Regulation of voltage-dependent Ca2+ channels of neuronal cells by chronic changes in membrane potential

DeLorme, E M; McGee, Richard

doi:10.1016/0006-8993(86)91385-5

Cited by 33 publications

(27 citation statements)

References 6 publications

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“…What signal might be produced by direct contact with the sympathetic nerve to produce increased expression of L-type calcium channels? Neurotransmitter(s) that induce differentiation (22,(25)(26)(27) or that might alter Gprotein expression (2,19,28) …”

Section: Discussionmentioning

confidence: 99%

Direct contact between sympathetic neurons and rat cardiac myocytes in vitro increases expression of functional calcium channels.

Ogawa¹,

Barnett²,

Sen³

et al. 1992

J. Clin. Invest.

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To test the hypothesis that direct contact between sympathetic neurons and myocytes regulates expression and function of cardiac Ca channels, we prepared cultures of neonatal rat ventricular myocytes with and without sympathetic ganglia. Contractile properties of myocytes were assessed by an optical-video system. Contractility-pCa curves showed a 60% greater increase in contractility for innervated myocytes compared with control cells at 63 mM [Cab (n = efficacy of Bay K 8644 was maintained for at least 24 h after denervation produced by removal of ganglia from the culture. Dihydropyridine binding sites were assessed with the L channel-specific radioligand 3[HJPN200-110. PN200-110 binding sites were increased by innervation (51±5 to 108±20 fmol/mg protein, P < 0.01), with no change in KD. Peak current-voltage curves were determined by whole-cell voltage clamp techniques for myocytes contacted by a neuron, control myocytes, and myocytes grown in conditioned medium. Current density of Ltype Ca channels was significantly higher in innervated myocytes (10.5±0.4 pA/pF, n = 5) than in control myocytes (5.9±03 pA/pF, n = 8, P < 0.01) or myocytes grown in conditioned medium (6.2±0.2 pA/pF, n = 10, P < 0.01). Thus, physical contact between a sympathetic neuron and previously uninnervated neonatal rat ventricular myocytes increases expression of functional L-type calcium channels as judged by contractile responses to Cao and Bay K 8644, as well as by electrophysiological and radioligand binding properties. (J.

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Section: Discussionmentioning

confidence: 99%

Direct contact between sympathetic neurons and rat cardiac myocytes in vitro increases expression of functional calcium channels.

Ogawa¹,

Barnett²,

Sen³

et al. 1992

J. Clin. Invest.

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“…ject to homologous and heterologous regulation by DHPs and f3-adrenergic ligands (1), may respond to membrane potential (2) or calcium itself (3), and might be altered in cardiomyopathies of animals (4) and man (5). Purification of the DHP receptor (DHPR) from transverse tubules of rabbit skeletal muscle (e.g., 6) and isolation ofthe corresponding cDNA (7,8) have made Ca2+ channel gene expression accessible to molecular analysis, at least in skeletal muscle.…”

Section: Introductionmentioning

confidence: 99%

Dihydropyridine receptor gene expression is regulated by inhibitors of myogenesis and is relatively insensitive to denervation.

Shih

Wathen²,

Marshall³

et al. 1990

J. Clin. Invest.

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To evaluate developmental and physiological signals that may influence expression of the dihydropyridine-sensitive "slow"Ca2" channel, we analyzed dihydropyridine receptor (DHPR) mRNA abundance in mouse skeletal muscle. Using synthetic oligonucleotide probes corresponding to the rabbit skeletal muscle DHPR, a 6.5 kb DHPR transcript was identified in postnatal skeletal muscle and differentiated C2 or BC3H1 myocytes, but not cardiac muscle or brain. DHPR gene expression was reversibly suppressed by 0.4 nM transforming growth factor j%-1 or by transfection with a mutant c-H-ras allele, nominal inhibitors of myogenesis that block the appearance of slow channels and DHPR. In contrast, both BC3HI and C2 myocytes containing the activated ras vector expressed the gene encoding the nicotinic acetylcholine receptor subunit, demonstrating that not all muscle-specific genes are extinguished by ras. Denervation stimulated DHPR gene expression less than 0.6-fold, despite 8-fold upregulation of 5-subunit mRNA and reciprocal effects on the skeletal and cardiac aactin genes. Thus, DHPR gene induction is prevented by inhibitors of other muscle-specific genes, whereas, at most, relatively small changes in DHPR mRNA abundance occur during adaptation to denervation. (J. Clin. Invest. 1990. 85:781-789.) calcium channels * differentiation * MyoDI -oncogenes * skeletal muscle transforming growth factor ,8-1

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“…That chronic ckpolarization down-regulates L-type voltage-gated Ca2 + channels in neuronal and neurosecretory cells is well established [ DeLorme arid McGee, 1986;DeLorme et al, 1988;Ferrante et al, 1991;Bcrdan et al, 19931. Treatment of PC12 cells or chick retinal neurons with elevated levels of K + for periods to 4 days reduced both the nomhers of 1,4-dihydropyridine sites arid clianiicl function.…”

Section: Calcium Channelsmentioning

confidence: 99%

Ion channels and diseases

Triggle¹

1994

Drug Development Research

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Regulation of voltage-dependent Ca2+ channels of neuronal cells by chronic changes in membrane potential

Cited by 33 publications

References 6 publications

Direct contact between sympathetic neurons and rat cardiac myocytes in vitro increases expression of functional calcium channels.

Direct contact between sympathetic neurons and rat cardiac myocytes in vitro increases expression of functional calcium channels.

Dihydropyridine receptor gene expression is regulated by inhibitors of myogenesis and is relatively insensitive to denervation.

Ion channels and diseases

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