ライフサイエンスコーパス: neurotransmitter

1 ramides, 3 branched chain amino acids, and 9 neurotransmitters).

2 mpulsivity in proportion to the loss of each neurotransmitter.

3 tors that match the presynaptically released neurotransmitter.

4 nal subtypes utilize more than one classical neurotransmitter.

5 ecture by altering the intestinal balance of neurotransmitters.

6 using a combination of glutamate and GABA as neurotransmitters.

7 h the opening of an ion pore upon binding of neurotransmitters.

8 ansmission by uptake and catabolism of major neurotransmitters.

9 han metabolism, and synthesis/degradation of neurotransmitters.

10 ebrates and cephalopods use many of the same neurotransmitters.

11 calcium signals in response to hormones and neurotransmitters.

12 ation by controlling the activity of ambient neurotransmitters.

13 nels that are directly activated by chemical neurotransmitters.

14 ical impulses into the exocytotic release of neurotransmitters.

15 l directions, and modulated by catecholamine neurotransmitters.

16 antidepressant medication that targets these neurotransmitters.

17 ella lenta that dehydroxylates catecholamine neurotransmitters.

18 DA discrimination in the presence of various neurotransmitters.

19 for responses to volatile anaesthetics(10), neurotransmitters(13) and G-protein-coupled receptors(13

20 cluster and synaptic vesicles release their neurotransmitters(2).

21 The endogenous neurotransmitter acetylcholine (ACh) is known to affect

22 The enteric neurotransmitter acetylcholine governs important intesti

23 The neurotransmitter acetylcholine influences how male finch

24 , converts the free energy of binding of the neurotransmitter acetylcholine into opening of its centr

25 rs, which are activated by the nerve-derived neurotransmitter acetylcholine, we show that muscarinic

26 Coherently, changes in neurotransmitters activity impact the functional configu

27 On the other hand, if one invokes unspecific neurotransmitter adsorption to the bilayer-a process not

28 iologically influenced by immune modulators, neurotransmitters, affective states, and even the underl

29 ptic shaping or through the trophic support, neurotransmitter and ion homeostasis, cytokine signaling

30 to disentangle effects of drugs on different neurotransmitters and clarify the biological mechanisms

31 mitochondrial enzyme that degrades monoamine neurotransmitters and dietary amines, in stromal cells e

32 zyme that catalyzes oxidative deamination of neurotransmitters and dietary amines.

33 ells is a convergence point of regulation by neurotransmitters and mediators of kidney injury, and ma

34 d investigated how this activity responds to neurotransmitters and mediators of kidney injury.

35 rate vocal patterns, as well as the roles of neurotransmitters and neuromodulators in activating the

36 d to relay these signals to immune cells via neurotransmitters and neuropeptides is indispensable for

37 Hereby we have focussed on signaling neurotransmitters and neuropeptides which may be a targe

38 We provide evidence for the use of multiple neurotransmitters and neuropeptides, and identify transc

39 urotransmission is based on the corelease of neurotransmitters and protons from synaptic vesicles, an

40 tion and provide an overview of the possible neurotransmitters and receptors involved.

41 to investigate the relationship between such neurotransmitters and RSNs in healthy, by reviewing the

42 onents (e.g., synaptic proteins, organelles, neurotransmitters and their receptors) are selectively d

43 in an imbalance of inhibitory and excitatory neurotransmitters, and as Gad1-/- mice die neonatally of

44 non-invasive cancer diagnosis, monitoring of neurotransmitters, and assessment of bone disease.

45 Neurotransmitters are important chemicals in human physi

46 obial regulation of short-chain fatty acids, neurotransmitters, as-yet-uncharacterized biochemicals,

47 membranes, reveal the structural aspects of neurotransmitters' association with zwitterionic and ani

48 es lack fast synaptotagmin isoforms, release neurotransmitter asynchronously, and are exclusively GAB

49 ators bind to sites that are remote from the neurotransmitter binding site, but modify coupling of li

50 es other roles, BH4 functions as cofactor in neurotransmitter biosynthesis.

