ライフサイエンスコーパス: M5 receptor

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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 The finding that M5 receptor activity modulates both morphine reward and

9 valuated for their affinity at muscarinic M1-M5 receptors and also assessed for their functional char

10 arent pK(I) = 8.78 +/- 0.24) and M1, M3, and M5 receptors (apparent pK(I) values <or= 8.0), and 3) ac

11 ors at submillimolar concentrations and from M5 receptors at 1 mM.

12 Further, a homology model of human M5 receptor based on the crystal structure of the rat M3

13 activation of "M1-like" mAChRs (M1, M3, and M5 receptors), but the specific receptor subtypes involv

14 on in the C-terminal tail of the M1, M3, and M5 receptors contributes to the ability of these recepto

15 ion of adenylyl cyclase, whereas m1, m3, and m5 receptors couple preferentially to activation of phos

16 biochemical, and neurochemical studies using M5 receptor-deficient mice (M5-/- mice) as novel experim

17 nforcing effects of cocaine are decreased in M5 receptor-deficient mice using chronic intravenous coc

18 M5 receptor deletion decreased self-administration of lo

19 Our results indicate that M5 receptor deletion diminished the reinforcing effects

20 Galphaq/11-coupled M1, M3, and M5 receptors each produced robust inhibition of Ca(V)1.2

21 rough ectopic expression of either the m1 or m5 receptor in combination with cPLA2 in COS-1, CHO and

22 potentiation of acetylcholine at M1, M3, and M5 receptors in cell-based Ca(2+) mobilization assays.

23 to increased neuronal firing, activation of M5 receptors in the striatum induces an inhibition in do

24 f the five muscarinic receptor subtypes, the M5 receptor is the only one detectable in midbrain dopam

25 (3)H]N-methylscopolamine binding site on the M5 receptor, is potent (IC50 = 0.45 nM) in inhibiting ox

26 significantly reduced (but not abolished) in M5 receptor KO mice.

27 ng only PLC-gamma2, overexpressed muscarinic M5 receptors (M5R) activated ACE.

28 eward and withdrawal processes suggests that M5 receptors may represent a novel target for the treatm

29 d that acetylcholine-dependent activation of M5 receptors might modulate the manifestations of opiate

30 These results suggest that M5 receptors on DA neuron terminals enhance DA release,

31 Although activation of somatodendritic M5 receptors on SNc neurons leads to increased neuronal

32 on depended on receptor subtype, with M3 and M5 receptors producing much larger CaV2.3 inhibition tha

33 Despite this, the M5 receptor still activated tyrosine kinases, induced ST

34 23 (KDKKE) with those conserved in the m1/m3/m5 receptor subtype family (ELAAL) had little effect on

35 In the brain, the M5 receptor subtype is preferentially expressed by dopam

36 ld-type mice and mice lacking M1, M3, and/or M5 receptors to determine the relative contribution of M

37 The cDNAs for the Ml, M2, and M5 receptors were not found.

38 Consistent with these observations, a mutant M5 receptor with these three key mutations, M5P179E, Q18

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