Effect of hydrogen sulfide on the characteristics of the neuromuscular synapse terminals of the rat diaphragm

2021 ◽  
Author(s):  
A.N. Kadenov ◽  
O.V. Yakovleva
Keyword(s):  
Hydrogen Sulfide ◽  
Synaptic Transmission ◽  
Key Words ◽  
Fluorescent Microscopy ◽  
Neuromuscular Synapse ◽  
Antioxidant Property ◽  
Postnatal Ontogenesis ◽  
Nerve Terminals ◽  
Rat Diaphragm ◽  
Biological Functions

Hydrogen sulfide is one of the gas-transmitters that also performs other biological functions. The antioxidant property of this substance is one of the important ones. The research was conducted on rats of both sexes between 6 and 18 days of age. We have shown that the offspring of females injected subcutaneously with hydrogen sulfide increased the area and luminescence of nerve terminals during postnatal ontogenesis, which can be further used to level the effects of hyperhomocysteinemia on synaptic transmission. Key words: neuromuscular synapse, fluorescent microscopy, hydrogen sulfide.

scholarly journals Synaptic transmission induces site-specific changes in sialylation on N-linked glycoproteins in rat nerve terminals

2020 ◽  
Author(s):  
Inga Boll ◽  
Pia Jensen ◽  
Veit Schwämmle ◽  
Martin R. Larsen
Keyword(s):  
Synaptic Transmission ◽  
Structure And Function ◽  
Synaptic Proteins ◽  
Nerve Terminals ◽  
Membrane Glycoproteins ◽  
Site Specific ◽  
Specific Alteration ◽  
And Function ◽  
Rat Nerve ◽  
Stimulation Of

AbstractSynaptic transmission leading to release of neurotransmitters in the nervous system is a fast and highly dynamic process. Previously, protein interaction and phosphorylation have been thought to be the main regulators of synaptic transmission. Here we show a novel potential modulator of synaptic transmission, sialylation of N-linked glycosylation. The negatively charged sialic acids can be modulated, similarly to phosphorylation, by the action of sialyltransferases and sialidases thereby changing local structure and function of membrane glycoproteins. We characterized site-specific alteration in sialylation on N-linked glycoproteins in isolated rat nerve terminals after brief depolarization using quantitative sialiomics. We identified 1965 formerly sialylated N-linked glycosites in synaptic proteins and found that the abundances of 430 glycosites changed after five seconds depolarization. We observed changes on essential synaptic proteins such as synaptic vesicle proteins, ion channels and transporters, neurotransmitter receptors and cell adhesion molecules. This study is to our knowledge the first to describe ultra-fast site-specific modulation of the sialiome after brief stimulation of a biological system.

The Case for Adaptability of the Neuromuscular Junction to Endurance Exercise Training

1998 ◽  
Vol 23 (4) ◽  
pp. 339-360 ◽  
Author(s):  
Robert Panenic ◽  
Phillip F. Gardiner
Keyword(s):  
Electrical Stimulation ◽  
Exercise Training ◽  
Neuromuscular Junction ◽  
Key Words ◽  
Endurance Exercise ◽  
Physiological Function ◽  
Trophic Factors ◽  
Nerve Terminals ◽  
Endurance Exercise Training

Although the adaptability of the neuromuscular junction (NMJ) has been demonstrated using the models of denervation/reinnervation, electrical stimulation, development, aging, and pathological states, relatively little is known about the effects of increased chronic voluntary use on the morphology and physiological function of the NMJ. A review of findings relating to adaptations in the various pre- and postsynaptic components of the NMJ with exercise training is presented. These findings are discussed as they pertain to NMJ function during exercise. Other physiological modulators of the NMJ, such as trophic factors released by nerve terminals and muscles, and circulating substances are discussed in terms of possible roles they may play in training-induced adaptations. Key words: neuromuscular junction, endurance exercise, adaptations, morphology, acetylcholinesterase, physiology, trophic factors

scholarly journals Enhanced Adenosine A2A Receptor Facilitation of Synaptic Transmission in the Hippocampus of Aged Rats