51 SCV) is widely used for in vivo detection of neurotransmitters, but identifying analytes, particularl

52 Some neurotransmitters can facilitate action potential firing

53 ions or rapid, robust, direct measurement of neurotransmitter concentration in isolated vesicles from

54 r the Ca(2+) ions that trigger the fusion of neurotransmitter-containing vesicles with the presynapti

55 Because these neurons release neurotransmitter continuously, synaptic ribbons are assu

56 crine control of hormonal signaling, altered neurotransmitter control of nervous system function, and

57 nd receptors in OPCs and oligodendrocytes by neurotransmitters converges on regulating intracellular

58 Using connectomic and neurotransmitter data, we propose a circuit model that c

59 ME) by sustaining the calcium transients and neurotransmitter-dependent communication among CRC cells

60 ation will be critical in achieving reliable neurotransmitter detection for the duration of long-term

61 and mechanistic basis of the effects of the neurotransmitter dopamine (DA) on inflammation remain un

62 -reward associations have been linked to the neurotransmitter dopamine in humans, the specific contri

63 When deciding to act, the neurotransmitter dopamine is implicated in a valuation o

64 The neurotransmitter dopamine is implicated in diverse funct

65 The neurotransmitter dopamine is required for the reinforcem

66 solimbic reward circuitry and release of the neurotransmitter dopamine that contribute to the develop

67 concept, sensors were produced to detect the neurotransmitter dopamine with high reproducibility and

68 so adapt the sensor design for detecting the neurotransmitter dopamine, illustrating versatility of t

69 se elevations in extracellular levels of the neurotransmitter dopamine.

70 tection performances were determined for the neurotransmitters dopamine and serotonin, exhibiting lin

71 and, via tyrosine, is the precursor for the neurotransmitters dopamine, norepinephrine, and epinephr

72 sive treatment of disorders characterized by neurotransmitter dysfunction.

73 Synaptic vesicles accumulate neurotransmitters, enabling the quantal release by exocy

74 de the perspective that ACh, like most other neurotransmitters, exhibits both fast and slow modes tha

75 a fundamental property of synapses in which neurotransmitter filled vesicles release their content i

76 phy (PET) enables non-invasive estimation of neurotransmitter fluctuations in the living human brain.

77 les fuse with the plasma membrane to release neurotransmitter following an action potential, after wh

78 strin-releasing peptide (GRP) functions as a neurotransmitter for non-histaminergic itch, but its sit

79 Calcium (Ca(2+))-evoked release of neurotransmitters from synaptic vesicles requires mechan

80 erstitial space, influences the diffusion of neurotransmitters from the synaptic cleft and the volume

81 ry neurotransmitter glutamate and inhibitory neurotransmitter GABA in regulating delay activity in rh

82 Efficient reuptake of the inhibitory neurotransmitter GABA is essential, and reuptake failure

83 the developmental switch of response to the neurotransmitter GABA, from excitatory depolarization to

84 group of cells that generate the inhibitory neurotransmitter GABA.

85 ought to arise from increased release of the neurotransmitter GABA.

86 pressed markers for the canonical inhibitory neurotransmitters GABA or glycine, but several expressed

87 (ipRGCs) in mice that release the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) at non-i

88 AD), a PLP-dependent enzyme synthesizing the neurotransmitter gamma-aminobutyric acid (GABA), define

89 fect of the p.R47H variant on the inhibitory neurotransmitter gamma-aminobutyric acid.

90 and only H1 store and release the inhibitory neurotransmitter, gamma-aminobutyric acid (GABA).

91 Thus, ASICs have become bona fide neurotransmitter-gated ion channels, activated by the sm

92 We probed the effects of excitatory neurotransmitter glutamate and inhibitory neurotransmitt

93 The excitatory neurotransmitter glutamate has been implicated in experi

94 VGLUTs) concentrate the principal excitatory neurotransmitter glutamate into synaptic vesicles, drive

95 reviously published paper indicated that the neurotransmitter glutamate, along with the compounds N-m

96 m and are responsible for fast uptake of the neurotransmitter glutamate, essential for neuronal funct

97 ceptors (AMPARs), which are activated by the neurotransmitter glutamate.

98 ctions through the release of the excitatory neurotransmitter glutamate.

99 f plasticity are initiated by the excitatory neurotransmitter glutamate.

100 Reductions in the neurotransmitters glutamate and GABA correlate with impu

101 ic mutant GlyRs became less sensitive to the neurotransmitter glycine.

