ライフサイエンスコーパス: sodium channel blocker

1 eptors but are unaffected by tetrodotoxin, a sodium channel blocker.

2 e effect would persist after withdrawal of a sodium channel blocker.

3 dicarboxamide (CDA54), a peripherally acting sodium channel blocker.

4 acerbated by GS967, a potent, unconventional sodium channel blocker.

5 ate onset epilepsies and lack of response to sodium channel blockers.

6 synthesized as voltage-gated skeletal muscle sodium channel blockers.

7 Lubeluzole moieties were modest sodium channel blockers.

8 Both riluzole and propranolol are efficient sodium channel blockers.

9 ch as carbamazepine and phenytoin, which are sodium channel blockers.

10 ut the side effect profile of broad spectrum sodium channel blockers.

11 opioid analgesics, such as subtype-selective sodium channel blockers.

12 ncreased from 32.7% to 78.6% with the use of sodium channel blockers.

13 By contrast, the sodium channel blocker 1 microM tetrodotoxin had no effe

14 oncealed and may be unmasked or modulated by sodium channel blockers, a febrile state, vagotonic agen

15 Sodium channel blockers also rescued the I1660V current,

16 on of sodium was minimized by the epithelial sodium channel blocker amiloride.

17 he degree seen with mM concentrations of the sodium channel blocker amiloride.

18 The epithelial sodium-channel blocker amiloride has been shown to inhib

19 CFM6104 was shown to be a state-selective, sodium channel blocker and a fluorescent p-glycoprotein

20 del of multiple sclerosis using conventional sodium channel blockers and a novel central nervous syst

21 on between age at disease onset, response to sodium channel blockers and the functional properties of

22 ating recombinant strains expressing AaIT1(a sodium channel blocker) and hybrid-toxin (a blocker of b

23 (SDLs) containing saxitoxin (STX), a site 1 sodium channel blocker, and the glucocorticoid agonist d

24 Sodium channel blockers are effective in unmasking carri

25 Sodium channel blockers are largely used to shorten QT i

26 Several clinical studies of sodium channel blockers are under way in patients with m

27 Sodium channel blockers are used as gene-specific treatm

28 Sodium channel blockers are used clinically to treat a n

29 Several sodium channel blockers are used clinically to treat neu

30 iate action potentials in brain neurons, and sodium channel blockers are used in therapy of epilepsy.

31 Considered as a sodium channel blocker, BBG is remarkably potent, acting

32 nist for ASICs), tetrodotoxin (0.5 microM, a sodium channel blocker), cadmium (100 microM, a nonselec

33 Sodium channel blockers can potentiate these findings an

34 Here we show that charged sodium-channel blockers can be targeted into nociceptors

35 BIIB074, a Nav1.7-selective, state-dependent sodium-channel blocker, can be administered at therapeut

36 length was ameliorated by the use-dependent sodium channel blocker carbamazepine and by a blocker of

37 r trigeminal neuralgia is treatment with the sodium channel blockers carbamazepine and oxcarbazepine,

38 Thus, the peripheral nerve sodium channel blocker CDA54 selectively inhibits sensor

39 and a novel central nervous system-excluded sodium channel blocker (CFM6104) that was synthesized wi

40 Further, a good response to sodium channel blockers clinically was found to be assoc

41 the efficacy of both drugs to mexiletine, a sodium channel blocker currently used to treat myotonia.

42 otent than anticonvulsant and antiarrhythmic sodium channel blockers currently used to treat neuropat

43 tes the high-affinity binding site for these sodium channel blocker drugs, and block may be mainly el

44 Internal perfusion with a fast sodium channel blocker eliminated spontaneous bursting b

45 s demonstrate unexpected efficacy of a novel sodium channel blocker in Dravet syndrome and suggest a

46 (NavMs) binds and is inhibited by eukaryotic sodium channel blockers in a manner similar to the human

47 ts, together with results showing effects of sodium channel blockers in immune cells, raise questions

48 ise questions about the long-term effects of sodium channel blockers in neuroinflammatory disorders,

49 orders, and suggest that clinical studies of sodium channel blockers in these disorders should be pla

50 combination with aerosolized amiloride, the sodium channel blocker, in normal human volunteers.

51 affected individuals and can be unmasked by sodium channel blockers, including antiarrhythmic drugs

52 Sodium channel blockers increase STE.

53 ines even in the presence of Tetrodotoxin, a sodium channel blocker, indicating that the morphine's e

54 Local perfusion of tetrodotoxin, a sodium channel blocker, into the striatum of an anesthet

55 Clinical utility of nonselective sodium channel blockers is limited due to serious advers

56 s show that CNS penetration by voltage-gated sodium channel blockers is not required for efficacy in

57 Na(v)1.1-1.8 demonstrated that the standard sodium channel blocker lamotrigine had modest activity a

58 hase 2 trial, we aimed to assess whether the sodium-channel blocker lamotrigine is also neuroprotecti

59 of MD, visual cortices were infused with the sodium channel blocker lidocaine in vehicle or vehicle o

60 Perfusion of the DRG with a sodium channel blocker (lidocaine) at a dose much less t

61 Nevertheless, compared with other known sodium channel blockers, lubeluzole adds a third pharmac

62 ta are converging to suggest next generation sodium channel blockers may offer the potential for nove

63 We report the characterization of a new sodium channel blocker, mu-conotoxin PIIIA(mu-PIIIA).

64 ort the discovery of two novel TTX-resistant sodium channel blockers, mu-conotoxins SIIIA and KIIIA,

65 litis (EAE) have shown protective effects of sodium channel blockers on central nervous system axons

66 eived HS containing a long acting epithelial sodium channel blocker (P308); isotonic saline; or no tr

67 Two sodium channel blockers, phenytoin and flecainide, have

68 the calcium channel blocker nifedipine, the sodium channel blocker quinidine, etc.

