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1 gest nicotine as a neuroprotective agent and nicotinic acetylcholine (ACh) receptors (nAChRs) as targ
3 nergic interneurons (CINs) and activation of nicotinic acetylcholine (ACh) receptors (nAChRs) in DA n
5 te, GABAergic GABAA , muscarinic M1 , M2 and nicotinic acetylcholine (nACh; alpha4 beta2 subtype), no
6 evidence to indicate that the stimulation of nicotinic acetylcholine alpha7 receptors (nAChRa7s) can
7 kynurenic acid, an antagonist of both alpha7 nicotinic acetylcholine and N-methyl-D-aspartate recepto
10 is (MG) without detectable antibodies to the nicotinic acetylcholine receptor (AChR) or to muscle-spe
13 SY5Y cells stably overexpressing the alpha-7 nicotinic acetylcholine receptor (alpha7-nAChR), a poten
14 ation in normal and cancer cells, the alpha7 nicotinic acetylcholine receptor (alpha7-nAChR), was mor
16 Here, we show that ILC2s express the alpha7-nicotinic acetylcholine receptor (alpha7nAChR), which is
17 septal cholinergic fibers through the alpha7-nicotinic acetylcholine receptor (alpha7nAChR), whose ac
19 s16969968 that alters function of the alpha5 nicotinic acetylcholine receptor (CHRNA5) and noncoding
20 er cognitive processes that are modulated by nicotinic acetylcholine receptor (nAChR) activation by c
21 linical trials suggest that drugs that alter nicotinic acetylcholine receptor (nAChR) activity can af
22 hether extending plasma levels of the alpha7-nicotinic acetylcholine receptor (nAChR) agonist 3-(2,4-
24 ation of nicotine or ABT-418, an alpha4beta2 nicotinic acetylcholine receptor (nAChR) agonist, normal
26 Conotoxin GeXIVA inhibits the alpha9alpha10 nicotinic acetylcholine receptor (nAChR) and is analgesi
31 t promote a desensitized state of the alpha7 nicotinic acetylcholine receptor (nAChR) have been assoc
32 associate with this soluble surrogate of the nicotinic acetylcholine receptor (nAChR) in a cooperativ
36 y a critical role in the characterization of nicotinic acetylcholine receptor (nAChR) structure and f
38 ar domain (ECD) of the human neuronal alpha2 nicotinic acetylcholine receptor (nAChR) subunit in comp
40 s for CHRNA7, the gene coding for the alpha7 nicotinic acetylcholine receptor (nAChR), and manifest a
43 ed transcripts of several targets, including nicotinic acetylcholine receptor alpha 1 and alpha 2 sub
44 agus nerve regulation of splenic cholinergic nicotinic acetylcholine receptor alpha7 (nAChRa7) signal
45 RV fibrosis, RV inflammation, and RV alpha-7 nicotinic acetylcholine receptor and muscarinic acetylch
46 ters = primary outcome variables) as well as nicotinic acetylcholine receptor expression, muscle mass
49 Isoform-specific mechanisms of alpha3beta4*-nicotinic acetylcholine receptor modulation by the proto
51 f nicotine dependence and stimulation of the nicotinic acetylcholine receptor on the ability to inter
52 "spiroimidates") and their utility as alpha7 nicotinic acetylcholine receptor partial agonists are de
54 ommon variants near the apolipoprotein E and nicotinic acetylcholine receptor subunit alpha 5 genes a
55 active with ion channels of the ligand-gated nicotinic acetylcholine receptor superfamily (namely alp
58 f the anti-inflammatory alpha7-nAChR (alpha7-nicotinic acetylcholine receptor) was similar in young S
59 may, by increasing activation of the alpha7-nicotinic acetylcholine receptor, alter the development
60 MS stem from molecular defects in the muscle nicotinic acetylcholine receptor, but they can also be c
62 ed tool to probe the ion channel pore of the nicotinic acetylcholine receptor, which is a prototypica
63 unique cell types expressing alpha8 subunit nicotinic acetylcholine receptor, while SPO and cOv are
64 te smoke (SS), or secondhand smoke, promoted nicotinic acetylcholine receptor-dependent exacerbation
65 clothianidin, but not imidacloprid, causes a nicotinic acetylcholine receptor-dependent rapid mitocho
66 ation of antiinflammatory effects via alpha7 nicotinic acetylcholine receptor-expressing splenic macr
69 d alpha3- and beta4-subunit-containing human nicotinic acetylcholine receptors (alpha3beta4*-nAChRs).