102 identified all the cells that express every neurotransmitter GPCR and genetically analyzed how each

103 This map of neurotransmitter GPCR expression and function in the egg

104 We found that many neurotransmitter GPCRs are expressed in each neuron, tha

105 we mapped which cells express each of the 26 neurotransmitter GPCRs of this organism and also genetic

106 To determine how neurotransmitter GPCRs together help regulate function o

107 One neurotransmitter, histamine (HA), has been well studied

108 formation from extracellular signals such as neurotransmitters, hormones, or drugs to cellular respon

109 rods microelectrodes were applied to detect neurotransmitters, i.e., dopamine (DA), serotonin (5-HT)

110 ctions in lineage 11A to promote cholinergic neurotransmitter identity and suppress the GABA fate.

111 rotransmitter switching, involves changes in neurotransmitter identity.

112 cular dysfunction, altered brain metabolism, neurotransmitter imbalance and impaired neuronal network

113 In addition to classical neurotransmitters, immunocytochemistry has provided evid

114 nical stimuli by releasing neuropeptides and neurotransmitters, implicating them as airway sensors.

115 Glutamate is the major excitatory neurotransmitter in the brain, and photochemical release

116 (beta-NAD) is an important inhibitory motor neurotransmitter in the enteric nervous system.

117 (VGluT2) and releases glutamate as a second neurotransmitter in the striatum, while only few adult s

118 uT2) and thus releases glutamate as a second neurotransmitter in the striatum.

119 bitory (gamma-amino butyric acid) amino acid neurotransmitters in brain, and is a source of energy du

120 imultaneous subsecond monitoring of multiple neurotransmitters in freely behaving rats.

121 the major excitatory (E) and inhibitory (I) neurotransmitters in the brain, respectively.

122 d glutamate are the most abundant amino acid neurotransmitters in the brain.

123 However, concentration of neurotransmitters in the human body is very low (nM or p

124 spatial resolution of fMRI to predict local neurotransmitters in the PFC.

125 t study aimed to elucidate the role of these neurotransmitters in the social learning process using a

126 neurons release chemical messengers, termed neurotransmitters, in response to action potential invas

127 e describe examples that include identifying neurotransmitters, including cases of apparent co-releas

128 neuronal activity, but the specifics of how neurotransmitter-induced calcium activity regulates neur

129 Tropane alkaloids from nightshade plants are neurotransmitter inhibitors that are used for treating n

130 Direct visualization of neurotransmitter inputs to LC11 confirmed the model conj

131 In neurons, the loading of neurotransmitters into synaptic vesicles uses energy fro

132 our understanding of the brain circuits and neurotransmitters involved in binge-eating disorder path

133 giotrophoblast to GC area suggests that this neurotransmitter is essential for maintaining cells with

134 And even when neurotransmitter is released, the resulting change in sy

135 GABA, an inhibitory neurotransmitter, is synthesized by glutamic acid decarb

136 ces deficits in social behaviors, and alters neurotransmitter levels in peripheral tissues in recipie

137 ynaptic signaling accompanied by recovery of neurotransmitter levels in the hippocampus.

138 oach provides greater spatial specificity on neurotransmitter levels, potentially improving the under

139 er, most psychoactive agents act on multiple neurotransmitters, limiting the ability of fMRI to ident

140 de orexin signaling are critical circuit and neurotransmitter mechanisms involved in this form of cog

141 easure equilibrium dissociation constants in neurotransmitter membrane association.

142 aspartate: lower in AD, p = 0.002); and (6) neurotransmitter metabolism (gamma-amino-butyric acid: l

143 s and breakdown, as well as abnormalities in neurotransmitter metabolism that are related to AD.

144 The neurotransmitter metabolite 3,4-dihydroxy-phenylglycolal

145 DA is one of the key neurotransmitters monitored for the diagnosis and during

146 igh charge injection capability and reliable neurotransmitters monitoring using amperometric techniqu

147 , proteins, immune molecules, neuropeptides, neurotransmitters, mRNA, and noncoding RNA expression si

148 The neurotransmitter N-acetyl-aspartyl-glutamate (NAAG) is t

149 many different signaling molecules, such as neurotransmitters, neurohormones and neuropeptides.

