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1                                              DMPP (1-4 microM) had no effect on the rate of spontaneo
2                                              DMPP produced robust increases with minimal release obse
3                                              DMPP-induced [3H]-5-HT release was neither sensitive to
4                                 Cytisine and DMPP seemed to be partial agonists.
5 k order of potency of EPI>>CYT approximately DMPP>NIC.
6           nNOS mRNA expression stimulated by DMPP was antagonized by a protein kinase C antagonist, a
7 receptor agonist dimethylphenylpiperazinium (DMPP) on the evoked release of ACh from motor terminals
8 5380), cytisine, dimethylphenylpiperazinium (DMPP).
9 gonists studied here were similar except for DMPP, which seemed to be a partial agonist compared with
10 th a differing rank order of potency of EPI>>DMPP approximately NIC approximately CYT.
11 of the IAS smooth muscle by EFS (0.25-5 Hz), DMPP, and VIP caused a significant increase in the HO ac
12 st evidence that the nitrification inhibitor DMPP can inhibit the N2 O production from nitrifier-indu
13 st 1,1-dimethyl-4-phenlypiperazinium iodide (DMPP) up to 77%.
14 C), 1,1-dimethyl-4-phenylpiperzinium iodide (DMPP), cytisine (CYT) and epibatidine (EPI) were investi
15 y 1,1-dimethyl-4-phenyl-piperazinium iodide (DMPP) approximately nicotine > acetylcholine > carbachol
16 t 1,1-dimethyl-4-phenyl-piperazinium iodide (DMPP) depolarized PPN neurons early in development, then
17 ulant dimethyl diphenyl piperazinium iodide (DMPP), and neuropeptide vasoactive intestinal polypeptid
18 d 1,1-dimethyl-4-phenyl-piperazinium iodide (DMPP, 100 microM).
19   1,1-Dimethyl-4-phenyl-piperazinium iodide (DMPP, 20 microM) or alpha,beta-methylene ATP (50-100 mic
20 t 1,1-dimethyl-4-phenyl-piperazinium iodide (DMPP; in vivo and in vitro) and by high K+ (in vitro); a
21 loride) and, in the presence of W7, 2 microM DMPP depressed evoked ACh release at 0.5 Hz.
22 n of evoked ACh release at 50 Hz by 2 microM DMPP was abolished by 10 microM of the calmodulin antago
23 , and was not impacted by the application of DMPP.
24                       Most of the effects of DMPP persisted following application of the sodium chann
25 hat PROG co-applied with DMPP inhibited peak DMPP-induced current up to 68% and with 3 min pre-incuba
26 , whereas 1,1-dimethyl-4-phenylpiperazinium (DMPP) was less potent than ACh in some cells (as in the
27  agonist, 1,1-dimethyl-4-phenylpiperizinium (DMPP, 10(-10)-10(-7) M), for 24 h significantly increase
28 on inhibitor 3,4-dimethylpyrazole phosphate (DMPP) significantly reduced the N2 O production from the
29 sing an electrophysiological technique, that DMPP can produce changes in the evoked ACh release from
30                                          The DMPP-induced increase in evoked ACh release was dependen
31 e in ammonia-oxidizing bacteria (AOB) in the DMPP-amended treatments.
32 echniques revealed that PROG co-applied with DMPP inhibited peak DMPP-induced current up to 68% and w

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