71 the integration of neural signals and alpha7 nicotinic acetylcholine receptors (alpha7nAChRs) on sple
73 level of nonsmokers following stimulation of nicotinic acetylcholine receptors (familywise error-corr
75 tional regulation and synaptic clustering of nicotinic acetylcholine receptors (nAChR) during neurotr
76 ificant associations between variants in the nicotinic acetylcholine receptors (nAChR) subunits and n
88 ives significant cholinergic innervation and nicotinic acetylcholine receptors (nAChRs) contribute gr
89 ng the most widely co-abused substances, and nicotinic acetylcholine receptors (nAChRs) contribute to
91 andoxin and shows high binding affinity with nicotinic acetylcholine receptors (nAChRs) expressed on
92 menthol enhances nicotine-induced changes in nicotinic acetylcholine receptors (nAChRs) expressed on
93 anatomical localisation and function of the nicotinic acetylcholine receptors (nAChRs) formed by the
95 The data suggest a complex interaction of nicotinic acetylcholine receptors (nAChRs) in regulating
96 X-12 over PhTX-343 for embryonic muscle-type nicotinic acetylcholine receptors (nAChRs) in TE671 cell
97 otine use induces functional upregulation of nicotinic acetylcholine receptors (nAChRs) in the mesoco
100 ulation of beta2 subunit-containing (beta2*) nicotinic acetylcholine receptors (nAChRs) is implicated
103 actions, but very little is known about how nicotinic acetylcholine receptors (nAChRs) regulate LHb
104 ng the expression and clustering of neuronal nicotinic acetylcholine receptors (nAChRs) remain poorly
105 and impact of aging on presynaptic neuronal nicotinic acetylcholine receptors (nAChRs) within the ci
107 al homologs of the ligand-binding domains of nicotinic acetylcholine receptors (nAChRs), and they rep
118 pamine neurons receive cholinergic input via nicotinic acetylcholine receptors from the Kenyon cells;
119 ore, phosphomimetic Dok-7 mutants aggregated nicotinic acetylcholine receptors in C2C12 myotubes with
120 texts that predict alcohol, and suggest that nicotinic acetylcholine receptors in the NAc are critica
121 Inactivation of 42 genes, including the nicotinic acetylcholine receptors nAChRalpha1 and nAChRa
123 sitivity and acute effects of stimulation of nicotinic acetylcholine receptors on behavioral and neur
124 survival in animal sepsis models via alpha7 nicotinic acetylcholine receptors on immunocompetent cel
125 r behaviour in animals through inhibition of nicotinic acetylcholine receptors present in the central
126 resting conformation, and in skeletal muscle nicotinic acetylcholine receptors there is an exponentia
127 sphorylation of the ER-resident chaperone of nicotinic acetylcholine receptors, RIC-3, leads to incre
134 control abilities.SIGNIFICANCE STATEMENT The nicotinic acetylcholine system plays a central role in n
137 se brain slices, we found that ACh generated nicotinic ACh receptor (nAChR)-mediated depolarizing pot
138 l FFA3 suppresses Cl(-) secretion induced by nicotinic ACh receptor activation via a Gi/o pathway.
