The role of a reactive disulphide bond in the function of the acetylcholine receptor at the frog neuromuscular junction

Ben-Haim, D.; Landau, Emmanuel M.; Silman, Israel

doi:10.1113/jphysiol.1973.sp010347

Cited by 70 publications

(33 citation statements)

References 39 publications

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“…Sigmoid movement depends on acetylcholine (ACh) neurotransmission as well but in our experiments appears unaffected by heat shock treatment. These results concurred with reports that ROS actions do not deactivate nicotinic acetylcholine receptors (nAChR) at the neuromuscular junction (Ben-Haim et al 1973;Giniatullin et al 2005) On the contrary, ROS and heat shock inhibit or deactivate enzyme acetylcholinesterase (Eichler and Silman 1995), keeping the ACh action longer in the synaptic cleft.…”

Section: Discussionsupporting

confidence: 91%

Inactivation of GABAA receptor is related to heat shock stress response in organism model Caenorhabditis elegans

Camargo

Elizalde

Trujillo

et al. 2016

Cell Stress and Chaperones

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The mechanisms underlying oxidative stress (OS) resistance are not completely clear. Caenorhabditis elegans (C. elegans) is a good organism model to study OS because it displays stress responses similar to those in mammals. Among these mechanisms, the insulin/IGF-1 signaling (IIS) pathway is thought to affect GABAergic neurotransmission. The aim of this study was to determine the influence of heat shock stress (HS) on GABAergic activity in C. elegans. For this purpose, we tested the effect of exposure to picrotoxin (PTX), gammaaminobutyric acid (GABA), hydrogen peroxide, and HS on the occurrence of a shrinking response (SR) after nose touch stimulus in N2 (WT) worms. Moreover, the effect of HS on the expression of UNC-49 (GABA A receptor ortholog) in the EG1653 strain and the effect of GABA and PTX exposure on HSP-16.2 expression in the TJ375 strain were analyzed. PTX 1 mM-or H 2 O 2 0.7 mM-exposed worms displayed a SR in about 80 % of trials. GABA exposure did not cause a SR. HS prompted the occurrence of a SR as did PTX 1 mM or H 2 O 2 0.7 mM exposure. In addition, HS increased UNC-49 expression, and PTX augmented HSP-16.2 expression. Thus, the results of the present study suggest that oxidative stress, through either H 2 O 2 exposure or application of heat shock, inactivates the GABAergic system, which subsequently would affect the oxidative stress response, perhaps by enhancing the activity of transcription factors DAF-16 and HSF-1, both regulated by the IIS pathway and related to hsp-16.2 expression.

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Section: Discussionsupporting

confidence: 91%

Inactivation of GABAA receptor is related to heat shock stress response in organism model Caenorhabditis elegans

Camargo

Elizalde

Trujillo

et al. 2016

Cell Stress and Chaperones

View full text Add to dashboard Cite

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“…If there are prejunctional cholinoceptors, DTT could reduce the action of ACh at this site and consequently diminish ADF directly by reducing the affinity of ACh for these receptors, if they are of the same type as those on the postjunctional membrane (Ben-Haim, Landau & Silman, 1973;Terrar, 1978) or like those in ganglia (Brown & Kwiatkowski, 1976;Bleehen, Clark & Hobbiger, 1983;see Webb & Bowman, 1974). Alternatively, DTT might reduce the prejunctional effect of ACh indirectly by an action on postjunctional cholinoceptors.…”

Section: Discussionmentioning

confidence: 99%

“…In the presence of an anticholinesterase, the diffusion of ACh from the synaptic cleft is delayed by its binding to postjunctional cholinoceptors (Katz & Miledi, 1973;Magleby & Terrar, 1975). Following exposure to DTT the affinity of ACh for these receptors is reduced (Ben-Haim, 1973;Terrar, 1978) and thus ACh would be expected to leave the synaptic cleft more rapidly (Terrar, 1976).…”