150 Acetylcholine acts as a neurotransmitter/neuromodulator of many central nervous

151 ombinatorial molecular codes that arise from neurotransmitters, neuropeptides and transcription facto

152 In addition to classical neurotransmitters, neuropeptides are emerging as modulat

153 In addition to classical neurotransmitters, neuropeptides have emerged to modulat

154 athetic nerves leads to burst release of the neurotransmitter noradrenaline (also known as norepineph

155 on gradient and that are stimulated with the neurotransmitter noradrenaline model the structure of th

156 According to the reviewed data, neurotransmitters nuclei diffusively project to subcorti

157 that fulfills diverse functional roles as a neurotransmitter or diffusible second messenger in the d

158 Na(+) -dependent symporters for amino acids, neurotransmitters, osmolytes, or creatine.

159 activity-dependent release of small-molecule neurotransmitters packaged into synaptic vesicles (SVs).

160 cification of a subset of spinal interneuron neurotransmitter phenotypes, as well as correct lateral

161 This neurotransmitter plasticity is activity-dependent, as wa

162 n and DNA methylation may contribute to this neurotransmitter plasticity.

163 Third, imbalances in neurotransmitter-positive GCs and an observed decrease i

164 ated ion channels, activated by the smallest neurotransmitter possible: protons.

165 Our results demonstrate that a neurotransmitter produced by gut bacteria mimics the fun

166 irectly from brain tissue and determined the neurotransmitter profiles of diverse brain regions in a

167 In the present study, we mapped the major neurotransmitter projections to the VTA through cell-typ

168 Local measures of neurotransmitters provide crucial insights into neurobio

169 lts identify roles for IRE1alpha and BARP in neurotransmitter receptor assembly and unlock drug disco

170 the complex biological processes defined by neurotransmitter receptor function.

171 cones and transsynaptically recruits the key neurotransmitter receptor mGluR6 in ON-BCs to enable syn

172 achinery play critical roles in postsynaptic neurotransmitter receptor trafficking, which is essentia

173 The actin cytoskeleton can regulate neurotransmitter receptors and ion channels by controlli

174 Neurotransmitter receptors and ion channels shape the bi

175 or the localization and activity of synaptic neurotransmitter receptors and ion channels.

176 brain depends on specialized organization of neurotransmitter receptors and scaffolding proteins with

177 The nanoscale co-organization of neurotransmitter receptors facing presynaptic release si

178 tors (AMPARs) are the predominant excitatory neurotransmitter receptors in the brain, where they medi

179 , the basis of specification of postsynaptic neurotransmitter receptors matching the newly expressed

180 s, from the sign of the response mediated by neurotransmitter receptors to the dynamics shaped by vol

181 ct receptors, epithelial cells often express neurotransmitter receptors, and receptors are often posi

182 ity features, such as expression of specific neurotransmitter receptors, ion channels and neuropeptid

183 increased signaling via forebrain Gq-coupled neurotransmitter receptors.

184 We found an enrichment in neurotransmitter-related pathways in microdissected-migr

185 ling" maintained the relative differences in neurotransmitter release across all inputs around a home

186 n which caused uniform downscaling of evoked neurotransmitter release across all inputs through decre

187 The eCBs mediates inhibition of neurotransmitter release and acts as a major homeostatic

188 ynaptic glutamate receptors (GluRs) modulate neurotransmitter release and are physiological targets f

189 n implicated in spontaneous and asynchronous neurotransmitter release and compete with Syt1 for bindi

190 cent glutamate indicators (iGluSnFRs) enable neurotransmitter release and diffusion to be visualized

191 del of SYT1 and SYT7 mediating all phases of neurotransmitter release and facilitation is not applica

192 Exogenous Mel inhibits neurotransmitter release and promotes sleep in wild-type

193 el synthesis) causes substantially increased neurotransmitter release and shortened sleep duration, a

194 notypes, specific alterations in spontaneous neurotransmitter release are a key factor to account for

195 release from intracellular stores can drive neurotransmitter release as well as subsequent signallin

196 Efficient neurotransmitter release at the presynaptic terminal req

197 not only the proximal Ca(2+) sensor for fast neurotransmitter release but also serves to clamp sponta

198 Ca(2+)-evoked release, RIM uniquely controls neurotransmitter release efficiency.

199 iour in an open-field assay, and depended on neurotransmitter release from VMHdm(SF1) neurons.