2003 ◽  
Vol 90 (2) ◽  
pp. 1295-1303 ◽  
Author(s):  
Nelson Rebola ◽  
Ana M. Sebastião ◽  
Alexandre de Mendonça ◽  
Catarina R. Oliveira ◽  
J. A. Ribeiro ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Synaptic Transmission ◽  
Receptor Agonist ◽  
Nerve Terminals ◽  
Aged Rats ◽  
Receptor Density ◽  
Young Rats ◽  
Kinase C ◽  
Fepsp Slope ◽  
Kinase A

Adenosine either inhibits or facilitates synaptic transmission through A1 or A2A receptors, respectively. Since A2A receptor density increases in the limbic cortex of aged (24 mo) compared with young adult rats (2 mo), we tested if A2A receptor modulation of synaptic transmission was also increased in aged rats. The A2A receptor agonist, CGS21680 (10 nM), caused a larger facilitation of the field excitatory postsynaptic potential (fEPSP) slope in hippocampal slices of aged (38%) than in young rats (19%), an effect prevented by the A2A receptor antagonist, ZM241385 (20 nM). In contrast to young rats, where CGS21680 facilitation of fEPSPs is prevented by the protein kinase C inhibitor, chelerythrine (6 μM), but not by the protein kinase A inhibitor, H-89 (1 μM), the CGS21680 -induced facilitation of fEPSP slope in aged rats was prevented by H-89 (1 μM) but not by chelerythrine (6 μM). Also, in contrast to the β–receptor agonist, isoproterenol (30 μM), CGS21680 (100–1,000 nM) enhanced cAMP levels in hippocampal nerve terminals of aged but not young rats. Finally, we observed a significant increase of both the binding density of [3H]CGS 21680 and the [3H]ZM241385 as well as of the anti-A2A receptor immunoreactivity in hippocampal nerve terminal membranes from aged compared with young rats. This shows that A2A receptor-mediated facilitation of hippocampal synaptic transmission is larger in aged than young rats due to increased A2A receptor density in nerve terminals and to the modified transducing system operated by A2A receptors, from a protein kinase C mediated control of A1 receptors into a direct protein kinase A dependent facilitation of synaptic transmission.

scholarly journals Glucose increases synaptic transmission from vagal afferent central nerve terminals via modulation of 5-HT3 receptors

2008 ◽  
Vol 295 (5) ◽  
pp. G1050-G1057 ◽  
Author(s):  
Shuxia Wan ◽  
Kirsteen N. Browning
Keyword(s):  
Synaptic Transmission ◽  
Glucose Concentration ◽  
Glutamate Release ◽  
Afferent Nerve ◽  
Excitatory Synaptic Transmission ◽  
Nerve Terminals ◽  
Extracellular Glucose Concentration ◽  
Extracellular Glucose ◽  
Vagal Afferent ◽  
Rat Brainstem

Acute hyperglycemia has profound effects on vagally mediated gastrointestinal functions. We have reported recently that the release of glutamate from the central terminals of vagal afferent neurons is correlated directly with the extracellular glucose concentration. The present study was designed to test the hypothesis that 5-HT3 receptors present on vagal afferent nerve terminals are involved in this glucose-dependent modulation of glutamatergic synaptic transmission. Whole-cell patch-clamp recordings were made from neurons of the nucleus tractus solitarius (NTS) in thin rat brainstem slices. Spontaneous and evoked glutamate release was decreased in a concentration-dependent manner by the 5-HT3 receptor selective antagonist, ondansetron. Alterations in the extracellular glucose concentration induced parallel shifts in the ondansetron-mediated inhibition of glutamate release. The changes in excitatory synaptic transmission induced by extracellular glucose concentration were mimicked by the serotonin uptake inhibitor, fenfluramine. These data suggest that glucose alters excitatory synaptic transmission within the rat brainstem via actions on tonically active 5-HT3 receptors, and the number of 5-HT3 receptors on vagal afferent nerve terminals is positively correlated with the extracellular glucose concentration. These data indicate that the 5-HT3 receptors present on synaptic connections between vagal afferent nerve terminals and NTS neurons are a strong candidate for consideration as one of the sites where glucose acts to modulate vagovagal reflexes.

