scholarly journals The voltage-gated calcium channel blocker lomerizine is neuroprotective in motor neurons expressing mutant SOD1, but not TDP-43

2014 ◽  
Vol 130 (3) ◽  
pp. 455-466 ◽  
Author(s):  
Luan T. Tran ◽  
Benoit J. Gentil ◽  
Kathleen E. Sullivan ◽  
Heather D. Durham
Keyword(s):  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Motor Neurons ◽  
Channel Blocker ◽  
Mutant Sod1 ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channel

scholarly journals Touch responsiveness in zebrafish requires voltage-gated calcium channel 2.1b

2012 ◽  
Vol 108 (1) ◽  
pp. 148-159 ◽  
Author(s):  
Sean E. Low ◽  
Ian G. Woods ◽  
Mathieu Lachance ◽  
Joel Ryan ◽  
Alexander F. Schier ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Motor Neurons ◽  
Motor Pattern ◽  
Pattern Generation ◽  
Gene Encoding ◽  
Physiological Basis ◽  
Voltage Gated ◽  
Normal Current ◽  
Voltage Gated Calcium Channel ◽  
Morpholino Oligonucleotides

The molecular and physiological basis of the touch-unresponsive zebrafish mutant fakir has remained elusive. Here we report that the fakir phenotype is caused by a missense mutation in the gene encoding voltage-gated calcium channel 2.1b ( CACNA1Ab). Injection of RNA encoding wild-type CaV2.1 restores touch responsiveness in fakir mutants, whereas knockdown of CACNA1Ab via morpholino oligonucleotides recapitulates the fakir mutant phenotype. Fakir mutants display normal current-evoked synaptic communication at the neuromuscular junction but have attenuated touch-evoked activation of motor neurons. NMDA-evoked fictive swimming is not affected by the loss of CaV2.1b, suggesting that this channel is not required for motor pattern generation. These results, coupled with the expression of CACNA1Ab by sensory neurons, suggest that CaV2.1b channel activity is necessary for touch-evoked activation of the locomotor network in zebrafish.

scholarly journals Ion-channel blocker sensitivity of voltage-gated calcium-channel homologue Cch1 in Saccharomyces cerevisiae

Microbiology ◽  
2008 ◽  
Vol 154 (12) ◽  
pp. 3775-3781 ◽  
Author(s):  
Jinfeng Teng ◽  
Rika Goto ◽  
Kazuko Iida ◽  
Itaru Kojima ◽  
Hidetoshi Iida
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Ion Channel ◽  
Calcium Channel ◽  
Channel Blocker ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channel

scholarly journals Synthesis and vasodilator activity of 3,4-dihydropyrimidin-2(1H)-ones bearing urea, thiourea, and sulfonylurea moieties

2019 ◽  
Vol 97 (1) ◽  
pp. 20-28 ◽  
Author(s):  
Tahir Habila ◽  
Mebrouk Belghobsi ◽  
Mohamed-Zakaria Stiti ◽  
Eric Goffin ◽  
Pascal de Tullio ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Channel Blocker ◽  
Vasodilator Agents ◽  
Biological Models ◽  
Urea Derivatives ◽  
Thiourea Derivatives ◽  
Voltage Gated ◽  
Vasodilator Activity ◽  
Potent Vasodilator

A series of novel 3,4-dihydropyrimidin-2(1H)-ones bearing urea, thiourea, and sulfonylurea moieties were synthesized and pharmacologically evaluated as vasodilator agents. The most interesting vasodilators were the thiourea derivatives 6a and 6b and the urea derivatives 6f–6i and 7f–7h, although the ureas were relatively more active than thioureas. Twenty-fold more active than diazoxide, the urea 6g was the most potent vasodilator (EC50 = 0.983 ± 0.061 μmol/L) and proved to act as a voltage-gated calcium channel blocker. The lack of activity of sulfonylureas, 6k and 7j, could be attributed to their partial ionization at the physiological pH because of their acidic character. It should be interesting to investigate a larger number of compounds, including N-methylated sulfonylureas, to increase the vasodilator activity and to explore other biological models.

scholarly journals Weaver granule neurons are rescued by calcium channel antagonists and antibodies against a neurite outgrowth domain of the B2 chain of laminin.

