Antidepressant-like effect of lamotrigine is reversed by veratrine: A possible role of sodium channels in bipolar depression

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.

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Mining the Virgin Land of Neurotoxicology: A Novel Paradigm of Neurotoxic Peptides Action on Glycosylated Voltage-Gated Sodium Channels

Journal of Toxicology ◽

10.1155/2012/843787 ◽

2012 ◽

Vol 2012 ◽

pp. 1-6 ◽

Cited By ~ 3

Author(s):

Zhirui Liu ◽

Jie Tao ◽

Pin Ye ◽

Yonghua Ji

Keyword(s):

Sodium Channels ◽

Network Activity ◽

Voltage Gated ◽

Virgin Land ◽

Neuronal Network Activity ◽

Voltage Gated Sodium Channels ◽

Pharmacological Targets ◽

Underlying Mechanisms ◽

Posttranslation Modification

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.

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The Role of Nonprotein Domains in the Function and Synthesis of Voltage-Gated Sodium Channels

Ion Channels ◽

10.1007/978-1-4615-7305-0_2 ◽

1990 ◽

pp. 33-64 ◽

Cited By ~ 5

Author(s):

S. R. Levinson ◽

W. B. Thornhill ◽

D. S. Duch ◽

E. Recio-Pinto ◽

B. W. Urban

Keyword(s):

Sodium Channels ◽

Voltage Gated ◽

Voltage Gated Sodium Channels

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On the role of Nav1.7 sodium channels in chronic pain: an experimental and computational study

10.1101/871236 ◽

2019 ◽

Author(s):

Alberto Capurro ◽

Jack Thornton ◽

Bruno Cessac ◽

Lyle Armstrong ◽

Evelyne Sernagor

Keyword(s):

Chronic Pain ◽

Sodium Channels ◽

Computational Study

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.

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