Types of Voltage-Gated Calcium Channels: Molecular and Electrophysiological Views

2014 ◽  
Vol 9 (3) ◽  
pp. 170-181 ◽  
Author(s):  
Taiji Furukawa
Keyword(s):  
Calcium Channels ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels

scholarly journals Presynaptic Paraneoplastic Disorders of the Neuromuscular Junction: An Update

2021 ◽  
Vol 11 (8) ◽  
pp. 1035
Author(s):  
Maria Pia Giannoccaro ◽  
Patrizia Avoni ◽  
Rocco Liguori
Keyword(s):  
Potassium Channels ◽  
Neuromuscular Junction ◽  
Calcium Channels ◽  
Myasthenia Gravis ◽  
Neuromuscular Transmission ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels ◽  
Immune Mediated ◽  
Recent Developments ◽  
Myasthenic Syndrome

The neuromuscular junction (NMJ) is the target of a variety of immune-mediated disorders, usually classified as presynaptic and postsynaptic, according to the site of the antigenic target and consequently of the neuromuscular transmission alteration. Although less common than the classical autoimmune postsynaptic myasthenia gravis, presynaptic disorders are important to recognize due to the frequent association with cancer. Lambert Eaton myasthenic syndrome is due to a presynaptic failure to release acetylcholine, caused by antibodies to the presynaptic voltage-gated calcium channels. Acquired neuromyotonia is a condition characterized by nerve hyperexcitability often due to the presence of antibodies against proteins associated with voltage-gated potassium channels. This review will focus on the recent developments in the autoimmune presynaptic disorders of the NMJ.

scholarly journals Voltage-gated calcium channel blockers for psychiatric disorders: genomic reappraisal

2019 ◽  
Vol 216 (5) ◽  
pp. 250-253 ◽  
Author(s):  
Paul J. Harrison ◽  
Elizabeth M. Tunbridge ◽  
Annette C. Dolphin ◽  
Jeremy Hall
Keyword(s):  
Calcium Channels ◽  
Calcium Channel ◽  
Psychiatric Disorders ◽  
Calcium Channel Blockers ◽  
Channel Blockers ◽  
Risk Genes ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels ◽  
Voltage Gated Calcium Channel ◽  
Second Use

SummaryWe reappraise the psychiatric potential of calcium channel blockers (CCBs). First, voltage-gated calcium channels are risk genes for several disorders. Second, use of CCBs is associated with altered psychiatric risks and outcomes. Third, research shows there is an opportunity for brain-selective CCBs, which are better suited to psychiatric indications.

Appearance of voltage-gated calcium channels following overexpression of ATPase II cDNA in neuronal HN2 cells

2003 ◽  
Vol 117 (2) ◽  
pp. 109-115 ◽  
Author(s):  
Gary Chin ◽  
Yasir El-Sherif ◽  
Farah Jayman ◽  
Rima Estephan ◽  
Andrzej Wieraszko ◽  
...  
Keyword(s):  
Calcium Channels ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels ◽  
Atpase Ii

scholarly journals Hyperoxic Vasoconstriction of Human Pulmonary Arteries: A Novel Insight into Acute Ventricular Septal Defects

2013 ◽  
Vol 2013 ◽  
pp. 1-4 ◽  
Author(s):  
Priyadharshanan Ariyaratnam ◽  
Mahmoud Loubani ◽  
Robert Bennett ◽  
Steven Griffin ◽  
Mubarak A. Chaudhry ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Calcium Channels ◽  
Pulmonary Arteries ◽  
Bronchial Carcinoma ◽  
Isometric Tension ◽  
Ventricular Septal Defects ◽  
High Oxygen Content ◽  
Voltage Gated ◽  
Septal Defects ◽  
Voltage Gated Calcium Channels

Objectives. Acute rises in pulmonary artery pressures following postinfarction ventricular septal defects present a challenge. We hypothesised that the abnormally high oxygen content exposure to the pulmonary arteries may be a factor. We investigated the contractile responses of human pulmonary arteries to changes in oxygen tension. Methods. Isometric tension was measured in large and medium sized pulmonary artery rings obtained from lung resections for patients with bronchial carcinoma (n=30). Fresh rings were mounted in organ baths bubbled under basal conditions with hyperoxic or normoxic gas mixes and the gas tensions varied during the experiment. We studied whether voltage-gated calcium channels and nitric oxide signalling had any role in responses to oxygen changes. Results. Hypoxia caused a net mean relaxation of 18.1% ± 15.5 (P<0.005) from hyperoxia. Subsequent hyperoxia caused a contraction of 19.2% ± 13.5 (P<0.005). Arteries maintained in normoxia responded to hyperoxia with a mean constriction of 14.8% ± 3.9 (P<0.005). Nifedipine inhibited the vasoconstrictive response (P<0.05) whilst L-NAME had no effect on any hypoxic vasodilatory response. Conclusions. We demonstrate that hyperoxia leads to vasoconstriction in human pulmonary arteries. The mechanism appears to be dependent on voltage-gated calcium channels. Hyperoxic vasoconstriction may contribute to acute rises in pulmonary artery pressures.

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