ライフサイエンスコーパス: M1 receptor

1 e 1,2,5-thiadiazole in the activation of the m1 receptor.

2 m channel Kv1.2 in a manner regulated by the m1 receptor.

3 yonic stem cells to produce mice lacking the m1 receptor.

4 m1 receptor using a nine amino model of the m1 receptor.

5 ient in the mechanism or pathway used by the m1 receptor.

6 and para-LRB-AC42 in a 3D model of the human M1 receptor.

7 is necessary for activation of TRPC5 by the M1 receptor.

8 c anxiolytic action mediated by postsynaptic M1 receptors.

9 serotonin transporters as well as muscarinic m1 receptors.

10 did not abolish interaction of Gq alpha with m1 receptors.

11 tors and negligible interactions at hERG and M1 receptors.

12 /allosteric binding properties at muscarinic M1 receptors.

13 on enhanced green fluorescent protein-fused M1 receptors.

14 42 to be used as a FRET tracer on EGFP-fused M1 receptors.

15 distinguish between the roles of mGluRs and m1 receptors.

16 ion, both triggered by pirenzepine-sensitive M1 receptors.

17 a1b and alpha2/delta subunits and muscarinic M1 receptors.

18 ptor antagonists and lost in neurons lacking M1 receptors.

19 producing much larger CaV2.3 inhibition than M1 receptors.

20 es stimulation was meticulously analyzed for M1 receptors.

21 sporter, and [3H]pirenzepine from muscarinic m1 receptors.

22 pha1B (Ca(V)2.2) Ca(2+) channel subunits and M1 receptors.

23 t do not block inhibition of alpha1E through M1 receptors.

24 e and pirenzepine, suggesting involvement of M1 receptors.

25 ors and increased binding in regions rich in M1 receptors.

26 whereas 1/TBPBd hybrids (5) did not activate M1-receptors.

27 The m1 receptor (7%) was detected in the ciliary processes a

28 In BHK cells expressing M1 receptors, a muscarinic agonist (carbachol) causes a

29 -term depression (LTD) induced by muscarinic M1 receptor activation (mLTD) is lost after medial septa

30 We show that M1 receptor activation also reduces the interaction of c

31 of residues, supporting the hypothesis that M1 receptor activation can occur through at least three

32 M1 receptor activation depolarizes pyramidal neurons by

33 ipitates with Kv1.2 in a manner dependent on m1 receptor activation.

34 e hippocampal NMDA receptor currents through M1 receptor activation.

35 the cue detection process, while muscarinic (M1) receptor activity was preferentially involved in the

36 is thought to enhance working memory via its M1 receptor agonist activity.

37 oinjection of ACh (5 pmol) or the muscarinic M1 receptor agonist McN-A-343 (30 ng) into the lateral h

38 nic cholinergic activation by muscarine, the M1 receptor agonist McN-A-343, and the M2 receptor antag

39 cetyl-beta-methylcholine (MCh), a muscarinic M1 receptor agonist or phorbol-12-myristate, 13-acetate

40 The M1 receptor agonist, NcN-A-343, increased the frequency

41 but slightly increased [(3)H]NMS binding to M1 receptors, an allosteric effect.

42 gulation of dopaminergic transmission by the M1 receptor and are consistent with the idea that M1 dys

43 acetylcholine signaling, via the muscarinic M1 receptor and epidermal growth factor receptor, increa

44 ], which has an IC50 value of 27.3 nM at the m1 receptor and possesses 100-fold (m2), 48-fold (m3), 7

45 esses an 11-fold selectivity for the M5 over M1 receptor and shows little activity at M2-M4.

46 sing current clamp recordings; activation of M1 receptors and blocking M-channels depolarized neurons

47 ) and D2 receptors, without interacting with M1 receptors and hERG channels.

48 ine is a potent, allosteric agonist at human M1 receptors and is able to potentiate hippocampal NMDA

49 idine derivatives displayed high efficacy at m1 receptors and lower activity at m3 receptors coupled

50 ps within seconds of arrestin binding to the M1 receptor, and it reverses within seconds of arrestin

51 Although the M1 receptor antagonist pirenzepine also reversed the inh

52 ptor antagonist methoctramine but not by the M1 receptor antagonist pirenzepine.

