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1 r can account for the acceleratory effect of FMRFamide.
2 hanges in excitability differed for 5-HT and FMRFamide.
3 s) are bidirectionally modulated by 5-HT and FMRFamide.
4 concentration tested, nor does it recognize FMRFamide.
5 six Tv neurons express the neuropeptide gene FMRFamide.
6 dentified by sera against the neuromodulator FMRFamide.
7 ' currents with the higher concentrations of FMRFamide.
8 seen following application of high doses of FMRFamide.
9 penings was shorter with FLRFamide than with FMRFamide.
10 und only FMRFamide- and HA immunoreactivity (FMRFamide: 4 optic ganglion cells, 4-5 hair cells; HA: 3
11 ally and in the periphery, the FRFamides and FMRFamide act in distinct ways, apparently through disti
15 ualitatively different from that produced by FMRFamide analogues with no obvious occurrence of subcon
18 monstrate the presence of both FRFamides and FMRFamide and their release, probably from the processes
21 atory peptides, Phe-Met-Arg-Phe-NH(2)-amide (FMRFamide) and gastrin cholecystokinin, demonstrate that
22 ctivity to the peptides Phe-Met-Arg-Phe-NH2 (FMRFamide) and gonadotropin-releasing hormone (GnRH).
25 ation kinetics of ICa,L were not affected by FMRFamide application, nor by internal perfusion with GT
27 t of synapses and the inhibitory transmitter FMRFamide at another, long-term facilitation is blocked
29 iously observed modulation of K+ currents by FMRFamide cannot account for this acceleratory effect in
33 osuppressin, short neuropeptides F, extended FMRFamides], crustacean cardioactive peptide, tachykinin
34 tivities of FaRPs encoded by D. melanogaster FMRFamide (dFMRFamide), myosuppressin (Dms), and sulfaki
35 C expressed in oocytes was less sensitive to FMRFamide (EC(50) = 70 microM) than HaFaNaC (EC(50) = 2
36 ress numerous neuropeptides including kinin, FMRFamides, eclosion hormone (EH), crustacean cardioacti
37 ction of chromatophore muscles; however, the FMRFamide effect is slower and longer lasting than that
41 Continuous application of a concentration of FMRFamide from 30 microM to 1 mM resulted in a reduction
42 ned a cDNA encoding a Phe-Met-Arg-Phe-NH(2) (FMRFamide)-gated Na(+) channel from nervous tissue of th
43 rtial inhibition of current flow through the FMRFamide- gated channel by some part of the agonist or
44 colon, lung, kidney, and tongue, a molluscan FMRFamide-gated channel (FaNaC), and the nematode degene
45 by HtFaNaC is 65 % identical to that of the FMRFamide-gated channel cloned from Helix aspersa (HaFaN
48 indicate that the products of the Drosophila FMRFamide gene function as neurohormones to modulate the
51 r branches, leading ultimately to a two-part FMRFamide-immunoreactive plexus and an apparently separa
53 A fifth bipolar neuron type (tubulin- and FMRFamide-immunoreactive) occurred deeper in the tissue,
54 ls, respectively, were mimicked by exogenous FMRFamide in culture (in vitro), implicating this or a r
55 ilies of RFamide peptides, the FRFamides and FMRFamide, in the central neuronal circuitry and the per
59 hosphate) (GDPbetaS, 100 microM) reduced the FMRFamide-induced inhibition of the peak Ca2+ current.
61 y internal perfusion with GTPgammaS, and the FMRFamide-induced reduction in ICa,L was not relieved by
62 non-hydrolysable GTP analogue, mimicked the FMRFamide inhibition of the Ca2+ current and occluded an
63 t late larval expression of the neuropeptide FMRFamide is dependent on correct levels of Zfh1 and tha
65 These properties include complex patterns of FMRFamide-like (FaRP) neuropeptides, serotonin (5HT) and
66 n summary, we did not observe either GnRH or FMRFamide-like immunoreactivity in the olfactory regions
68 l behaviors, we explored the function of the FMRFamide-like neuropeptide (flp) gene family in regulat
70 s requires ALA depolarization and release of FMRFamide-like neuropeptides encoded by the flp-13 gene.
71 Conformational properties of several similar FMRFamide-like neuropeptides from mollusks were investig
72 here identified a major biological role for FMRFamide-like neuropeptides in nematodes, and we sugges
73 n the nematode, and for normal expression of FMRFamide-like neurotransmitters in the AVK interneurons
77 pment of the NMJ and expression of myoactive FMRFamide-like peptides in specific central neurons, the
78 It does not recognize 35 other AF (A. suum FMRFamide-like) peptides at the highest concentration te
82 neurones high doses of Phe-Met-Arg-Phe-NH2 (FMRFamide) often evoke biphasic inward whole-cell curren
84 (Phe-Leu-Phe-Gln-Pro-Gln-Arg-Phe amide) and FMRFamide (Phe-Met-Arg-Phe amide) generated no current o
90 ective for processing endogenously expressed FMRFamide (Phe-Met-Arg-Phe-NH2)-related peptides (FaRPs)
91 We map the expression of the FRFamide and FMRFamide precursors in the feeding circuitry using in s
94 Ligands for EGL-6 are Phe-Met-Arg-Phe-NH(2) (FMRFamide)-related peptides encoded by the genes flp-10
95 d this information back into the CNS via the FMRFamide-related neuropeptide FLP-21 and its cognate re
97 Evidence is also presented suggesting that FMRFamide-related peptides (FaRPs) also function as neur
100 eptor (GPCR) (C10C6.2) as a receptor for the FMRFamide-related peptides (FaRPs) encoded on the flp15
101 latostatins A, B, C, SIFamide, allatotropin, FMRFamide-related peptides [myosuppressin, short neurope
102 Allatostatin A, allatotropin, SIFamide, FMRFamide-related peptides, short neuropeptide F, myoinh
106 -N-isopropyl)-amiloride (EIPA), enhanced the FMRFamide response in oocytes expressing HtFaNaC cRNA.
110 he greater whole-cell response observed with FMRFamide than with FLRFamide results mostly from a slow
112 rmine halothane' 5 site of action, exogenous FMRFamide was applied to both PeA(E) and PeA(I) cells in
113 ility decreases in SNs were evoked only when FMRFamide was applied to regions along the L7 axon with
114 aptic efficacy were evoked only when 5-HT or FMRFamide was applied to regions with SN varicosities al
116 olished, whereas the inhibitory responses to FMRFamide were maintained and enhanced in duration in 1%
117 othane, the excitatory responses produced by FMRFamide were substantially reduced or abolished, where
118 olism becomes anaerobic in ischaemia) and by FMRFamide (which may mimic the action of related mammali
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