1996 ◽  
Vol 134 (2) ◽  
pp. 477-486 ◽  
Author(s):  
P Liesi ◽  
J M Wright
Keyword(s):  
Calcium Channel ◽  
Neurite Outgrowth ◽  
Calcium Channel Blocker ◽  
Neuronal Migration ◽  
Channel Blocker ◽  
Postnatal Life ◽  
Granule Neurons ◽  
Mk 801 ◽  
Voltage Gated ◽  
High Concentrations

The weaver mutation impairs migration of the cerebellar granular neurons and induces neuronal death during the first two weeks of postnatal life. To elucidate the molecular mechanisms for the impaired neuronal migration, we investigated the rescue mechanisms of the weaver (wv/wv) granule neurons in vitro. We found that Fab2 fragments of antibodies against a neurite outgrowth domain of the B2 chain of laminin enhanced neurite outgrowth and neuronal migration of the weaver granule neurons on a laminin substratum and in the established cable culture system. The rescue of the weaver granule neurons by antibodies against the B2 chain of laminin may result from the neutralizing effect of these antibodies against the elevated B2 chain levels of the weaver brain. The L-type calcium channel blocker, verapamil (1-5 microM), also rescued the weaver granule neurons. High concentrations of MK-801 (10-20 microM), a glutamate receptor antagonist and voltage-gated calcium channel blocker, rescued the weaver granule neurons similar to verapamil, but low concentrations of MK-801 (1 microM) had no rescue effect. Simultaneous patch-clamp studies indicated that the weaver granule neurons did not express functional N-methyl-D-aspartate receptors further indicating that the rescue of the weaver granule neurons by MK-801 resulted from its known inhibition of voltage-gated calcium channels. The present results indicate that antibodies against the B2 chain of laminin, verapamil, and high concentrations of MK-801 protect the weaver granule neurons from the otherwise destructive action of the weaver gene. Thus, both the laminin system and calcium channel function contribute to the migration deficiency of the weaver granule neurons.

Chronic treatment by the calcium channel blocker ± PN 200-110 in the rat counteracts the stimulations of pituitary weight, prolactin release and pituitary C-kinase activity induced by a chronic estradiol treatment, in vivo

1990 ◽  
Vol 122 (3) ◽  
pp. 403-408
Author(s):  
Ph. Touraine ◽  
P. Birman ◽  
F. Bai-Grenier ◽  
C. Dubray ◽  
F. Peillon ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Channel Blocker ◽  
Plasma Prolactin ◽  
Estradiol Treatment ◽  
Kinase C ◽  
Protein Kinase C Activity

Abstract In order to investigate whether a calcium channel blocker could modulate the protein kinase C activity in normal and estradiol pretreated rat pituitary, female Wistar rats were treated or not (controls) with ± PN 200-110 (3 mg · kg−1 · day−1, sc) for 8 days or with estradiol cervical implants for 8 or 15 days, alone or in combination with PN 200-110 the last 8 days. Estradiol treatment induced a significant increase in plasma prolactin levels and pituitary weight. PN 200-110 administered to normal rats did not modify these parameters, whereas it reduced the effects of the 15 days estradiol treatment on prolactin levels (53.1 ± 4.9 vs 95.0 ±9.1 μg/l, p<0.0001) and pituitary weight (19.9 ± 0.4 vs 23.0 ± 0.6 mg, p <0.001), to values statistically comparable to those measured after 8 days of estradiol treatment. PN 200-110 alone did not induce any change in protein kinase C activity as compared with controls. In contrast, PN 200-110 treatment significantly counteracted the large increase in soluble activity and the decrease in the particulate one induced by estradiol between day 8 and day 15. We conclude that PN 200-110 opposed the stimulatory effects of chronic in vivo estradiol treatment on plasma prolactin levels and pituitary weight and that this regulation was related to a concomitant modulation of the protein kinase C activity.

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