53 use the effects of carbachol were blocked by M1 receptor antagonists and lost in neurons lacking M1 r

54 increased approximately 2-fold by brucine at m1 receptors, approximately 3-fold by N-chloromethyl bru

55 m1 receptors are also expressed by 60% of calbindin-immu

56 In cells coexpressed with muscarinic M1 receptors, bath application of muscarinic agonist red

57 largely absent in neurons from mice lacking M1 receptors, but most were robust in neurons lacking M3

58 in response to carbachol, and stimulation of m1 receptors, but not direct JNK activation, induced exp

59 monstrated that activation of the muscarinic M1 receptor by a subtype-selective positive allosteric m

60 Stimulation of M1 receptors by 10 microM oxotremorine-M (Oxo-M) strongl

61 -desmethylclozapine preferentially activated M1 receptors by interacting with a site that does not fu

62 rt, immunohistochemistry revealed muscarinic M1 receptor, CaV3.2, and KV7.2/7.3 subunit localization

63 Stimulation of the cortical muscarinic M1 receptor (CHRM1) is proposed as a treatment for schiz

64 It is concluded that M1 receptors couple to all known KCNQ subunits and that

65 ounding basic residues to facilitate partial m1 receptor coupling after full agonist stimulation.

66 ext of Gi1alpha were not sufficient to allow M1 receptor coupling, nor were C-terminal amino acids of

67 the KKAAR365 motif participate in efficient m1 receptor coupling.

68 prevented M2 receptor coupling nor permitted M1 receptor coupling.

69 mpal CA3 pyramidal neurons and are absent in M1 receptor-deficient mice.

70 onselective pharmacological antagonists, the M1 receptor deletion produced a selective phenotype that

71 forms nor overexpression of PKCdelta induced M1 receptor desensitization, excluding a contribution of

72 produced stabilization and enrichment of the M1 receptor dimer population, but the receptor subtype n

73 TRPL channels together with the muscarinic (M1) receptor, enabling the openings of TRPL channels via

74 -receptors, and 8200-fold lower affinity for M1-receptors expressed in CHO cells.

75 Together, our results demonstrate that M1 receptors facilitate cue detection behaviors and are

76 died with the human muscarinic acetylcholine M1-receptor (hM1) with respect to receptor binding and G

77 Docking into an M1 receptor homology model revealed that AC-42 and TBPB

78 g some 50 molecules.mum(-2) human muscarinic M1 receptor identified a approximately 75:25 mixture of

79 tein or transcript, both the fraction of the M1 receptor in the synaptic plasma membrane and the biot

80 Finally, we confirm a role for M1 receptors in behavior by demonstrating cue detection

81 Double-labeling immunocytochemistry revealed m1 receptors in calbindin-D28k--positive medium spiny pr

82 inephrine (NET) transporters, and muscarinic M1 receptors in rat brain.

83 implicate M3 receptors in the inhibition and M1 receptors in the enhancement of transmitter releaseat

84 ta1b and alpha2delta subunits and muscarinic M1 receptors in the Xenopus oocytes and the expressed cu

85 e of M1 muscarininc acetylcholine receptors (m1 receptors) in metabotropic glutamate receptor (mGluR)

86 By comparison, though m1 receptors induce the tyrosine phosphorylation of the

87 P) kinase kinase (MEK), had no effect on the m1 receptor-induced inhibition of Kir2.1, suggesting tha

88 Activation of M1 receptors inhibits Abeta signaling by enhancing the c

89 ention of receptor immunoreactivity, whereas M1 receptor internalization was not affected by loss of

90 ion of a muscarinic depolarizing current and M1 receptor internalization.

91 to be, at least in part, the consequence of M1 receptor internalization.