69 lencing motor neurons with the intracellular sodium channel blocker QX-314 also disrupted premotor rh

70 vity, by introducing the membrane-impermeant sodium channel blocker QX-314 into these axons via the T

71 Most sodium channel blockers reduce the early (peak) and late

72 f tetrodotoxin (TTX), a potent voltage-gated sodium channel blocker, reduces neurological deficits an

73 esensitization blocker cyclothiazide and the sodium channel blockers riluzole, mexiletine and QX-314

74 nd carvedilol), flecainide, and the neuronal sodium-channel blocker riluzole; a direct antiarrhythmic

75 ionally, inhibition of sodium influx using a sodium channel blocker saxitoxin completely prevented th

76 Antiepileptic drugs were categorized by MOA: sodium channel blockers (SC), gamma-aminobutyric acid an

77 in many patients, but can be unmasked using sodium channel blockers such as flecainide, ajmaline or

78 Amiloride, an epithelial sodium channel blocker, suppresses the responsiveness of

79 produce SLRs followed by an injection of the sodium channel blocker tetrodotoxin (TTX) into the MCP.

80 ked this large outward component because the sodium channel blocker tetrodotoxin (TTX) is typically u

81 e tested this by measuring the effect of the sodium channel blocker tetrodotoxin (TTX) on depolarizat

82 nvestigated this concept with the reversible sodium channel blocker tetrodotoxin (TTX) to determine (

83 DMPP persisted following application of the sodium channel blocker tetrodotoxin (TTX), and in the pr

84 using glutamate receptor antagonists and the sodium channel blocker tetrodotoxin (TTX).

85 ither in the presence or absence of the fast sodium channel blocker tetrodotoxin (TTX).

86 ivation of the basolateral amygdala with the sodium channel blocker tetrodotoxin disrupted both the a

87 Conversely, the sodium channel blocker tetrodotoxin fully abolished the

88 mpletely abolished by the application of the sodium channel blocker tetrodotoxin or by replacement of

89 In all experiments the sodium channel blocker tetrodotoxin was used to prevent

90 The astrocytic responses were blocked by the sodium channel blocker tetrodotoxin, the voltage-depende

91 ught to induce hyperpolarized arrest) or the sodium-channel blocker tetrodotoxin (which induces polar

92 The highly selective sodium channel blocker, tetrodotoxin (TTX) has been inst

93 f the study was to examine the effect of the sodium channel blocker, tetrodotoxin (TTX), in order to

94 The sodium channel blocker, tetrodotoxin (TTX), is an effect

95 intravitreal injections of the voltage-gated sodium channel blocker, tetrodotoxin (TTX), the metabotr

96 Then, the BC was microinjected with a sodium channel blocker, tetrodotoxin, during 4 extinctio

97 The sodium-channel blocker, tetrodotoxin (TTX; 2 micromol/l)

98 S represents a structurally novel and potent sodium channel blocker that may be used as a template fo

99 We report here the discovery of A-803467, a sodium channel blocker that potently blocks tetrodotoxin

100 Tetrodotoxin (TTX) is a sodium channel blocker that temporarily inactivates both

101 , we demonstrated that tetrodotoxin (TTX), a sodium channel blocker that temporarily inactivates neur

102 after incubation with tetrodotoxin (TTX), a sodium channel blocker, there was a significant increase

103 The development of subtype-specific sodium channel blockers, though clearly desirable, has b

104 orms of the disease and the effectiveness of sodium channel blockers to unmask the syndrome and, thus

105 ranch block, as well as the effectiveness of sodium channel blockers to unmask the syndrome and, thus

106 The clinical suspicion and use of a sodium-channel blocker to unmask BrS has allowed earlier

107 receptor antagonist CNQX (20 microM) or the sodium channel blocker TTX (1 microM) did not.

108 Application of the voltage-gated sodium channel blocker TTX enhanced the on-centre respon

109 Third, the sodium channel blocker TTX mimicked the effects of D2 re

110 Application of the voltage-gated sodium channel blocker TTX produced effects on AII amacr

111 ted dilation was inhibited completely with a sodium channel blocker (TTX), an NOS inhibitor (L-NNA),

112 ist, bicuculline (10 microM) and by the fast sodium channel blocker, TTX, suggesting that 5-HT had in

113 We find that the use of sodium channel blockers was often associated with clinic

114 sory axons by targeted delivery of a charged sodium-channel blocker, we found that functional blockad

115 -onset forms and an insufficient response to sodium channel blockers were associated with loss-of-fun

116 In contrast, sodium channel blockers were rarely effective in epileps