The Role of Slow Sodium Channels in GABAergic and NOergic Modulation of Nociceptive Neuron Excitability

2021 ◽  
Vol 51 (6) ◽  
pp. 831-836
Author(s):  
V. B. Plakhova ◽  
V. A. Penniyaynen ◽  
S. G. Terekhin ◽  
S. A. Podzorova ◽  
A. D. Kalinina ◽  
...  
1992 ◽  
Vol 70 (5) ◽  
pp. 695-700 ◽  
Author(s):  
Martín Ansaldo ◽  
María Cristina Damasco ◽  
María Silvina de Lavallaz ◽  
Carlos Pedro Lantos ◽  
Gerhard Malnic

The role of amiloride-dependent sodium channels in the action of adrenal cortical steroids on urine–blood [Formula: see text] (U–B [Formula: see text]) differences was studied in bicarbonate-infused and amiloride-treated adrenalectomized rats. U–B [Formula: see text] was significantly reduced by amiloride in bicarbonate-infused control rats. Adrenalectomy further reduced U–B [Formula: see text] in amiloride-treated, bicarbonate-infused rats (from 27.9 ± 1.82 mmHg in sham-operated rats to 21.3 ± 1.58 mmHg in adrenalectomized (ADX) rats) (1 mmHg = 133.322 Pa). Acute administration of corticosterone and 18-hydroxycorticosterone (18-OH-B), but not of aldosterone, caused recovery of U–B [Formula: see text] to the level of sham-operated animals treated with amiloride. Aldosterone did not affect U–B [Formula: see text] in the presence of amiloride (21.9 mmHg ADX group vs. 20.98 mmHg aldosterone group). Results are compatible with aldosterone affecting distal H ion secretion mostly by a sodium and potential difference dependent mechanism, while corticosterone and 18-OH-B should act by other mechanisms (e.g., increased luminal buffer level).Key words: distal H ion secretion, corticosteroids, amiloride, adrenalectomy, aldosterone, corticosterone, 18-hydroxycorticosterone.


2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Zhirui Liu ◽  
Jie Tao ◽  
Pin Ye ◽  
Yonghua Ji

Voltage-gated sodium channels (VGSCs) are important membrane protein carrying on the molecular basis for action potentials (AP) in neuronal firings. Even though the structure-function studies were the most pursued spots, the posttranslation modification processes, such as glycosylation, phosphorylation, and alternative splicing associating with channel functions captured less eyesights. The accumulative research suggested an interaction between the sialic acids chains and ion-permeable pores, giving rise to subtle but significant impacts on channel gating. Sodium channel-specific neurotoxic toxins, a family of long-chain polypeptides originated from venomous animals, are found to potentially share the binding sites adjacent to glycosylated region on VGSCs. Thus, an interaction between toxin and glycosylated VGSC might hopefully join the campaign to approach the role of glycosylation in modulating VGSCs-involved neuronal network activity. This paper will cover the state-of-the-art advances of researches on glycosylation-mediated VGSCs function and the possible underlying mechanisms of interactions between toxin and glycosylated VGSCs, which may therefore, fulfill the knowledge in identifying the pharmacological targets and therapeutic values of VGSCs.


Ion Channels ◽  
1990 ◽  
pp. 33-64 ◽  
Author(s):  
S. R. Levinson ◽  
W. B. Thornhill ◽  
D. S. Duch ◽  
E. Recio-Pinto ◽  
B. W. Urban

2014 ◽  
Author(s):  
Erin C. McKiernan

Motor activity, like that producing locomotion, is generated by networks of neurons. At the last output level of these networks are the motor neurons, which send signals to the muscles, causing them to contract. Current research in motor control is focused on finding out how motor neurons contribute to shaping the timing of motor behaviors. Are motor neurons just passive relayers of the signals they receive? Or, do motor neurons shape the signals before passing them on to the muscles, thereby influencing the timing of the behavior? It is now well accepted that motor neurons have active, intrinsic membrane properties - there are ion channels in the cell membrane that allow motor neurons to respond to input in non-linear and diverse ways. However, few direct tests of the role of motor neuron intrinsic properties in shaping motor behavior have been carried out, and many questions remain about the role of specific ion channel genes in motor neuron function. In this study, two potassium channel transgenes were expressed in Drosophila larvae, causing motor neurons to fire at lower levels of current stimulation and at higher frequencies, thereby increasing excitability. Mosaic animals were created in which some identified motor neurons expressed the transgenes while others did not. Motor output underlying crawling was compared in muscles innervated by control and experimental neurons in the same animals. Counterintuitively, no effect of the transgenic manipulation on motor output was seen. Future experiments are outlined to determine how the larval nervous system produces normal motor output in the face of altered motor neuron excitability.


2019 ◽  
Author(s):  
Alberto Capurro ◽  
Jack Thornton ◽  
Bruno Cessac ◽  
Lyle Armstrong ◽  
Evelyne Sernagor

This manuscript has been withdrawn by the authors as they no longer stand by part of their conclusions and wish not to be cited for this work. If you have any questions, please contact the corresponding authors.


2019 ◽  
Vol 9 ◽  
Author(s):  
Weijia Mao ◽  
Jie Zhang ◽  
Heinrich Körner ◽  
Yong Jiang ◽  
Songcheng Ying

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