The expression of neuronal voltage-dependent calcium channels in human cerebellum

Volsen, Stephen G.; Day, Nicola C.; McCormack, Alison L.; Smith, William K.; Craig, Peter J.; Beattie, Ruth E.; Ince, Paul G.; Shaw, Pamela J.; Ellis, Steven B.; Gillespie, Alison; Harpold, Michael M.; Lodge, David

doi:10.1016/0169-328x(95)00234-j

Cited by 98 publications

(82 citation statements)

References 38 publications

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“…The regulation of N channels that we have observed in HEK293 cells closely resembles that frequently described in neurons (Hille, 1994). Little is known as yet, however, about the normal properties and functions of the Ca channels that are formed by expression of ␣ 1E , although the protein is widely expressed on the soma and dendrites of neurons throughout the brain (Williams et al, 1994;Volsen et al, 1995;Yokoyama et al, 1995). The experiments reported here suggest that direct G-protein regulation of Figure 2.…”

Section: Discussionsupporting

confidence: 78%

Selective G-Protein Regulation of Neuronal Calcium Channels

Tóth¹,

Shekter²,

Hui³

et al. 1996

J. Neurosci.

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We examined the properties and regulation of Ca channels resulting from the expression of human ␣ 1B and ␣ 1E subunits stably expressed in HEK293 cells. The ancillary subunits ␤ 1B and ␣ 2 /␦ were also stably expressed in these cell lines. Ca currents in ␣ 1B -expressing cells had the properties of N-type currents. Ca currents in cells expressing ␣ 1E exhibited a novel profile that was similar to the properties of the "R type" Ca current. Introduction of GTP-␥-S into ␣ 1B cells greatly enhanced the extent of prepulse facilitation of the Ca current, whereas it had only a very small effect in ␣ 1E -expressing cells. Activation of somatostatin receptors endogenous to HEK293 cells or opioid receptors, expressed in the cells after transfection, inhibited Ca currents in ␣ 1B -expressing cells. This inhibition was blocked by pertussis toxin and was partially relieved by a depolarizing prepulse. In contrast, no inhibitory effects were noted in cells expressing ␣ 1E channels under the same circumstances. HEK293 cells normally contained G-proteins from all of the four major families. Inhibition of Ca currents by agonists in ␣ 1B -expressing cells was enhanced slightly by the cotransfection of several G-protein ␣ subunits. agonists, however, had no effect in ␣ 1E -containing cells, even after overexpression of different G-protein ␣-subunits. In summary, these results demonstrate that there is a large difference in the susceptibility of ␣ 1B -and ␣ 1E -based Ca channels to regulation by G-proteins. This is so despite the fact that the two types of Ca channels show substantial similarities in their primary sequences.

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Section: Discussionsupporting

confidence: 78%

Selective G-Protein Regulation of Neuronal Calcium Channels

Tóth¹,

Shekter²,

Hui³

et al. 1996

J. Neurosci.

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“…No staining was observed in the glomerulus ( Figure 7G) or in the negative control incubated with preimmune serum ( Figure 7H). Identical patterns were observed with the anti-␣1E-com or the serum received from Dr. S.G. Volsen (Volsen et al 1995). Similar immunohistochemical results were obtained from rat kidney (not shown).…”

Section: Immunohistochemical Detection Of ␣1e In Kidneysupporting

confidence: 83%

“…Two sera were created by linking peptides to hemocyanin ) and one was independently created by fusing a peptide to gluthathion S-transferase (Volsen et al 1995). Identical results were obtained with all three ␣1E-directed sera.…”

Section: Detection Of ␣1e By Immunoblottingmentioning

confidence: 99%

“…In some experiments, the purified anti-␣ 1E serum against an ␣ 1E fusion protein (Volsen et al 1995) and a monoclonal antibody against ␣ 1E, a gift from Dr. R.E. Beattie and Dr. S.G. Volsen (E. Lilly; Windlesham, UK), were used as additional antibodies to compare the staining results with different primary antibodies.…”

Section: Preparation Of Paraffin-embedded Tissue and Immunostaining Omentioning

confidence: 99%

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Immunodetection of α1E Voltage-gated Ca²⁺ Channel in Chromogranin-positive Muscle Cells of Rat Heart, and in Distal Tubules of Human Kidney

Weiergräber

Pereverzev

Vajna

et al. 2000

J Histochem Cytochem.

