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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 sporter, and [3H]pirenzepine from muscarinic m1 receptors.
9 pha1B (Ca(V)2.2) Ca(2+) channel subunits and M1 receptors.
10 t do not block inhibition of alpha1E through M1 receptors.
11 e and pirenzepine, suggesting involvement of M1 receptors.
12 ors and increased binding in regions rich in M1 receptors.
13 c anxiolytic action mediated by postsynaptic M1 receptors.
14 serotonin transporters as well as muscarinic m1 receptors.
15 did not abolish interaction of Gq alpha with m1 receptors.
16  synaptic transmission in the cortex via non-M1 receptors.
17 tors and negligible interactions at hERG and M1 receptors.
18 /allosteric binding properties at muscarinic M1 receptors.
19  on enhanced green fluorescent protein-fused M1 receptors.
20 42 to be used as a FRET tracer on EGFP-fused M1 receptors.
21  distinguish between the roles of mGluRs and m1 receptors.
22 ion, both triggered by pirenzepine-sensitive M1 receptors.
23 a1b and alpha2/delta subunits and muscarinic M1 receptors.
24 ptor antagonists and lost in neurons lacking M1 receptors.
25 producing much larger CaV2.3 inhibition than M1 receptors.
26 es stimulation was meticulously analyzed for M1 receptors.
27 ation of heterologously expressed muscarinic M1 receptors.
28 whereas 1/TBPBd hybrids (5) did not activate M1-receptors.
29                                          The m1 receptor (7%) was detected in the ciliary processes a
30 ersing MS is remyelination by inhibiting the M1 receptor, a member of the muscarinic acetylcholine re
31                      In BHK cells expressing M1 receptors, a muscarinic agonist (carbachol) causes a
32 -term depression (LTD) induced by muscarinic M1 receptor activation (mLTD) is lost after medial septa
33                                 We show that M1 receptor activation also reduces the interaction of c
34  of residues, supporting the hypothesis that M1 receptor activation can occur through at least three
35 he activity of PI3K-Akt signaling induced by M1 receptor activation could be abolished by cAMP-PKA in
36                                              M1 receptor activation depolarizes pyramidal neurons by
37  Taken together, these data demonstrate that M1 receptor activation induces membrane insertion of Glu
38 the postsynaptic excitability of PT neurons, M1 receptor activation promotes corticofugal output by a
39 ipitates with Kv1.2 in a manner dependent on m1 receptor activation.
40 5 and membrane insertion of GluA1 induced by M1 receptor activation.
41 e hippocampal NMDA receptor currents through M1 receptor activation.
42 the cue detection process, while muscarinic (M1) receptor activity was preferentially involved in the
43 is thought to enhance working memory via its M1 receptor agonist activity.
44 oinjection of ACh (5 pmol) or the muscarinic M1 receptor agonist McN-A-343 (30 ng) into the lateral h
45 nic cholinergic activation by muscarine, the M1 receptor agonist McN-A-343, and the M2 receptor antag
46 cetyl-beta-methylcholine (MCh), a muscarinic M1 receptor agonist or phorbol-12-myristate, 13-acetate
47                                          The M1 receptor agonist, NcN-A-343, increased the frequency
48  classes used clinically, such as muscarinic M1 receptor agonists, and is therefore a potential targe
49  but slightly increased [(3)H]NMS binding to M1 receptors, an allosteric effect.
50 gulation of dopaminergic transmission by the M1 receptor and are consistent with the idea that M1 dys
51  acetylcholine signaling, via the muscarinic M1 receptor and epidermal growth factor receptor, increa
52 ], which has an IC50 value of 27.3 nM at the m1 receptor and possesses 100-fold (m2), 48-fold (m3), 7
53 esses an 11-fold selectivity for the M5 over M1 receptor and shows little activity at M2-M4.
54 sing current clamp recordings; activation of M1 receptors and blocking M-channels depolarized neurons
55 ) and D2 receptors, without interacting with M1 receptors and hERG channels.
56 ine is a potent, allosteric agonist at human M1 receptors and is able to potentiate hippocampal NMDA
57 idine derivatives displayed high efficacy at m1 receptors and lower activity at m3 receptors coupled
58 ant neuroprotective property inherent to the M1-receptor and indicate that next generation M1-recepto
59 ps within seconds of arrestin binding to the M1 receptor, and it reverses within seconds of arrestin
60 c model to quantify binding of the tracer to M1 receptors, and the reliability of the chosen quantifi
61                                 Although the M1 receptor antagonist pirenzepine also reversed the inh
62 ptor antagonist methoctramine but not by the M1 receptor antagonist pirenzepine.
