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1 m entry through a pharmacologically distinct voltage-dependent calcium channel.
2 d immunostaining for any of nine subtypes of voltage-dependent calcium channel.
3 sensitive calcium release (RyR-dependent) or voltage dependent calcium channels.
4 e surface charge associated with the pore of voltage-dependent calcium channels.
5 tein kinase A and requires calcium entry via voltage-dependent calcium channels.
6 ed [Ca2+]i decrease required deactivation of voltage-dependent calcium channels.
7 and/or S1P2 receptors, partially via L-type voltage-dependent calcium channels.
8 these effects are dependent on activation of voltage-dependent calcium channels.
9 activation and calcium influx through T type voltage-dependent calcium channels.
10 ng pathways that result in the inhibition of voltage-dependent calcium channels.
11 tworks of intracellular effectors, including voltage-dependent calcium channels.
12 ter is completely abolished by inhibitors of voltage-dependent calcium channels.
13 s studies of the mechanisms of modulation of voltage-dependent calcium channels.
14 g extracellular calcium or by antagonists of voltage-dependent calcium channels.
15 nventional TTX-sensitive sodium channels and voltage-dependent calcium channels.
16 hippocalcin might play a role in regulating voltage-dependent calcium channels.
17 ar localization of the rat beta2a subunit of voltage-dependent calcium channels.
18 h the peptide omega-grammotoxin-SIA inhibits voltage-dependent calcium channels.
19 rpolarization-activated cation current Ih or voltage-dependent calcium channels.
20 omolar range, but not the activity of native voltage-dependent calcium channels.
21 t modulation by an auxiliary beta subunit of voltage-dependent calcium channels, a recombinant beta3
22 hloride channels, and there is evidence that voltage-dependent calcium channels, along with the recep
23 peptide antibody targeted at a region of the voltage-dependent calcium channel alpha 1D subunit C-ter
24 n, the metabotropic glutamate receptor 6 and voltage-dependent calcium channel alpha1.4, are not dete
25 curs indirectly through activation of L-type voltage-dependent calcium channels, an event that is als
26 azin, both as a modulatory gamma subunit for voltage-dependent calcium channels and as a regulator of
28 coded by the gene is a regulatory subunit of voltage-dependent calcium channels and is expressed in b
29 encodes the pore-forming protein of P/Q-type voltage-dependent calcium channels and is predominantly
30 aling cascade initiated by Ca(2+) influx via voltage-dependent calcium channels and the N-methyl-D-as
31 nctional assay useful to characterize L-type voltage-dependent calcium channels and their antagonists
32 cal synaptic events included NMDA receptors, voltage-dependent calcium channels, and Ca2+-induced Ca2
33 mediated in part by secondary activation of voltage-dependent calcium channels, and in part by ligan
34 hway that involves extracellular calcium and voltage-dependent calcium channels, and that this respon
35 cific cation, calcium-activated chloride and voltage-dependent calcium channels, angiotensin II also
36 nd were only slightly affected by the L-type voltage-dependent calcium channel antagonists, nifedipin
37 cium channels, this study determined whether voltage dependent calcium channels are also involved in
39 The CaV2.2 (N-type) and CaV2.1 (P/Q-type) voltage-dependent calcium channels are prevalent through
40 he emerging model is that calcium influx via voltage-dependent calcium channels at the calcium microd
41 h microprofiles, generated by the opening of voltage-dependent calcium channels at the presynaptic pl
43 -terminal tail of the skeletal muscle L-type voltage-dependent calcium channel binds Ca2+, Ca2+ calmo
44 the sodium channel blocker tetrodotoxin, the voltage-dependent calcium channel blocker omega-conotoxi
45 nase A inhibitor H-89 (20 micromol/L) or the voltage-dependent calcium channel blockers diltiazem and
47 ologic agents that specifically block L-type voltage-dependent calcium channels, but not P/Q-type cal
51 nase (PI3K) has been shown to enhance native voltage-dependent calcium channel (Ca(v)) currents both
60 upport previous evidence for a major role of voltage-dependent calcium channels in driving pacemaking
61 -delta subunit protein of widely distributed voltage-dependent calcium channels in the brain and spin
62 eviously unknown yet critical role of L-type voltage-dependent calcium channels in the expression and
63 cation (AMPA receptors) and cell regulation (voltage-dependent calcium channels) in a relatively rapi
66 Ca2+ sources, including distinct subtypes of voltage-dependent calcium channels, intracellular Ca2+ s
68 CAM(flx) sprouts were associated with L-type voltage-dependent calcium channel (L-VDCC) immunoreactiv
70 tretrieval bilateral blockade of long-acting voltage-dependent calcium channels (L-VDCCs), but not of
71 ated inhibitory peptide; or the blocker of L-voltage-dependent calcium channels (L-VDCCs), nifedipine
72 ion, which would limit calcium entry through voltage-dependent calcium channels leading to relaxation
73 DA-mediated long-term potentiation (LTP) and voltage-dependent calcium channel LTP in hippocampus.
74 rations of cadmium, a nonspecific blocker of voltage-dependent calcium channels mediating vesicle rel
75 lu5 antagonist MPEP but not by inhibitors of voltage dependent calcium channels or by the AMPA/KA rec
76 ent role in neurons as a regulator of either voltage-dependent calcium channels or AMPA receptors.
78 n contrast, CaMKIIbeta activation via L-type voltage-dependent calcium channels promotes GKAP recruit
81 onists of ionotropic glutamate receptors and voltage-dependent calcium channels, suggesting that the
82 or G protein-mediated modulation of neuronal voltage-dependent calcium channels that involves the des
83 rfold increase in the contribution of L-type voltage-dependent calcium channels to contraction that o
84 e examined the contribution of two intrinsic voltage-dependent calcium channels to the light-evoked r
86 ifs is inducible by influx of Ca(2+) through voltage-dependent calcium channels upon beta-adrenergic
87 ontrolled by different mechanisms, including voltage-dependent calcium channel (VDCC) activation and
88 el invokes the modulation of CaV2.3 (R-type) voltage-dependent calcium channel (VDCC) currents observ
90 ed to the gamma-1 subunit of skeletal muscle voltage-dependent calcium channel (VDCC), and a deficit
93 Calcium influx through NMDA receptors and voltage-dependent calcium channels (VDCC) mediates an ar
95 ndent on the activation of either the L-type voltage dependent calcium channel (vdccLTP) or the N-met
97 strongly depends on the distance between the voltage-dependent calcium channels (VDCCs) and the presy
100 arization that is sufficient to activate the voltage-dependent calcium channels (VDCCs) expressed in
104 th, is involved in the tonic upregulation of voltage-dependent calcium channels (VDCCs) in rat sensor
106 Here, we describe how surface mobility of voltage-dependent calcium channels (VDCCs) modulates rel
107 c buffering of calcium ions entering through voltage-dependent calcium channels (VDCCs) only, (iii) t
112 A can trigger GABA release after blockade of voltage-dependent calcium channels (VDCCs) with Cd.
113 This effect was occluded by block of R-type voltage-dependent calcium channels (VDCCs), but not by i
115 lationship between [Capre]t via presynaptic, voltage-dependent calcium channels (VDCCs), measured opt
116 xin-sensitive action potentials and P/Q-type voltage-dependent calcium channels (VDCCs), thereby conv
118 (CACNL1A3) of the dihydropyridine-sensitive voltage-dependent calcium channel was determined by isol
120 gh a calcium pool controlled by postsynaptic voltage-dependent calcium channels, whereas sustained st
121 gh N-methyl-D-aspartate receptors and L-type voltage-dependent calcium channels, which occurs in the
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