戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 W84 (>100-fold), compared with the wild-type M5 receptor.
2 lator with unprecedented selectivity for the M5 receptor.
3 st in neurons lacking M3, M5, or both M3 and M5 receptors.
4 has no effect on ACh affinity at M1 to M3 or M5 receptors.
5 tivity with [3H]NMS at M1 to M4 and possibly M5 receptors.
6 f morphine remained unaltered by the lack of M5 receptors.
7 ciliary processes and iris sphincter and the m5 receptor (5%), which is usually found only in the cen
8            These data indicate that boosting M5 receptor activity may be a useful therapeutic target
9                             The finding that M5 receptor activity modulates both morphine reward and
10 valuated for their affinity at muscarinic M1-M5 receptors and also assessed for their functional char
11 arent pK(I) = 8.78 +/- 0.24) and M1, M3, and M5 receptors (apparent pK(I) values <or= 8.0), and 3) ac
12                             We conclude that M5 receptors are critical for both engaging with the env
13 ors at submillimolar concentrations and from M5 receptors at 1 mM.
14           Further, a homology model of human M5 receptor based on the crystal structure of the rat M3
15  activation of "M1-like" mAChRs (M1, M3, and M5 receptors), but the specific receptor subtypes involv
16                    Furthermore, we show that M5 receptors can modulate exploratory behavior in a sex-
17 on in the C-terminal tail of the M1, M3, and M5 receptors contributes to the ability of these recepto
18 ion of adenylyl cyclase, whereas m1, m3, and m5 receptors couple preferentially to activation of phos
19 biochemical, and neurochemical studies using M5 receptor-deficient mice (M5-/- mice) as novel experim
20 nforcing effects of cocaine are decreased in M5 receptor-deficient mice using chronic intravenous coc
21                                              M5 receptor deletion decreased self-administration of lo
22                    Our results indicate that M5 receptor deletion diminished the reinforcing effects
23               Galphaq/11-coupled M1, M3, and M5 receptors each produced robust inhibition of Ca(V)1.2
24             Yet, most preclinical studies of M5 receptor function have primarily focused on substance
25                            Unlike M1-M4, the M5 receptor has relatively restricted expression in the
26 rough ectopic expression of either the m1 or m5 receptor in combination with cPLA2 in COS-1, CHO and
27 potentiation of acetylcholine at M1, M3, and M5 receptors in cell-based Ca(2+) mobilization assays.
28           Here, we characterized the role of M5 receptors in potentiating dopamine transmission in th
29  to increased neuronal firing, activation of M5 receptors in the striatum induces an inhibition in do
30 f the five muscarinic receptor subtypes, the M5 receptor is the only one detectable in midbrain dopam
31 (3)H]N-methylscopolamine binding site on the M5 receptor, is potent (IC50 = 0.45 nM) in inhibiting ox
32 significantly reduced (but not abolished) in M5 receptor KO mice.
33 ng only PLC-gamma2, overexpressed muscarinic M5 receptors (M5R) activated ACE.
34 eward and withdrawal processes suggests that M5 receptors may represent a novel target for the treatm
35 d that acetylcholine-dependent activation of M5 receptors might modulate the manifestations of opiate
36                   These results suggest that M5 receptors on DA neuron terminals enhance DA release,
37       Although activation of somatodendritic M5 receptors on SNc neurons leads to increased neuronal
38                                 We show that M5 receptors potentiate dopamine transmission by acting
39 on depended on receptor subtype, with M3 and M5 receptors producing much larger CaV2.3 inhibition tha
40       We found that constitutive deletion of M5 receptors reduced exploration of the center of an ope
41 l and behavioral functions of the muscarinic M5 receptor remain understudied.
42                            Despite this, the M5 receptor still activated tyrosine kinases, induced ST
43 23 (KDKKE) with those conserved in the m1/m3/m5 receptor subtype family (ELAAL) had little effect on
44                            In the brain, the M5 receptor subtype is preferentially expressed by dopam
45 ld-type mice and mice lacking M1, M3, and/or M5 receptors to determine the relative contribution of M
46  illustrate the therapeutic potential of the M5 receptor, warranting further research in the context
47                The cDNAs for the Ml, M2, and M5 receptors were not found.
48 Consistent with these observations, a mutant M5 receptor with these three key mutations, M5P179E, Q18