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S U M M A R YThe calcium channel ␣ 1E subunit was originally cloned from mammalian brain. A new splice variant was recently identified in rat islets of Langerhans and in human kidney by the polymerase chain reaction. The same isoform of ␣ 1E was detected in rat and guinea pig heart by amplifying indicative cDNA fragments and by immunostaining using peptide-specific antibodies. The apparent molecular size of cardiac ␣ 1E was determined by SDS-PAGE and immunoblotting (218 Ϯ 6 kD; n ϭ 3). Compared to ␣ 1E from stably transfected HEK-293 cells, this is smaller by 28 kD. The distribution of ␣ 1E in cardiac muscle cells of the conducting system and in the cardiomyoblast cell line H9c2 was compared to the distribution of chromogranin, a marker of neuroendocrine cells, and to the distribution of atrial natriuretic peptide (ANP). In serial sections from atrial and ventricular regions of rat heart, co-localization of ␣ 1E with ANP was detected in atrium and with chromogranin A/B in Purkinje fibers of the conducting system in both rat atrium and ventricle. The kidney is another organ in which natriuretic peptide hormones are secreted. The detection of ␣ 1E in the distal tubules of human kidney, where urodilatin is stored and secreted, led to the conclusion that the expression of ␣ 1E in rat heart and human kidney is linked to regions with endocrine functions and therefore is involved in the Ca 2 ϩ -dependent secretion of peptide hormones such as ANP and urodilatin.

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“…Calcium channels containing the 1A subunit (Ca V 2.1 or P/Q-type) are expressed throughout the human and mammalian brain with a higher concentration in the cerebellum and are localized in most presynaptic terminals (Catterall 1998, Wu et al 1999, Mintz et al 1995 as well as in the cell body and dendrites of many neurons (Volsen et al 1995, Westenbroek et al 1995. In many central synapses, Ca V 2.1 channels are preferentially located at the release sites and are more effectively coupled to neurotransmitter release than other Ca 2+ channel types (Li et al 2007, Matsushita et al 2002, Qian and Noebels 2001, 2000, Dunlap et al 1995, Mintz et al 1995, Wu et al 1999, Iwasaki et al 2000.…”

Section: Discussionmentioning

confidence: 99%

CaV2.1 voltage activated calcium channels and synaptic transmission in familial hemiplegic migraine pathogenesis

Uchitel

Inchauspe

Urbano

et al. 2012

Journal of Physiology-Paris

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The expression of neuronal voltage-dependent calcium channels in human cerebellum

Cited by 98 publications

References 38 publications

Selective G-Protein Regulation of Neuronal Calcium Channels

Selective G-Protein Regulation of Neuronal Calcium Channels

Immunodetection of α1E Voltage-gated Ca²⁺ Channel in Chromogranin-positive Muscle Cells of Rat Heart, and in Distal Tubules of Human Kidney

CaV2.1 voltage activated calcium channels and synaptic transmission in familial hemiplegic migraine pathogenesis

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The expression of neuronal voltage-dependent calcium channels in human cerebellum

Cited by 98 publications

References 38 publications

Selective G-Protein Regulation of Neuronal Calcium Channels

Selective G-Protein Regulation of Neuronal Calcium Channels

Immunodetection of α1E Voltage-gated Ca2+ Channel in Chromogranin-positive Muscle Cells of Rat Heart, and in Distal Tubules of Human Kidney

CaV2.1 voltage activated calcium channels and synaptic transmission in familial hemiplegic migraine pathogenesis

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Immunodetection of α1E Voltage-gated Ca²⁺ Channel in Chromogranin-positive Muscle Cells of Rat Heart, and in Distal Tubules of Human Kidney