140 ocation and function of presynaptic neuronal nicotinic ACh receptors (nAChRs) at the major inputs to
141 naptic function and pharmacology of neuronal nicotinic ACh receptors (nAChRs) in young adult and the
142 it striatal DA release through activation of nicotinic ACh receptors (nAChRs) on DA axonal projection
143 itter acetylcholine (ACh) activates calyceal nicotinic ACh receptors (nAChRs); however, it is unclear
146 thyl-5,6,7,8-tetrahydronaphthalen-2-yl)amino)nicotinic acid (NEt-TMN) were synthesized and assessed f
147 unctionalized substituents introduced at the nicotinic acid 5-position are recognized by the sea urch
148 hat LarB carboxylates the pyridinium ring of nicotinic acid adenine dinucleotide (NaAD) and cleaves t
150 metabolites by phosphorylating nicotinamide/nicotinic acid adenine dinucleotide at the adenosine 3'-
151 Both products of AvrRxo1, 3'-NADP and 3'-nicotinic acid adenine dinucleotide phosphate (3'-NAADP)
158 e-targeted calcium release channels gated by nicotinic acid adenine dinucleotide phosphate, as also a
159 ases the myocardial levels of 3 metabolites, nicotinic acid adenine dinucleotide, methylnicotinamide,
160 ve substituted at both the 5-position of the nicotinic acid and at the 8-adenosyl position was also r
161 nadC in B. bronchiseptica was influenced by nicotinic acid and by a NadQ family transcriptional repr
164 thalpy of the OHN LBHB formed in crystalline nicotinic acid is only 7.7+/-0.5 kcal mol(-1) , suggesti
165 onucleotides nicotinamide mononucleotide and nicotinic acid mononucleotide (NAMN) and thus catalyze N
169 related to the consumption of peas (N-methyl nicotinic acid), apples (rhamnitol), and onions (N-acety
171 , flufuran, gregatin B, hydroxysydonic acid, nicotinic acid, phomaligin A, spinulosin and terrein.
173 onjugated with neuroactive carriers, namely, nicotinic acid, valproic acid, theophylline-7-acetic aci
174 improved by a more stable but still reactive nicotinic acid-derived tetrazine and by changing the key
179 or binding pose that differs from classical nicotinic agonists and antagonists and from the previous
182 tion of this projection elicits monosynaptic nicotinic and GABAergic currents in glomerular layer-pro
184 tween gamma and theta oscillations, and both nicotinic and muscarinic receptor activity contributed t
185 ne release, through distinct actions at both nicotinic and muscarinic receptors, triggers a processio
188 modeling of DPA docking to GABArho1, alpha7 nicotinic, and 5-HT3A receptors suggests that a hydropho
189 s of DPA on human homomeric GABArho1, alpha7 nicotinic, and 5-HT3A serotonin receptors expressed in X
192 duced seizures, and validated TGFBR2 and the nicotinic antiinflammatory acetylcholine receptor nAChRa
194 city, we found that the deletion of Lynx1, a nicotinic "brake" for functional plasticity, doubled the
198 Here we used the selective expression of the nicotinic cholinergic receptor alpha2 (Chrna2) in mice t
200 xpressed in the nervous system that modulate nicotinic cholinergic signaling, but their functions and
201 igestion (CHGA360-373) selectively inhibited nicotinic cholinergic stimulated catecholamine release f
203 data support the notion that modulating the nicotinic cholinergic system might help to maintain long
204 Existing programs attempting to develop nicotinic drugs that might exert this apparent neuroprot
206 neurons have been shown to provide intrinsic nicotinic excitation of local GABAergic interneurons, wh
207 tation in NGF interneurons and a disynaptic, nicotinic excitation through cholinergic interneurons.
208 Maternal cigarette smoke, including prenatal nicotinic exposure (PNE), is responsible for sudden infa
211 eover, converging data are consistent with a nicotinic-GABAergic mechanism of multisensory integratio
216 icotinic receptors or biphasic GABAergic and nicotinic neurotransmission conveyed by GABA and ACh cor
217 teral DA neurons received mainly excitatory (nicotinic or glutamatergic) mediated cholinergic neurotr
221 ing homozygous variants of cholinergic gamma nicotinic receptor (CHRNG, 6 subjects) and endothelin co
223 f long-term depression by nicotine relied on nicotinic receptor activation and key regulators of NRG3
224 rular sensitivity to weak odor input whereas nicotinic receptor activation decreases sensitivity to s
225 and safety of 3 doses of ABT-126, an alpha7 nicotinic receptor agonist, for the treatment of cogniti
227 d a common polymorphism of the high-affinity nicotinic receptor alpha4beta2 (rs1044396 on the CHRNA4
228 f a common polymorphism of the high-affinity nicotinic receptor alpha4beta2 that is consistent across
229 nic (atropine, 0.1 mumol l(-1) , n = 6) or a nicotinic receptor antagonist (mecamylamine, 10 mumol l(