63 use the effects of carbachol were blocked by M1 receptor antagonists and lost in neurons lacking M1 r
64 increased approximately 2-fold by brucine at m1 receptors, approximately 3-fold by N-chloromethyl bru
65                                              m1 receptors are also expressed by 60% of calbindin-immu
66  B (Akt) inhibitor IV blocked the effects of M1 receptors as well.
67         In cells coexpressed with muscarinic M1 receptors, bath application of muscarinic agonist red
68  largely absent in neurons from mice lacking M1 receptors, but most were robust in neurons lacking M3
69 in response to carbachol, and stimulation of m1 receptors, but not direct JNK activation, induced exp
70 monstrated that activation of the muscarinic M1 receptor by a subtype-selective positive allosteric m
71                               Stimulation of M1 receptors by 10 microM oxotremorine-M (Oxo-M) strongl
72 -desmethylclozapine preferentially activated M1 receptors by interacting with a site that does not fu
73 of the M1 muscarinic acetylcholine receptor (M1-receptor) can not only restore memory loss in AD pati
74 rt, immunohistochemistry revealed muscarinic M1 receptor, CaV3.2, and KV7.2/7.3 subunit localization
75       Stimulation of the cortical muscarinic M1 receptor (CHRM1) is proposed as a treatment for schiz
76                         It is concluded that M1 receptors couple to all known KCNQ subunits and that
77 ounding basic residues to facilitate partial m1 receptor coupling after full agonist stimulation.
78 ext of Gi1alpha were not sufficient to allow M1 receptor coupling, nor were C-terminal amino acids of
79  the KKAAR365 motif participate in efficient m1 receptor coupling.
80 prevented M2 receptor coupling nor permitted M1 receptor coupling.
81 mpal CA3 pyramidal neurons and are absent in M1 receptor-deficient mice.
82 onselective pharmacological antagonists, the M1 receptor deletion produced a selective phenotype that
83 forms nor overexpression of PKCdelta induced M1 receptor desensitization, excluding a contribution of
84 produced stabilization and enrichment of the M1 receptor dimer population, but the receptor subtype n
85  TRPL channels together with the muscarinic (M1) receptor, enabling the openings of TRPL channels via
86 -receptors, and 8200-fold lower affinity for M1-receptors expressed in CHO cells.
87                        We have reported that M1 receptors facilitate cognition by promoting membrane
88       Together, our results demonstrate that M1 receptors facilitate cue detection behaviors and are
89 ation of an effective medicine targeting the M1-receptor has however been severely hampered by associ
90 died with the human muscarinic acetylcholine M1-receptor (hM1) with respect to receptor binding and G
91                              Docking into an M1 receptor homology model revealed that AC-42 and TBPB
92 g some 50 molecules.mum(-2) human muscarinic M1 receptor identified a approximately 75:25 mixture of
93 tein or transcript, both the fraction of the M1 receptor in the synaptic plasma membrane and the biot
94               Finally, we confirm a role for M1 receptors in behavior by demonstrating cue detection
95 Double-labeling immunocytochemistry revealed m1 receptors in calbindin-D28k--positive medium spiny pr
96 inephrine (NET) transporters, and muscarinic M1 receptors in rat brain.
97 implicate M3 receptors in the inhibition and M1 receptors in the enhancement of transmitter releaseat
98 and is a highly promising ligand to quantify M1 receptors in the human brain.
99 ta1b and alpha2delta subunits and muscarinic M1 receptors in the Xenopus oocytes and the expressed cu
100 e of M1 muscarininc acetylcholine receptors (m1 receptors) in metabotropic glutamate receptor (mGluR)
101                        By comparison, though m1 receptors induce the tyrosine phosphorylation of the
102 dence of these Kv7 homomeric channels or the m1 receptor-induced activation of phospholipase C or pro
103 P) kinase kinase (MEK), had no effect on the m1 receptor-induced inhibition of Kir2.1, suggesting tha
104 nd the G(q)-coupled muscarinic acetylcholine M1 receptor inhibited the activity of TRPM3 heterologous
105                                Activation of M1 receptors inhibits Abeta signaling by enhancing the c
106 ention of receptor immunoreactivity, whereas M1 receptor internalization was not affected by loss of
107 ion of a muscarinic depolarizing current and M1 receptor internalization.
108  to be, at least in part, the consequence of M1 receptor internalization.
109                 Our results suggest that the M1 receptor is specifically involved in memory processes
110  Clozapine's potent antagonism of muscarinic M1 receptors is thought to worsen working memory deficit
111             The M1-muscarinic acetylcholine (M1) receptor is the target of choice but has been hamper
112 om a combination of blockade of postsynaptic m1 receptors, leading to reduced excitability, with bloc
113 1-receptor and indicate that next generation M1-receptor ligands designed to drive receptor phosphory
114                               The muscarinic M1 receptors localized to the submucosal glands do not a
115                     Activation of muscarinic M1 receptors (M1-Rs) caused robust and reversible inhibi
116 eral amygdalar nucleus (BLa) mediated by the M1 receptor (M1R) is critical for memory consolidation.
