vestibular ganglion cells. Their peripheral processes are labeled in the vestibular endorgan, predominantly in the posterior crista. Some GABA-positive fibers are present in the olfactory nerve (after E5) and in the optic nerve (after E9.5); their immunoreactivity persists throughout the period investigated. Transient GABA immunoreactivity follows "pioneer" fiber outgrowth and coincides with the formation of early synaptic contacts. GABA-containing neurons may change their neuronal phenotype (loss of GABA expression) or they may be eliminated by embryological cell death. Periods of cell death were determined in cranial ganglia and motor nuclei by aggregations of pycnotic cells in the same embryonic material. The periods of embryonic cell death partly coincide with transient GABA immunoreactivity. The function(s) of transient GABA expression is unknown. Some lines of evidence suggest that GABA has neurotrophic functions in developing cranial nerves or their target tissue. In the developing neuromuscular junction, GABA may be involved in the regulation of acetylcholine receptors.

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Do Motor‐nerve Terminals Have Γ‐aminobutyric Acid Receptors?

Abstract: 1 y-Aminobutyric acid (GABA, 0.1 to 1 mM) had no significant effect on the amplitude, rise time, half decay time or frequency of miniature endplate potentials (m.e.p.ps) at the frog or mouse neuromuscular junctions in vitro.

Cited by 9 publications

References 32 publications

Metabotropic GABA_B receptors mediate GABA inhibition of acetylcholine release in the rat neuromuscular junction

Metabotropic GABA_B receptors mediate GABA inhibition of acetylcholine release in the rat neuromuscular junction

Enhancement of mouse diaphragm contractility in the presence of antagonists of GABA_A and GABA_B receptors

Transient GABA immunoreactivity in cranial nerves of the chick embryo

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Do Motor‐nerve Terminals Have Γ‐aminobutyric Acid Receptors?

Abstract: 1 y-Aminobutyric acid (GABA, 0.1 to 1 mM) had no significant effect on the amplitude, rise time, half decay time or frequency of miniature endplate potentials (m.e.p.ps) at the frog or mouse neuromuscular junctions in vitro.

Cited by 9 publications

References 32 publications

Metabotropic GABAB receptors mediate GABA inhibition of acetylcholine release in the rat neuromuscular junction

Metabotropic GABAB receptors mediate GABA inhibition of acetylcholine release in the rat neuromuscular junction

Enhancement of mouse diaphragm contractility in the presence of antagonists of GABAA and GABAB receptors

Transient GABA immunoreactivity in cranial nerves of the chick embryo

Contact Info

Product

Resources

About

Metabotropic GABA_B receptors mediate GABA inhibition of acetylcholine release in the rat neuromuscular junction

Metabotropic GABA_B receptors mediate GABA inhibition of acetylcholine release in the rat neuromuscular junction

Enhancement of mouse diaphragm contractility in the presence of antagonists of GABA_A and GABA_B receptors