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1 ral excitability through a process involving galanin.
2 nist counteracted MAPK activation induced by galanin.
3 ding tyrosine hydroxylase, prodynorphin, and galanin.
4 ivity prevented the proliferative effects of galanin.
5 roduced a complete reversal of the effect of galanin.
6 ular mechanism for the behavioral effects of galanin.
7 e neuroanatomical locus for these effects of galanin.
8 n-specific enolase, mu opioid receptors, and galanin.
9 release was the first reported activity for galanin.
11 whereas the galanin receptor antagonist M40 (galanin-(1-12)-Pro3-(Ala-Leu)2-Ala amide) prevented the
14 The first experiment examined the effects of galanin (10, 20 microg i.c.v.) on the performance of a s
15 e second experiment looked at the effects of galanin (5, 20 microg i.c.v.) on the performance of non-
16 those encoding KLF2, a transcription factor; galanin, a hypothalamic neurohormone; BAX, a proapoptoti
17 and demonstrate the potential involvement of galanin, acetylcholine and serotonin in mediation of the
19 support the hypothesis that GAL-R1 mediates galanin actions on gastrointestinal motility and secreti
24 affects morphine withdrawal signs by using a galanin agonist, galnon, that crosses the blood-brain ba
25 ct opiate withdrawal and that small molecule galanin agonists could be effective in diminishing the p
27 calcitonin gene-related peptide (CGRP), and galanin all are known to have central effects on food in
28 e blood-brain barrier, we designed truncated galanin analogues in which nonessential amino acid resid
29 almitoyl, and cationization into a series of galanin analogues yielded systemically active anticonvul
32 sion of pain mediating sensory neuropeptides galanin and calcitonin gene related peptide (CGRP) in a
33 owed that glial NF-kappaB inhibition reduces galanin and CGRP expression, which are neuropeptides tha
34 ition, co localization of neurons containing galanin and choline acetyl transferase (ChAT) and seroto
35 view here what is known about the ability of galanin and galanin receptors to alter neuronal activity
37 in and LY294002 inhibition demonstrated that galanin and GALR1 induce ERK1/2 activation via Galphai,
39 tion of the transcripts for the neuropeptide galanin and its receptors (GalR1-R3), tryptophan hydroxy
40 scription factor 3 (ATF3), the neuropeptides galanin and neuropeptide Y (NPY), brain-derived neurotro
44 the terminals of RTN-Phox2b neurons contain galanin and VGLUT2 proteins, to identify the specific pr
46 differentiation and define the neuropeptide Galanin as a novel target of this transcription factor.
47 e for this behavior and a potential role for galanin as neuromodulator remains to be identified.SIGNI
48 d GalR3 largely recapitulates the pattern of galanin binding throughout the brain, some discrepancies
49 oughout the brain, correlate with widespread galanin binding, and colocalize with tyrosine hydroxylas
50 ibited no detectable affinity for the (125)I galanin-binding site of GalR2 receptor, an effect consis
52 ediates the inhibition of insulin release by galanin by regulating both K(ATP) and Ca(2+) channels in
53 is of the distributions of the neuropeptides galanin, calcitonin gene related peptide (CGRP), substan
54 distributions of met-enkephalin, vasotocin, galanin, calcitonin gene-related peptide, tyrosine hydro
61 t study examined whether genetic deletion of galanin could affect the locomotor and reinforcing effec
62 l1R ligands: a negative cross talk, by which galanin counteracted MAPK activation induced by the endo
65 cture and expression and the consequences of galanin deficiency in developing zebrafish are unknown.
