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1 phase advancement was mediated via intrinsic cholinergic nerves.
2 tinal polypeptide (VIP) are co-released from cholinergic nerves.
3 The results indicate that baseline airway cholinergic nerve activity is necessarily dependent upon
4 dentified an age-related mechanism along the cholinergic nerve-airway smooth muscle (ASM) axis that u
5 d paradigm wherein osteocytes interface with cholinergic nerves and bone mechanotransduction is regul
11 Specifically, pharmacological inhibition of cholinergic nerve function reduces cardiomyocyte prolife
13 tric oxide, released from non-adrenergic/non-cholinergic nerves, is considered the principle stimulat
21 ted that the homozygous PDAPP mouse exhibits cholinergic nerve terminal degenerative pathology and th
22 have validated these structural metrics with cholinergic nerve terminal in vivo imaging in Parkinson'
23 of the cholinergic basal forebrain predicted cholinergic nerve terminal loss, with most robust correl
24 cellular choline is transported into central cholinergic nerve terminals by 'high' and 'low' affinity
25 xtracellular acetate uptake into hippocampal cholinergic nerve terminals by metabolizing it to acetyl
27 lular acetate is recycled by rat hippocampal cholinergic nerve terminals for the formation and releas
28 Conclusion: Vesamicol receptor mapping of cholinergic nerve terminals in murine brain can be achie
29 s an age-related reduction in the density of cholinergic nerve terminals in the cerebral cortex; at 2
31 itrosative stress in the microenvironment of cholinergic nerve terminals would diminish cholinergic t
32 rotoxin inhibits neurotransmitter release at cholinergic nerve terminals, causing a descending flacci
33 d the rate of nonquantal release of ACh from cholinergic nerve terminals, were computer-simulated, an
38 ure in mice resulted in increased density of cholinergic nerves, which was prevented by inhibiting Tr