117                               The muscarinic M1 receptor (M1R) is highly involved in cognition, and s
118 gms, an effect primarily associated with the M1 receptor (M1R).
119 is study investigated the role of muscarinic M1 receptors (M1Rs) in the dlPFC using iontophoresis cou
120 uron-1 as an accessory subunit of muscarinic M1 receptors (M1Rs).
121 ed M1-receptor, we recently established that M1-receptor mediated adverse responses can be minimized
122 ced Ca2+ influx, these sites may account for M1 receptor-mediated regulation of neurotransmission at
123 ediated cholinergic actions in the striatum: m1 receptors modulate extrinsic glutamatergic and monoam
124 ed M2-class (m2, m4) receptor mRNAs, whereas m1 receptor mRNA was found in only a subset (approximate
125 ation of rapamycin attenuated the effects of M1 receptors on GluA1.
126 s induced by muscarine require activation of M1 receptors on hippocampal CA3 pyramidal neurons and ar
127  oligodendroglial deletion of the muscarinic M1 receptor or systemic administration of the pro-myelin
128  the study of procholinergic agents, such as M1 receptor-positive allosteric modulators, to enhance c
129 enzepine (3.0 mM), which blocks postsynaptic m1 receptors, produced a significant increase only in ou
130 e primary interneuronal subtype in the bulb, M1 receptors regulate the degree of adaptation that occu
131 phospholipids in CHO cells stably expressing M1 receptors shows that PIP2 and PIP are nearly depleted
132       We propose a 'unifying hypothesis' for M1 receptor signalling whereby inhibitory and excitatory
133 tyrosine kinase activity is critical for the m1 receptor-stimulated tyrosine phosphorylation of PYK2.
134 ses chronic inhibition of IRK3 channels, and m1 receptor stimulation may lead to an increase of cytop
135                                    Thus, the m1 receptor subtype mediates M current modulation in sym
136 nic receptor antagonists telenzepine for the M1 receptor subtype, methoctramine for the M2 subtype an
137 a) gained the ability to productively couple M1 receptors suggesting that the proper context of both
138  we have developed classification models for M1 receptor that will enable rapid screening of large ch
139  with a null mutation of the gene coding the M1 receptor, the most densely distributed muscarinic rec
140 , dynamic ligand binding can be exploited in M1 receptors to design partial agonists with graded effi
141 xpressed in JEG-3 cells, the m2, but not the m1, receptor undergoes agonist-induced sequestration.
142  interaction of muscarinic agonists with the m1 receptor using a nine amino model of the m1 receptor.
143                          Immunoreactivity to M1 receptor was not on goblet cells but was on the strat
144                           Specificity of the M1 receptor was tested by the MT-7 toxin.
145 r the dopamine transporter versus muscarinic m1 receptors was achieved by substitution of the N-methy
146               The presynaptic requirement of m1 receptors was confirmed by the lack of DHPG-induced m
147  The modulation of CaV1.3 channels by D2 and M1 receptors was disrupted by intracellular dialysis of
148                   Channel inhibition through M1 receptors was studied in detail and was found to be k
149 arboxyl-terminal third intracellular loop of m1 receptors, was mutated to AAAAA365, thereby generatin
150 ty, which is downstream from both mGluRs and m1 receptors, was reduced in CA3 but not in CA1.
151 mouse models that express a G protein-biased M1-receptor, we recently established that M1-receptor me
152                           Ultrastructurally, m1 receptors were predominantly localized in asymmetric
153 inin receptors became nearly as effective as M1 receptors when PIP2 synthesis, IP3 receptors, or the
154                     Activation of muscarinic m1 receptors which are coupled to the phosphoinositide (
155  antagonized the effects of carbachol at the M1 receptor, while only 4d completely antagonized carbac
156 f Gq(alpha), prevents coupling to muscarinic M1 receptors, while the C-terminus of Gq(alpha), when pl
157 tion caused by stimulation of the muscarinic m1 receptor with 100 microM carbachol.
158 volume after selectively blocking muscarinic M1 receptors with dicyclomine during SDH.
159 in transporters, but all bound to muscarinic m1 receptors with high affinity (K1 = 0.41-2.52 nM).
160 tassium channels or activation of muscarinic M1 receptors with selective allosteric agonist 77-LH-28-
161  accumulation, while being a full agonist at M1-receptors with an EC50 of 23 nM and a partial agonist

 
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