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1 that this channel is a low-voltage-activated T-type calcium channel.
2 selective blocker of low-voltage-activated, T-type calcium channels.
3 lcium transients due to strong expression of T-type calcium channels.
4 sect the contribution of genetic variants in T-type calcium channels.
5 of spinal pain neurons under the control of T-type calcium channels.
6 none or graded manner, due to recruitment of T-type calcium channels.
7 differentially inhibit Cav3 isoforms of the T-type calcium channels.
8 neurons are almost exclusively dependent on T-type calcium channels.
9 sufficiently hyperpolarized to de-inactivate T-type calcium channels.
10 logically distinct from L-, N-, P/Q-, R- and T-type calcium channels.
11 a low-threshold calcium current mediated by T-type calcium channels.
12 perpolarization "primes" (deinactivates) the T-type calcium channel, a depolarizing input will "trigg
14 te to A-currents, thus potentially unmasking T-type calcium channel activity and membrane hyperexcita
15 e inhibits rebound activity independently of T-type calcium channels and A-type potassium channels.
16 aracterization of the subunit composition of T-type calcium channels and help determine their involve
17 This toxin distinguishes between alpha 1G T-type calcium channels and other types of voltage-gated
19 ogy in vivo showed that TTA-P2 (a blocker of T-type calcium channels) and gabapentin (inhibitor of tr
20 were consistent with the known properties of T-type calcium channels, and the voltage dependence was
21 pretreatment with the novel mixed N-type and T-type calcium channel antagonist 1-(6,6-bis(4-fluorophe
22 ient synthetic routes for the synthesis of a T-type calcium channel antagonist MK-8998 were developed
25 dependence was blocked by application of the T-type calcium channel antagonists Ni2+ and mibefradil.
31 s suggest that both alpha1A P/Q- and alpha1G T-type calcium channels are required for the dynamic con
34 the alpha1G subunit of the thalamus-enriched T-type calcium channel, are associated with absence seiz
36 ene encoding Ca(v)3.2 low-voltage-activated, T-type calcium channels associated with bursting behavio
38 (100 nM), and by 26+/-3% (n=90 cells) by the T-type calcium channel blocker flunarizine (1 microM).
39 centration of nickel and by Z944, a specific T-type calcium channel blocker in advanced clinical deve
40 we demonstrated for the first time that the T-type calcium channel blocker ML218 acts similarly to m
41 c suppression of RT excitability via Z944, a T-type calcium channel blocker, and via C21 activation o
43 ility and burst firing, and selective triple T-type calcium channel blockers could offer a new way to
52 anic blocker to selectively block the native T-type calcium channel, but the potency and mechanism of
53 mutations in the CACNA1H gene (encoding the T-type calcium channel Ca(V)3.2) cause autosomal-dominan
55 e-activated calcium currents are mediated by T-type calcium channels Ca(V)3.1, Ca(V)3.2, and Ca(V)3.3
56 e found that pulvinar neurons expressed more T-type calcium channels (Ca(v) 3.2) and more small condu
57 block of this drug on the three recombinant T-type calcium channels (Ca(V)3.1, Ca(V)3.2, and Ca(V)3.