scholarly journals Cholinesterases in Tripartite Neuromuscular Synapse

2021 ◽  
Vol 14 ◽  
Author(s):  
Konstantin A. Petrov ◽  
Svetlana E. Proskurina ◽  
Eric Krejci
Keyword(s):  
Synaptic Transmission ◽  
Motor Neuron ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Neuromuscular Synapse ◽  
Genetic Studies ◽  
Pathological Conditions ◽  
Α7 Nicotinic Acetylcholine Receptors ◽  
Terminal Schwann Cells

The neuromuscular junction (NMJ) is a tripartite synapse in which not only presynaptic and post-synaptic cells participate in synaptic transmission, but also terminal Schwann cells (TSC). Acetylcholine (ACh) is the neurotransmitter that mediates the signal between the motor neuron and the muscle but also between the motor neuron and TSC. ACh action is terminated by acetylcholinesterase (AChE), anchored by collagen Q (ColQ) in the basal lamina of NMJs. AChE is also anchored by a proline-rich membrane anchor (PRiMA) to the surface of the nerve terminal. Butyrylcholinesterase (BChE), a second cholinesterase, is abundant on TSC and anchored by PRiMA to its plasma membrane. Genetic studies in mice have revealed different regulations of synaptic transmission that depend on ACh spillover. One of the strongest is a depression of ACh release that depends on the activation of α7 nicotinic acetylcholine receptors (nAChR). Partial AChE deficiency has been described in many pathologies or during treatment with cholinesterase inhibitors. In addition to changing the activation of muscle nAChR, AChE deficiency results in an ACh spillover that changes TSC signaling. In this mini-review, we will first briefly outline the organization of the NMJ. This will be followed by a look at the role of TSC in synaptic transmission. Finally, we will review the pathological conditions where there is evidence of decreased AChE activity.

scholarly journals Depolarization-dependent Induction of Site-specific Changes in Sialylation on N-linked Glycoproteins in Rat Nerve Terminals

2020 ◽  
Vol 19 (9) ◽  
pp. 1418-1435
Author(s):  
Inga Boll ◽  
Pia Jensen ◽  
Veit Schwämmle ◽  
Martin R. Larsen
Keyword(s):  
Synaptic Transmission ◽  
Neurotransmitter Release ◽  
Synaptic Proteins ◽  
Nerve Terminals ◽  
Membrane Glycoproteins ◽  
Site Specific ◽  
Specific Alteration ◽  
And Function ◽  
Rat Nerve ◽  
Stimulation Of

Synaptic transmission leading to release of neurotransmitters in the nervous system is a fast and highly dynamic process. Previously, protein interaction and phosphorylation have been thought to be the main regulators of synaptic transmission. Here we show that sialylation of N-linked glycosylation is a novel potential modulator of neurotransmitter release mechanisms by investigating depolarization-dependent changes of formerly sialylated N-linked glycopeptides. We suggest that negatively charged sialic acids can be modulated, similarly to phosphorylation, by the action of sialyltransferases and sialidases thereby changing local structure and function of membrane glycoproteins. We characterized site-specific alteration in sialylation on N-linked glycoproteins in isolated rat nerve terminals after brief depolarization using quantitative sialiomics. We identified 1965 formerly sialylated N-linked glycosites in synaptic proteins and found that the abundances of 430 glycosites changed after 5 s depolarization. We observed changes on essential synaptic proteins such as synaptic vesicle proteins, ion channels and transporters, neurotransmitter receptors and cell adhesion molecules. This study is to our knowledge the first to describe ultra-fast site-specific modulation of the sialiome after brief stimulation of a biological system.

