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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
13             Both forms of plasticity rely on T-type calcium channel activation to confer synapse spec
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
18                                       Cav3.2 T-type calcium channels and their dysregulation by the d
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
23                            Using a selective T-type calcium channel antagonist, we describe a T-type
24 ry of a novel series of potent and selective T-type calcium channel antagonists is reported.
25 dependence was blocked by application of the T-type calcium channel antagonists Ni2+ and mibefradil.
26 sed by AMPA-R and NMDA-R antagonists but not T-type calcium channel antagonists.
27                    Our results indicate that T-type calcium channels are critical regulators of a C.
28 quency band (0.75-1.5 Hz) only when thalamic T-type calcium channels are functionally active.
29                                              T-type calcium channels are important modulators of both
30                      Low-threshold activated T-type calcium channels are present at the synapse, alth
31 s suggest that both alpha1A P/Q- and alpha1G T-type calcium channels are required for the dynamic con
32                                              T-type calcium channels are responsible for generating l
33                       Low-voltage-activated (T-type) calcium channels are responsible for burst firin
34 the alpha1G subunit of the thalamus-enriched T-type calcium channel, are associated with absence seiz
35                                    We define T-type calcium channels as a target of Abeta-NgR signali
36 ene encoding Ca(v)3.2 low-voltage-activated, T-type calcium channels associated with bursting behavio
37                                The effect of T-type calcium channel block was more pronounced after B
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
42                              Ethosuximide, a T-type calcium channel blocker, eliminated busting in le
43 ility and burst firing, and selective triple T-type calcium channel blockers could offer a new way to
44                                        These T-type calcium channel blockers produced an insurmountab
45                               In contrast to T-type calcium channel blockers that prevent all modes o
46 ives as potent, selective, brain-penetrating T-type calcium channel blockers.
47 ines as brain penetrant and selective triple T-type calcium channel blockers.
48  as potent, selective, and brain-penetrating T-type calcium channel blockers.
49  was unaltered in the presence of L-, R- and T-type calcium channel blockers.
50                                          The T-type calcium-channel blockers, nickel (3 micromol/l) a
51                     In burst mode, dendritic T-type calcium channels boosted small synaptic inputs an
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
54      We show that calcium spikes rely on the T-type calcium channel Ca-alpha1T and argue via analytic
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
61 approved drug mibefradil, which inhibits the T-type calcium channel Cav3.2.
62 sion of L-type calcium channel (Cav1.2), not T-type calcium channel (Cav3.2), was up-regulated.
63                     Pharmacological block of T-type calcium channels (Cav3), although not noticeably
64 at remains poorly understood with respect to T-type calcium channels (Cav3).
65                                              T-type calcium channels (Cav3.1 to Cav3.3) regulate low-
66 ut interestingly was a potent blocker of the T-type calcium channel, Cav3.1 (IC(50) = 1.05 muM).
67       The corresponding mutations affect the T-type calcium channel CCA-1 and symmetrically re-tune i
68                  The robust E2 regulation of T-type calcium channels could be an important mechanism
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
71                                       CaV3.2 T-type calcium channels, encoded by CACNA1H, are express
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
74 ripts (alpha1G, alpha1H, and alpha1I) of the T-type calcium channel family (CaVT).
75                         Other members of the T-type calcium channel family were also regulated by syn
76                                         Cav3 T-type calcium channels from great pond snail Lymnaea st
77                 External pH (pH(o)) modifies T-type calcium channel gating and permeation properties.
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
80                      The Ca(v)3.2 subtype of T-type calcium channels has been targeted for developing
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
84                  Low-voltage-activated (LVA) T-type calcium channels have a wide tissue distribution
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
95                         The role of P/Q- and T-type calcium channels in the rhythmic oscillatory beha
96 alpha-adrenergic receptors and modulation of T-type calcium channels in the thalamus and was not due
97  inhibition of CaV3.2 low-voltage-activated (T-type) calcium channels in pain pathways.
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
102  is a useful tool for probing the effects of T-type calcium channel inhibition.
103                       Conversely, ABT-639, a T-type calcium channel inhibitor that failed in Phase 2
104 k analysis showed trimethadione, a selective T-type calcium channel inhibitor, but not riluzole nor v
105                                       Cav3.2 T-type calcium channel is a major molecular actor of neu
106 more, we find that coexpression of TRPC5 and T-type calcium channels is sufficient to reconstitute a
107            Previous data have indicated that T-type calcium channels (low-voltage activated T-channel
108                                          The T-type calcium channel may play a role in this process.
109  their spontaneous activity, suggesting that T-type calcium channels may represent a pharmacological
110                 Low voltage-activated (LVA), T-type, calcium channels mediate diverse biological func
111        The vulnerable population expresses a T-type calcium channel-mediated afterdepolarization (ADP
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
116                                              T-type calcium channels play a key role in neuronal exci
117                                              T-type calcium channels play essential roles in regulati
118  membrane potential allows activation of the T-type calcium channels, promoting rhythmic high-frequen
119                                              T-type calcium channels represent a key pathway for Ca(2
120 H channels determined impact of 1 variant on T-type calcium channel responsiveness to ethosuximide.
121                     Our analysis with R- and T-type calcium channels revealed that differences in the
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
127                 Recent studies indicate that T-type calcium channels (T-channels) in the thalamus are
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
130                                              T-type calcium channels (T/Ca(v)3-channels) are implicat
131 ons in a hyperpolarized state for recruiting T-type calcium channels that are important for burst fir
132          We examined a homology model of the T-type calcium channel to look for possible routes of dr
133 tion of a potent and selective antagonist of T-type calcium channels, TTA-A2, to normal-weight animal
134                  We previously proposed that T-type calcium channel (TTCC) expression may serve as a
135                         INTERPRETATION: Four T-type calcium channel variants and 1 ABCB1 transporter
136                                           In T-type calcium channels, verapamil blocks with micromola
137 gene of the pore-forming alpha1G subunit for T-type calcium channel were used.
138                                     Although T-type calcium channels were first described in sensory
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

 
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