58 etinoic acid receptor beta 2 (RAR beta), and T-type calcium channel (CACNA1G) genes, and methylated i
59 1), retinoic acid receptor beta 2 (RARbeta), T-type calcium channel (CACNA1G), and multiple endocrine
60 d this area, we identified a gene encoding a T-type calcium channel, CACNA1G, as a target for hyperme
69 zation-activated cation channel currents and T-type calcium channel currents may account for some of
70 cal blockers we showed that L-, P/Q-, R- and T-type calcium channels do not contribute to the spontan
72 tch between firing modes depends on Ca(v)3.1 T-type calcium channels enriched in thalamic relay neuro
73 Although 17beta-estradiol (E2) modulates T-type calcium channel expression and function, little i
78 models shows how a non-linear dependence of T-type calcium channel gating on GABA(B) receptor activi
79 lectively identify Cacna1g, one of the three T-type calcium channel genes, as a key component of a ge
81 cular cloning of low-voltage activated (LVA) T-type calcium channels has enabled the study of their r
82 nce of motor function and that modulation of T-type calcium channels has therapeutic potential for SC
83 w calcium antagonist that selectively blocks T-type calcium channels, has been shown to be an effecti
85 ously, it was shown that mice lacking CaV3.1 T-type calcium channels have altered sleep/wake activity
86 the canonical rebound-related ion channels: T-type calcium channels, hyperpolarization-activated cat
87 regulates the expression of Cacna1h/Cav3.2 a T-type calcium channel implicated in autism and epilepsy
88 The aim was to investigate the role of the T-type calcium channel in HMSM by characterizing mRNA ex
89 tivity in vivo, supporting a contribution of T-type calcium channels in driving nociceptors' hyperexc
90 befradil completely and reversibly inhibited T-type calcium channels in freshly isolated rat cerebell
91 based on our biophysical characterization of T-type calcium channels in Purkinje cells suggests that
92 have identified a potential central role for T-type calcium channels in regulating body weight mainte
93 acologic inhibition or knockdown of Ca(v)3.1 T-type calcium channels in the auditory thalamus substan
94 believe to be a previously unknown role for T-type calcium channels in the regulation of sleep and w
96 alpha-adrenergic receptors and modulation of T-type calcium channels in the thalamus and was not due
98 I rats showed that the increased activity of T-type calcium channels induced by SCI contributes to dr
99 Here, we show that the increased activity of T-type calcium channels induced by the injury plays a ma
100 data suggest that the increased activity of T-type calcium channels induced by the injury plays a pr
101 increased activity of low voltage activated T-type calcium channels induced by the injury sustains t
104 k analysis showed trimethadione, a selective T-type calcium channel inhibitor, but not riluzole nor v
106 more, we find that coexpression of TRPC5 and T-type calcium channels is sufficient to reconstitute a
109 their spontaneous activity, suggesting that T-type calcium channels may represent a pharmacological
112 se in total firing and the ictal increase of T-type calcium channel-mediated burst firing of thalamoc
113 sociated with calpain-1 activation following T-type calcium channel opening, and resulted in the trun
114 ting sodium channel inactivation, inhibiting T-type calcium channels, or enhancing gamma-aminobutyric
115 This research expands our understanding of T-type calcium channel pharmacology and supports the sui
118 membrane potential allows activation of the T-type calcium channels, promoting rhythmic high-frequen
120 H channels determined impact of 1 variant on T-type calcium channel responsiveness to ethosuximide.
122 s of Ca(v)3.2 alone and in complex with four T-type calcium channel selective antagonists with overal
123 port the existence of a syntaxin-1A/Ca(v)3.2 T-type calcium channel signaling complex that relies on
124 +), using whole-cell recordings from alpha1G T-type calcium channels stably expressed in HEK 293 cell
125 t studies have highlighted the importance of T-type calcium channels (T-channels) in peripheral nocic
126 te a prominent role of low-voltage-activated T-type calcium channels (T-channels) in the firing activ
128 e CaV3.1 isoform of low-voltage-activated or T-type calcium channels (T-channels) in this process.
129 usly documented that the Ca(V)3.3 isoform of T-type calcium channels (T-channels) is inhibited by cli
131 ons in a hyperpolarized state for recruiting T-type calcium channels that are important for burst fir
133 tion of a potent and selective antagonist of T-type calcium channels, TTA-A2, to normal-weight animal
139 overexpressing the Cacna1g gene for alpha1G T-type calcium channels were generated with low and high
140 at estrogen regulates the mRNA expression of T-type calcium channels, which leads to increased functi
141 toxin (kurtoxin) that binds to the alpha 1G T-type calcium channel with high affinity and inhibits t
142 In current-clamp recordings, inhibition of T-type calcium channels with 1 mum TTA-P2 reduced both t