68 ptors alone is not sufficient to mediate the galanin effect on resting membrane potential and spontan
71 des, including substance P, neurotensin, and galanin, emerged as important mediators in the developme
72 o report of pathogenic mutations in GAL, the galanin-encoding gene, and therefore its role in human e
73 increased expression of orexigenic peptides, galanin, enkephalin, and dynorphin, in the paraventricul
76 tudies, SNAP 37889 partially antagonized the galanin-evoked reduction in hippocampal serotonin (5-hyd
77 ave shown that the endogenous peptide ligand galanin exerts powerful anticonvulsant effect through ac
78 se key markers of specific neurons, although galanin-expressing fibers were in a close spatial proxim
82 these observations underscore heterogeneous galanin expression and raise potential implications for
86 nsight into the biological implication(s) of galanin expression in the PVN and SON will depend, at le
88 r damage, and inflammation, whereas blocking galanin expression with specific vivo-morpholino sequenc
90 (PVN(p)) was predominantly as varicose thin galanin fiber processes while the magnocellular PVN (PVN
92 for NPY as a more appropriate candidate than galanin for future gene therapy trials in pharmacoresist
95 Here we report that variants in genes for galanin (GAL) and its receptors (GALR1, GALR2, GALR3), d
96 nt experiments suggest that the neuropeptide galanin (GAL) and its three G protein-coupled receptors,
98 activity in muscle (mLPL); and (4) elevated galanin (GAL) expression and peptide levels in the anter
99 ditioning (CFC) and messenger RNA (mRNA) for galanin (GAL) in the locus coeruleus (LC) and brain-deri
100 quantitative PCR revealed markedly enhanced galanin (GAL) in the paraventricular nucleus and reduced
105 wild-type (GAL-WT) and knockout mice lacking galanin (GAL-KO) maintained on the 129/OlaHsd background
108 on increases sleep and induces expression of galanin (galn), a hypothalamic sleep-inducing peptide.
111 - and amphetamine-related transcript (CART), galanin, gastrin-releasing peptide (GRP), neuropeptide Y
114 in in the nervous system of vertebrates, the galanin gene structure and expression and the consequenc
116 ranscripts in the following order in the LC: galanin >> GalR3 >> GalR1 > GalR2; in the DRN the rankin
124 ments based on viral vectors encoding NPY or galanin have been shown to effectively suppress seizures
126 se-activating polypeptide, nitric oxide, and galanin), hormonal (e.g. gastrin, cholecystokinin, and g
128 divisions, i.e., a medial portion containing galanin-immunoreactive (-IR) axons and a lateral portion
131 eavy concentration of CCK-, CGRP-, NPY-, and galanin-immunoreactive fibers in the capsular fiber laye
132 l subdivision contains a dense population of galanin-immunoreactive fibers, originating from galanin
134 try and stereology to quantify the number of galanin-immunoreactive intermediate nucleus neurons in e
135 Moreover, they demonstrate that a paucity of galanin-immunoreactive intermediate nucleus neurons is a
137 ed significant increases (P < or = 0.001) in galanin immunoreactivity (IR) in these regions of the S1
138 nucleotides caused complete disappearance of galanin immunoreactivity in the brain until 7 dpf and di
140 atomical studies have shown the existence of galanin immunoreactivity in the medulla oblongata, but a
144 AL-KO mice does not support a major role for galanin in cocaine-induced hyperlocomotion and self-admi
145 ter understand this potential involvement of galanin in executive control, the present study tested t
147 fiber layer and reactivity for CCK, NPY, and galanin in the deeper sensory and fiber layers are relat
150 atment of sham and BDL rats with recombinant galanin increased cholangiocyte proliferation and intrah
155 f other neurotransmitters and contributes to galanin-induced inhibition of gastric acid secretion by
157 n human islets, so that it reads (GALR3) and galanin inhibited insulin secretion only from mouse isle
161 the L4-L6 segments except for an increase in galanin-IR in the dorsal commissure in the L4 segment.
162 centage of bladder afferent cells expressing galanin-IR significantly increased (4-19-fold) after chr
177 Our results indicate that wild-type and galanin knockout mice on a congenic 129/OlaHsd backgroun
181 d containing several neuropeptides including galanin, located in laminas 7 and 10 of the lumbar segme
183 lified by receptors for melanocortins, GnRH, galanin, MCH, orexin, and some chemokine receptors vario
185 , and thus can be targeted to manipulate the galanin-mediated physiological and behavioral responses.
186 ng that GalR1 may play a predominant role in galanin-mediated regulation of dopamine neurotransmissio
187 ing that these isoforms may be important for galanin-mediated regulation of noradrenergic transmissio
190 physical activity in rats upregulates prepro-galanin messenger RNA levels in the locus coeruleus.