200 tion converted synchronous into asynchronous neurotransmitter release in projections from cerebellar

201 Spontaneous neurotransmitter release is a fundamental property of sy

202 2 voltage-gated calcium channels for driving neurotransmitter release is broadly conserved.

203 Synchronous neurotransmitter release is triggered by Ca(2+) binding

204 and postsynaptic compartments, organizes the neurotransmitter release machinery, and provides a frame

205 is an essential component of the presynaptic neurotransmitter release machinery.

206 Thus, defects in excitatory neurotransmitter release may represent a general and con

207 cross the postsynaptic membrane, rather than neurotransmitter release per se, a result consistent wit

208 f release.SIGNIFICANCE STATEMENT Spontaneous neurotransmitter release that occurs independent of pres

209 xpression of dSol-1 is sufficient to enhance neurotransmitter release through a DKaiR1D-dependent mec

210 Synaptotagmin 1 (Syt1) synchronizes neurotransmitter release to action potentials (APs) acti

211 ofmeister series and the cellular process of neurotransmitter release via exocytosis and provide a be

212 is protein, resulting in loss of synchronous neurotransmitter release with a concomitant increase in

213 1) acts as a Ca(2+) sensor that synchronizes neurotransmitter release with Ca(2+) influx during actio

214 nsmembrane protein 2 (PRRT2), a regulator of neurotransmitter release, at glycine-305 was previously

215 powerful tool to elucidate the mechanism of neurotransmitter release, but it is important to underst

216 the primary interface, which strongly impair neurotransmitter release, disrupt and enhance synaptotag

217 gmin-2, the fastest Ca2+ sensor for synaptic neurotransmitter release, from parvalbumin neurons in mi

218 spontaneous vesicle fusion and asynchronous neurotransmitter release, regulate vesicle priming, medi

219 function of GPCRs is to inhibit presynaptic neurotransmitter release, requiring ligand-activated rec

220 Surprisingly, spontaneous neurotransmitter release, synaptic strength, the time co

221 exocytosis to maintain SV pool size and thus neurotransmitter release.

222 unctionally important for SNARE assembly and neurotransmitter release.

223 ing the balance among the different modes of neurotransmitter release.

224 se machinery, but dramatically impaired fast neurotransmitter release.

225 plasticity that is associated with enhanced neurotransmitter release.

226 in essential for synaptic vesicle fusion and neurotransmitter release.

227 um influx to exocytosis, thereby suppressing neurotransmitter release.

228 mains, C2A and C2B, act as Ca(2+) sensors of neurotransmitter release.

229 25, forms the essential fusion machinery for neurotransmitter release.

230 anges in the Ca(2+) channel subtypes driving neurotransmitter release.

231 ritical to its central role in orchestrating neurotransmitter release.

232 than not, action potentials fail to trigger neurotransmitter release.

233 1 and the SNARE complex cooperate to trigger neurotransmitter release.

234 potent homeostatic reduction in presynaptic neurotransmitter release.

235 t1), an SV protein essential for synchronous neurotransmitter release.

236 t7), and spontaneous (Doc2a/Doc2b) phases of neurotransmitter release.

237 us contribution of L-type Ca(2+) channels to neurotransmitter release.

238 (Ca(v)) channels to trigger Ca(2+)-dependent neurotransmitter release.

239 Maps of the synapses made and neurotransmitters released by all neurons in model syste

240 However, the neurotransmitters released by cortical ChAT(+) neurons a

241 Recently developed genetically encoded neurotransmitter sensors, when combined with superresolu

242 ion channel that converts the binding of the neurotransmitter serotonin (5-HT) into a transient catio

243 The neurotransmitter serotonin is primarily synthesized in t

244 other neural circuits.SIGNIFICANCE STATEMENT Neurotransmitters signal through GPCRs to modulate activ

245 We hypothesize that neurotransmitter signaling in immune cells can contribut

246 izing cancer-associated G-protein mutants to neurotransmitter signaling in primary neurons.

247 This study has uncovered a novel neurotransmitter signaling pathway in Ixodes SG, and sug

248 hesis/catabolism, including abnormalities in neurotransmitter signaling, urea cycle, aspartate-glutam

249 In turn, alterations in neurotransmitters signaling (or its disconnection) may f

250 (SN), and default-mode network (DMN)-and in neurotransmitters signaling-such as dopamine (DA) and se

251 hich operate as dimers to transform synaptic neurotransmitter signals into a cellular response throug

252 easurements revealed no group differences in neurotransmitter signals.