SYMPOSIUM: BEHAVIOR MODIFICATION BY DRUGS

PEDIATRICS ◽  
1972 ◽  
Vol 49 (5) ◽  
pp. 694-701
Author(s):  
Ross J. Baldessarini
Keyword(s):  
Basal Ganglia ◽  
Synaptic Transmission ◽  
Tissue Distribution ◽  
Behavior Modification ◽  
Nerve Terminals ◽  
Median Forebrain Bundle ◽  
Stereotyped Behaviors ◽  
Synaptic Receptors ◽  
Oxidative Processes ◽  
Stimulation Of

The pharmacology of the amphetamines has been studied for several decades. There is now a great deal of information about their tissue distribution and catabolism, largely by enzymatic oxidative processes. The most clearly characterized actions of the amphetamines occur at catecholamineconaining nerve terminals and tend to enhance the availability of the transmitter to post-synaptic receptors. The actions of the drugs in the CNS include stimulation of the ascending reticular formation of the brainstem, and probably enhancement of the activity of a behavior reinforcement system mediated by the median forebrain bundle. Toxic effects of amphetamine include apparent interactions at the basal ganglia to produce stereotyped behaviors in animals and man. All of these actions might involve catecholaminergic synaptic transmission systems. Under careful, controlled medical supervision the amphetamines are remarkably safe, although in excessive doses they can produce severe toxic, sympathomimetic and psychotic effects and can be lethal. They are subject to gross abuses, and to habituation. Tolerance develops to some of their actions, but usually not to their legitimate and rational uses in narcolepsy and hyperkinesis. Withdrawal symptoms are relatively minor.

scholarly journals Norepinephrine as a possible transmitter involved in synaptic transmission in frog taste organs and Ca dependence of its release.

1985 ◽  
Vol 85 (3) ◽  
pp. 431-442 ◽  
Author(s):  
S Nagahama ◽  
K Kurihara
Keyword(s):  
Synaptic Transmission ◽  
Great Reduction ◽  
Sensory Nerve ◽  
Lingual Artery ◽  
Nerve Terminals ◽  
Taste Cells ◽  
Artificial Solution

In order to explore the role of catecholamine and Ca2+ in the synaptic transmission from taste cells to sensory nerve terminals, the effects of various agents added to an artificial solution perfusing the lingual artery on the frog taste nerve responses were examined. The injection of reserpine or guanetidine, which are catecholamine-depleting agents, led to a great reduction of the frog taste nerve responses. The addition of catecholamines to the perfusing solution did not practically enhance the spontaneous impulse discharges, but did recover the response to all the taste stimuli examined. Norepinephrine was most effective and is the most likely candidate for the transmitter. The enhancement of the responses by norepinephrine was suppressed by desipramine, cocaine, or imipramine, which suggests that the enhancement was brought about by incorporation of norepinephrine into taste cells. In a previous paper (Nagahama, S., Y. Kobatake, and K. Kurihara, 1982. J. Gen. Physiol. 80:785), we showed that the responses to the stimuli of one group depended on Ca2+, cGMP, and cAMP added to the perfusing solution and those to the stimuli of another group did not depend on these agents. After the injection or addition of reserpine to the lingual artery, which probably modified injection or addition of reserpine to the lingual artery, which probably modified the permeability of the artery, the responses to the stimuli of the latter group also came to exhibit dependences on these agents, which indicates that the responses to all the taste stimuli have dependences on Ca2+, cGMP, and cAMP.

Altered synaptic transmission at olfactory and vomeronasal nerve terminals in mice lacking N-type calcium channel Cav2.2

2014 ◽  
Vol 40 (10) ◽  
pp. 3422-3435 ◽  
Author(s):  
Jan Weiss ◽  
Martina Pyrski ◽  
Petra Weissgerber ◽  
Frank Zufall
Keyword(s):  
Synaptic Transmission ◽  
Calcium Channel ◽  
Nerve Terminals
Sign in / Sign up

Export Citation Format

Share Document