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 imaging of an allosteric binding site of the M4 receptor.
2 inhibits modulation of Ca(2+) current by the M4 receptor.
3 one of which was identical to the endogenous M4 receptor.
4 rs, but it increases ACh potency 3.5-fold at M4 receptors.
5 cells transfected with the Gi-coupled M2 and M4 receptors.
6 approximately 1.5-fold by brucine-N-oxide at m4 receptors.
7 n the levels of mRNA encoding the M1, M2 and M4 receptors.
8 ddition to the canonical antikinetic role of M4 receptors.
11 e self-administration through the muscarinic M4 receptor and the histone acetyltransferase Kat5/Tip60
13 acetylcholine dip must interact, via D1 and M4 receptor, and a dopamine dip must interact with adeno
14 ments in rats were related to stimulation of M4 receptors, and that these movements could be suppress
15 Remarkably, pretreatment with muscarinic (m2/m4) receptor antagonists resulted in robust oxotremorine
18 gested that the dopamine release-stimulating M4 receptors are probably located on neuronal cell bodie
20 were found not to be mediated via M1, M2 or M4 receptors, as they were not blocked by the M1-selecti
21 it inhibits [3H]NMS dissociation from M1 to M4 receptors at submillimolar concentrations and from M5
22 and a full agonist with an IC50 of 11 nM at M4-receptors, based on inhibition of cyclic AMP accumula
23 o increases the direct binding of [3H]ACh to M4 receptors but decreases it slightly at M2 receptors.
24 to 5-fold for inhibiting [3H]NMS binding to M4 receptors but has no effect on ACh affinity at M1 to
25 um, which contain autoinhibitory presynaptic M4 receptors, but not from hippocampal slices, which con
26 blocked cloned M2 receptors had no effect on M4 receptors, but slightly increased [(3)H]NMS binding t
27 , suggesting that preferential expression of m4 receptors by striatonigral neurons may contribute to
29 or histological defects, and the m2, m3, and m4 receptors continue to be expressed in brain with no e
34 tivity of N-chloromethyl brucine with ACh on M4 receptor function was also observed, thereby demonstr
35 adaptation was due to a reduced postsynaptic M4 receptor function, resulting from down-regulated rece
36 mediate early gene expression and muscarinic M4 receptor in dopamine D1 receptor-expressing medium sp
38 R-neurons by selectively blocking muscarinic M4 receptors in the NAc-S, which tightly regulate the ac
39 half of all projection neurons, and mRNA for M4 receptors is prevalent only in striatonigral neurons.
40 riatal [3H]dopamine release was abolished in M4 receptor KO mice, significantly increased in M3 recep
41 ability, with blockade of presynaptic m2 and m4 receptors, leading to increased out-of-field firing.
42 hese fibers In contrast, changes in nNOS and M4 receptor location on spinal cord neurons are not resp
43 e most specific antagonists known for M1 and M4 receptors (m1-toxin and m4-toxin), it was screened fo
44 xin that binds with very high specificity to M4 receptors (m4-toxin) was biotinylated for use as a se
45 d selectively to one of five mAChR subtypes, M4 receptors (M4Rs), at their C-terminal regions of seco
47 uculline methochloride suggested that M3 and M4 receptors mediate their dopamine release-modulatory e
48 ggest that pharmacological antagonism of the M4 receptor modulates select behavioral responses in the
49 s tested, nearly all expressed M2-class (m2, m4) receptor mRNAs, whereas m1 receptor mRNA was found i
50 more rigorously compare the distribution of M4 receptors on rat neurons in these pathways a toxin th
52 s a novel, brain-penetrant, highly selective M4 receptor positive allosteric modulator in development
55 ide on acetylcholine (ACh) potency at M1 and M4 receptors respectively have been confirmed in guanosi
56 elease studies with brain slices from M2 and M4 receptor single KO mice indicated that autoinhibition
60 th of cholinergic transmission at muscarinic M4 receptor synapses on direct pathway medium spiny neur
62 expressed in the same zone as the endogenous M4 receptor, the two expression patterns were, in large
64 e muscarinic agonist oxotremorine-M, M2, and M4 receptors underwent significantly reduced internaliza
70 ne (1.0 mM), which blocks presynaptic m2 and m4 receptors, were initially strong but then diminished
71 the orthosteric and allosteric sites of the M4 receptor, which provides new insight into how alloste
72 e M2AChR and a partial agonist at the M1 and M4 receptors, with full antagonist activity at M3- and M