253 how neural circuits integrate and respond to neurotransmitter signals.

254 Neurotransmitter:sodium symporters (NSS) are conserved f

255 The anatomic organization of neurotransmitter-specific inputs to the VTA remains poor

256 Neurons also release neurotransmitters spontaneously.

257 ely on fast and tightly regulated release of neurotransmitters stored in secretory vesicles through S

258 pharmacologically by targeting receptors for neurotransmitters such as acetylcholine (ACh).

259 , diminishing sensitivity and selectivity to neurotransmitters such as dopamine.

260 c spine formation, and increases turnover of neurotransmitters, such as dopamine.

261 appropriate transmitter receptors following neurotransmitter switching and may contribute to the pro

262 Neurotransmitter switching is a form of brain plasticity

263 he activity-dependent molecular mechanism of neurotransmitter switching is increasingly well understo

264 , we investigate whether photoperiod-induced neurotransmitter switching persists during aging and whe

265 We suggest that neurotransmitter switching provides the basis by which s

266 esents prospects for future investigation of neurotransmitter switching, considering opportunities an

267 A newly discovered form of neuroplasticity, neurotransmitter switching, involves changes in neurotra

268 contain fast synaptotagmin isoforms, release neurotransmitter synchronously, and are mediated by comb

269 Use of immunostaining for the octopamine neurotransmitter synthesis enzyme Tdc2, along with a nov

270 uding oxidative metabolism, myelination, and neurotransmitter synthesis.

271 ehaviors, and rescued ACE-impaired GABAergic neurotransmitter system and PV interneurons in PrL.

272 cement of the gamma-aminobutyric acid (GABA) neurotransmitter system in the prelimbic cortex (PrL) of

273 that provides the far-reaching noradrenergic neurotransmitter system of the brain.

274 o citalopram administration on the serotonin neurotransmitter system was studied in the hippocampus,

275 se stressor engagement through modulation of neurotransmitter systems and are used to investigate str

276 ggesting that interactions between these two neurotransmitter systems are necessary to achieve an ant

277 and behavior, we examined the development of neurotransmitter systems from larval to male adult mutan

278 digm shift away from dysregulation of single neurotransmitter systems in depression towards circuit l

279 Alterations across multiple neurotransmitter systems in SZ suggest that this illness

280 the OUD-related negative affect, and several neurotransmitter systems were identified (i.e., serotoni

281 g function across multiple brain regions and neurotransmitter systems.

282 cal mutual coupling between the neuronal and neurotransmitter systems.

283 from stress coping styles to sensitivity of neurotransmitter systems.

284 f opioids in sleep-related brain regions and neurotransmitter systems.

285 hough many molecules have been identified as neurotransmitters, technical limitations have precluded

286 Some bacteria produce bioactive neurotransmitters that have previously been proposed to

287 o numerous neurohormones, neuropeptides, and neurotransmitters that reach it via the vasculature or s

288 ease of neuronal excitability in response to neurotransmitters through the suppression of this curren

289 m cells through synapse-like connections and neurotransmitters to couple tissue production with deman

290 mission are based on the specific binding of neurotransmitters to ligand-gated receptor ion channels.

291 been difficult because binding affinities of neurotransmitters to the lipid bilayer are low.

292 owever, little is known about the control of neurotransmitter transport into synaptic vesicles, which

293 Specific neurotransmitter transporters are responsible for this a

294 maging, electrophysiological recordings, and neurotransmitter typing in two transgenic lines, the wid

295 OS), and can be enhanced in frequency by the neurotransmitter tyramine via the TyrRII receptor.

296 pses in (1) bouton and active zone size, (2) neurotransmitter vesicle pool size, (3) distribution of

297 hat also depend on this indirect coupling of neurotransmitters via their membrane interaction.

298 ental stimulus causes neurons to replace one neurotransmitter with another, often resulting in change

299 to homeostatic roles, astrocytes respond to neurotransmitters with calcium transients stimulating th

300 obutyric acid (GABA) is the major inhibitory neurotransmitter within the central nervous system (CNS)