193 rgic Phox2b(+)/TH(-) neurons of the RTN, but galanin mRNA identifies only half of these putative cent
195 d that 14 days of FLX treatment up-regulated galanin mRNA levels by 100% and GalR2-binding sites by 5
196 gic nuclei: Electroconvulsive shock elevated galanin mRNA levels in dorsal raphe nucleus, whereas sle
197 nucleus, whereas sleep deprivation increased galanin mRNA levels in the locus coeruleus, further unde
207 cystokinin, corticotropin releasing hormone, galanin, neuropeptide Y, neurotensin, preproenkephalin a
210 y by attenuating the inhibitory influence of galanin on 5-HT transmission at the level of the dorsal
211 mechanisms that may underlie the effects of galanin on behaviors involved in responses to stress and
215 xplain previous results showing antagonistic galanin-opioid interactions and offers a new therapeutic
219 h galanin gene encoded for a single amidated galanin peptide and a galanin message-associated peptide
220 gnal with the coding sequence for the active galanin peptide significantly attenuated in vivo focal s
224 versus caudal DRN, and a high proportion of galanin-positive cells in the midline also contained NAD
225 in situ hybridization, we found that pre-pro-galanin (PPGal) mRNA is expressed by an isolated cluster
226 of Nmb, but low levels of Kcnk5/Gpr4/pre-pro-galanin/pre-pro-enkephalin, and do not respond to hyperc
227 monstrate that the RA-mediated activation of Galanin promoter activity and Brn-3a N-terminal transcri
228 rgistically with RA treatment to up-regulate Galanin promoter activity; that the activity of the N-te
231 we identified the sites of expression of the galanin receptor 1 (GAL-R1) subtype in the rat stomach a
236 mutant showed antagonistic activity against galanin receptor 1 (GalR1)-mediated response, and decrea
237 ve effects of galanin were via activation of galanin receptor 1 expressed specifically on cholangiocy
238 different models of chronic pain requires a galanin receptor 1-triggered depression of excitatory sy
240 riment indicated that galnon, a nonselective galanin receptor agonist, did not affect cocaine-induced
241 Direct activation of galanin receptors by a galanin receptor agonist, galnon, was found to produce a
242 ) neurons, inhibited OX neurons, whereas the galanin receptor antagonist M40 (galanin-(1-12)-Pro3-(Al
245 For example, GalR3 seems to be the important galanin receptor in both the human LC and DRN versus Gal
248 ese MORs form functional heteromers with the galanin receptor subtype Gal1 (Gal1R), which modulate th
251 discrepancies exist, suggesting that another galanin receptor(s) may be present in some brain areas.
254 -NH(2) motif and exhibited high affinity for galanin receptors (K(i) = 3.5 nM and 51.5 nM for GalR1 a
257 data further implicate brain and spinal cord galanin receptors as drug targets and provide an example
258 The pharmacological exploitation of the galanin receptors as drug targets for treatment of epile
262 at is known about the ability of galanin and galanin receptors to alter neuronal activity, and we dis
265 tivity for the three identified neuropeptide galanin receptors, GalR1, GalR2, and GalR3, was determin
266 inding revealed the presence of both NPY and galanin receptors, while functional receptor binding was
275 may also be relevant to the understanding of galanin signaling in other biological systems, especiall
276 suggest that the p.A39E mutant could impair galanin signaling in the hippocampus, leading to increas
277 together, these data suggest that targeting galanin signaling may be effective for the maintenance o
279 receptors may serve as a molecular gate for galanin signaling, and thus can be targeted to manipulat
280 al evidence that the mutant protein disrupts galanin signaling, strongly supports GAL as the causal g
285 ate analysis revealed a greater relevance of galanin system genes in highly stressed subjects compare
286 Using the same method, the effect of the galanin system genes was stronger than the effect of the
287 near models demonstrated that interaction of galanin system genes with life stressors explained more
288 Previous studies have demonstrated that the galanin system modulates responses to drugs of abuse suc
289 with special relevance for the neuropeptide galanin that also revealed DNA methylation changes at it
291 ivation of GABA(B) receptors is required for galanin to accomplish its modulation on the membrane pro
292 tide selectively counteracted the ability of galanin to block the dendritic dopamine release in the r
295 ts via bile duct ligation (BDL) surgery, and galanin was increased in serum and liver homogenates fro
296 (ATP)) and inhibition of calcium currents by galanin were disrupted by anti-G(o)2alpha antibodies.
297 ations in the expression of the neuropeptide galanin were examined in micturition reflex pathways 6 w
299 Although Nts did not alter OX activity, galanin, which is coexpressed in LepRb(Nts) neurons, inh
300 pes (GALR1, GALR2, and GALR3), which bind to galanin with different affinities and have their own uni
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