92 Our results suggest that the M1 receptor is specifically involved in memory processes

93 Clozapine's potent antagonism of muscarinic M1 receptors is thought to worsen working memory deficit

94 om a combination of blockade of postsynaptic m1 receptors, leading to reduced excitability, with bloc

95 The muscarinic M1 receptors localized to the submucosal glands do not a

96 Activation of muscarinic M1 receptors (M1-Rs) caused robust and reversible inhibi

97 eral amygdalar nucleus (BLa) mediated by the M1 receptor (M1R) is critical for memory consolidation.

98 The muscarinic M1 receptor (M1R) is highly involved in cognition, and s

99 gms, an effect primarily associated with the M1 receptor (M1R).

100 ced Ca2+ influx, these sites may account for M1 receptor-mediated regulation of neurotransmission at

101 ediated cholinergic actions in the striatum: m1 receptors modulate extrinsic glutamatergic and monoam

102 ed M2-class (m2, m4) receptor mRNAs, whereas m1 receptor mRNA was found in only a subset (approximate

103 s induced by muscarine require activation of M1 receptors on hippocampal CA3 pyramidal neurons and ar

104 the study of procholinergic agents, such as M1 receptor-positive allosteric modulators, to enhance c

105 enzepine (3.0 mM), which blocks postsynaptic m1 receptors, produced a significant increase only in ou

106 e primary interneuronal subtype in the bulb, M1 receptors regulate the degree of adaptation that occu

107 phospholipids in CHO cells stably expressing M1 receptors shows that PIP2 and PIP are nearly depleted

108 We propose a 'unifying hypothesis' for M1 receptor signalling whereby inhibitory and excitatory

109 tyrosine kinase activity is critical for the m1 receptor-stimulated tyrosine phosphorylation of PYK2.

110 ses chronic inhibition of IRK3 channels, and m1 receptor stimulation may lead to an increase of cytop

111 Thus, the m1 receptor subtype mediates M current modulation in sym

112 nic receptor antagonists telenzepine for the M1 receptor subtype, methoctramine for the M2 subtype an

113 a) gained the ability to productively couple M1 receptors suggesting that the proper context of both

114 with a null mutation of the gene coding the M1 receptor, the most densely distributed muscarinic rec

115 , dynamic ligand binding can be exploited in M1 receptors to design partial agonists with graded effi

116 xpressed in JEG-3 cells, the m2, but not the m1, receptor undergoes agonist-induced sequestration.

117 interaction of muscarinic agonists with the m1 receptor using a nine amino model of the m1 receptor.

118 Immunoreactivity to M1 receptor was not on goblet cells but was on the strat

119 Specificity of the M1 receptor was tested by the MT-7 toxin.

120 r the dopamine transporter versus muscarinic m1 receptors was achieved by substitution of the N-methy

121 The presynaptic requirement of m1 receptors was confirmed by the lack of DHPG-induced m

122 The modulation of CaV1.3 channels by D2 and M1 receptors was disrupted by intracellular dialysis of

123 Channel inhibition through M1 receptors was studied in detail and was found to be k

124 arboxyl-terminal third intracellular loop of m1 receptors, was mutated to AAAAA365, thereby generatin

125 ty, which is downstream from both mGluRs and m1 receptors, was reduced in CA3 but not in CA1.

126 Ultrastructurally, m1 receptors were predominantly localized in asymmetric

127 inin receptors became nearly as effective as M1 receptors when PIP2 synthesis, IP3 receptors, or the

128 Activation of muscarinic m1 receptors which are coupled to the phosphoinositide (

129 antagonized the effects of carbachol at the M1 receptor, while only 4d completely antagonized carbac

130 f Gq(alpha), prevents coupling to muscarinic M1 receptors, while the C-terminus of Gq(alpha), when pl

131 tion caused by stimulation of the muscarinic m1 receptor with 100 microM carbachol.

132 volume after selectively blocking muscarinic M1 receptors with dicyclomine during SDH.

133 in transporters, but all bound to muscarinic m1 receptors with high affinity (K1 = 0.41-2.52 nM).

134 accumulation, while being a full agonist at M1-receptors with an EC50 of 23 nM and a partial agonist