Section: Discussionmentioning

confidence: 99%

The relationship between stimulus‐induced antidromic firing and twitch potentiation produced by paraoxon in rat phrenic nerve‐diaphragm preparations

Clark

Hobbiger

Terrar

1983

British J Pharmacology

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1 The relationship between stimulus-induced repetitive antidromic firing (ADF) in the motor nerve and twitch potentiation produced by the organophosphate anticholinesterase paraoxon, has been investigated in rat diaphragm preparations. 2 Little or no ADF was produced by paraoxon in preparations bathed in a Tyrode solution containing 1 mM calcium and 1 mM magnesium ions although the preparations showed marked twitch potentiation. 3 Increases in the calcium: magnesium ion ratio produced a ratio-dependent increase in the ADF but had no consistent effect on peak twitch potentiation. 4 Dithiothreitol, a disulphide bond reducing agent which decreases the affinity of acetylcholine for nicotinic cholinoceptors, abolished ADF but only modified the time course of twitch potentiation. 5 It is concluded that the initiation of ADF is a consequence of the prolonged action of acetylcholine within the synaptic cleft following inhibition of acetylcholinesterase, and that ADF is not the only mechanism by which twitch potentiation can be produced.

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“…The presence of a disulfide bond has been confirmed with other ACh-receptor preparations : rat denervated muscle (ALBUQUERQUE et al, 1968), frog rectus (MITTAG and TORMAY, 1970), chick biventer cervix (RANG and BITTER, 1971), frog sartorius (DEL CASTILLO et al, 1971;BEN-HAIM et a!., 1973), and leech muscle (Ross and TRIGGLE,1972). However, it should be noted that the ACh-receptors studied so far were all excitatory, and curare-sensitive type.…”

mentioning

confidence: 78%

Effects of various enzymes and chemical modification reagents on the Na+- and Cl--dependent responses of the ganglion cells to acetylcholine.

et al. 1983

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Using the abdominal ganglion cells of Aplysia, we analyzed the effects of various enzymes and chemical modification reagents on the acetylcholine (ACh)-induced responses of the excitatory (Natdependent) and inhibitory (Cl--dependent) types. (1) Phospholipase A (2 mg/ml) caused no appreciable effects on either type of response.(2) Phospholipase C (2 mg/ml) markedly depressed both types of response. These suggested that the phosphoryl group of the phospholipid is an important site related to the binding of ACh, common to both types of ACh-receptors. (3) Carboxypeptidase A (10 mg/ml) caused no observable effects on either type of response. (4) Carboxypeptidase B (10 mg/ml) depressed the inhibitory type of response without affecting the excitatory one. (5) Pyridoxal-5'-phosphate (1 mM) also depressed the inhibitory response without affecting the excitatory one. These findings (4, 5) suggested that the Cl--channel in the inhibitory AChreceptor complex includes a C-terminal lysine which may play an active role in the movement of Cl-across the receptor membrane. (6) LLeucine aminopeptidase (1 mg/ml) depressed the excitatory response without altering the inhibitory one. (7) p-Nitrothiophenol (1 mM) also depressed the excitatory response without affecting the inhibitory one. These findings (6, 7) suggested the presence of a certain N-terminal amino acid near a glutamate or aspartate residue within a molecular moiety of Na+-channel included in the excitatory ACh-receptor complex.

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The role of a reactive disulphide bond in the function of the acetylcholine receptor at the frog neuromuscular junction

Cited by 70 publications

References 39 publications

Inactivation of GABAA receptor is related to heat shock stress response in organism model Caenorhabditis elegans

Inactivation of GABAA receptor is related to heat shock stress response in organism model Caenorhabditis elegans

The relationship between stimulus‐induced antidromic firing and twitch potentiation produced by paraoxon in rat phrenic nerve‐diaphragm preparations

Effects of various enzymes and chemical modification reagents on the Na+- and Cl--dependent responses of the ganglion cells to acetylcholine.

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