230 tion of carbamylcholine was prevented by the nicotinic receptor antagonist mecamylamine, inhibitors o
231 croinfusions of mecamylamine, a nonselective nicotinic receptor antagonist, highlight a major role fo
232 protective effect could also be induced by a nicotinic receptor antagonist, suggesting that xenobioti
234 evoked dopamine release, with muscarinic and nicotinic receptor antagonists causing suppression and a
235 tion of enteric neurons was inhibited by the nicotinic receptor antagonists hexamethonium and dihydro
236 we demonstrate that splenic injection of the nicotinic receptor blocker alpha-bungarotoxin increased
239 The same peptides significantly altered a nicotinic receptor induced behaviour in C. elegans and i
240 tor was described in landmark studies of the nicotinic receptor isolated from the electric organ of T
243 cy and safety of ABT-126, a selective alpha7 nicotinic receptor partial agonist, in stable patients w
244 esting that xenobiotic exposure, rather than nicotinic receptor signaling, is responsible for program
245 on VFT that depends upon both muscarinic and nicotinic receptor stimulation, where the generation of
246 on VFT that depends upon both muscarinic and nicotinic receptor stimulation, where the generation of
248 centrations of ethanol inhibit activity of a nicotinic receptor subtype that is expressed in brain ar
249 nsynonymous variant rs16969968 in the alpha5 nicotinic receptor subunit gene (CHRNA5) is the stronges
251 NIC) treatment or specific deletion of beta2 nicotinic receptor subunits in dopamine neurons mitigate
252 ale neuroimaging genetics study of the human nicotinic receptor system (two cohorts, males and female
254 her loci include genes such as a cholinergic nicotinic receptor, CHRNA2, and the telomere-related gen
255 lographic structure of the human alpha4beta2 nicotinic receptor, the most abundant nicotinic subtype
258 ed nicotine upregulation of alpha4beta2-type nicotinic receptors (alpha4beta2Rs) in live cells and ne
261 two neurotransmitters activate two types of nicotinic receptors (nAChRs) (the homomeric alpha7 recep
263 search shows that compounds acting at alpha7 nicotinic receptors (nAChRs) can reduce nicotine self-ad
264 mine release in the striatum via presynaptic nicotinic receptors (nAChRs) on dopamine axon terminals.
265 d/or receptor expression of beta2-containing nicotinic receptors alters presynaptic and postsynaptic
266 le Renshaw cell is more than halved when the nicotinic receptors are blocked, confirming that the two
267 the fields of pharmacology and neurobiology, nicotinic receptors are important therapeutic targets fo
269 an IC50 of 1.6 microM, an enhancer of alpha7 nicotinic receptors at relatively high concentrations of
270 tor activity attenuated, whereas blockade of nicotinic receptors augmented cue-induced invigoration o
271 an alpha-conotoxin that inhibits Drosophila nicotinic receptors but not its vertebrate counterparts.
272 current study found that ACh stimulation of nicotinic receptors comprised of alpha4 and beta2 subuni
274 acetylcholine receptors, including neuronal nicotinic receptors comprising alpha4 and beta2 subunits
275 r antagonist, highlight a major role for the nicotinic receptors expressed in medial habenula and int
277 bited acetylcholine responses of alpha4beta2 nicotinic receptors in vitro, as did full length ectodom
278 o be due, at least in part, to activation of nicotinic receptors on GABAergic NPY-neurogliaform inter
279 tually mediated by activation of presynaptic nicotinic receptors on nigrostriatal terminals that evok
280 y GABAergic currents mediated by presynaptic nicotinic receptors or biphasic GABAergic and nicotinic
282 tion or a downregulation of beta2-containing nicotinic receptors protects the striatal network agains
284 ometry, and the expression of muscarinic and nicotinic receptors was evaluated by flow cytometry or q
285 elease is (1) dependent of the activation of nicotinic receptors, (2) independent on the spontaneous
287 stigmine can potentiate and inhibit neuronal nicotinic receptors, in addition to inhibiting the activ
288 ffects of KYNA on cannabinoid reward involve nicotinic receptors, in the present study we used rat an
294 tudies identify Ash2l as a target induced by nicotinic stimulation that couples developmental nicotin
296 earning, because selective deletion of beta2 nicotinic subunits in dopamine neurons reduced D2R-media
297 srupted premotor rhythms, as did blockade of nicotinic synapses in the motor nucleus (the putative lo
300 rplay is underpinned by marked remodeling of nicotinic systems, causing increased ventral tegmental a
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