ライフサイエンスコーパス: neurotransmitter

1 fects of recurrent hypoglycemia (RH) on this neurotransmitter.

2 to match the identity of the newly expressed neurotransmitter.

3 e and increasing the likelihood of releasing neurotransmitter.

4 al step in the activity-dependent release of neurotransmitter.

5 -releasing peptide (GRP) is an itch-specific neurotransmitter.

6 nels mediate the actions of inhibitory brain neurotransmitters.

7 eurotransmission by the reuptake of released neurotransmitters.

8 s using acetylcholine, GABA, or serotonin as neurotransmitters.

9 des exhibit rapid and selective detection of neurotransmitters.

10 ising platform for point-of-care testing for neurotransmitters.

11 ted by endogenous compounds, including major neurotransmitters.

12 e by mapping the synaptic wiring diagram and neurotransmitters.

13 s, synaptic transmission, neuropeptides, and neurotransmitters [15-20].

14 n CD afferents when the predominant efferent neurotransmitter acetylcholine (ACh) activates calyceal

15 a critical determinant of signalling by the neurotransmitter acetylcholine at both central and perip

16 gnitive enhancers.SIGNIFICANCE STATEMENT The neurotransmitter acetylcholine is known to be important

17 ks inhibitory effects of the parasympathetic neurotransmitter acetylcholine on heart rate leading to

18 In addition to the endogenous neurotransmitter acetylcholine, nicotine also binds and

19 sferase (ChAT), the enzyme that produces the neurotransmitter acetylcholine.

20 (ACh) receptors have a high affinity for the neurotransmitter ACh and a low affinity for its metaboli

21 Delivery of neurotransmitters across the T-B-cell synapse may be adv

22 ABSTRACT: Fast neurotransmitters act in conjunction with slower modulat

23 e locus coeruleus as an additional source of neurotransmitter acting on dopaminergic receptors in the

24 These two neurotransmitters activate two types of nicotinic recept

25 nctional imaging of the brain by sensing the neurotransmitter activity directly.

26 amine is a catecholamine that acts both as a neurotransmitter and as a hormone, exerting its function

27 ological conditions, d-serine functions as a neurotransmitter and coagonist for NMDA receptors and is

28 roxytryptamine; 5-HT), which is an important neurotransmitter and endocrine, autocrine and paracrine

29 f the synaptic cleft due to the corelease of neurotransmitter and H(+) from synaptic vesicles.

30 r example, the amount of damage to forebrain neurotransmitter and neuromodulator circuits, most notab

31 UNC-18, which regulates neurotransmitter and neuropeptide release from synaptic

32 eurotransmitter switching is the gain of one neurotransmitter and the loss of another in the same neu

33 ically relevant target for endogenous opioid neurotransmitters and analgesics, has been a major focus

34 the biological effects of many hormones and neurotransmitters and are important pharmacological targ

35 trongly support the hypothesis of protons as neurotransmitters and demonstrate that presynaptic relea

36 l of early morphogenesis that is mediated by neurotransmitters and ion channel activity.Functions of

37 whose potential efficacy is tied to specific neurotransmitters and neurocircuits as well as specific

38 highly specialized regions of a neuron where neurotransmitters and neurohormones are released.

39 Many of these neurons can co-release neurotransmitters and neuropeptides in a use-dependent m

40 inverse relationship between levels of these neurotransmitters and premature responding normally evid

41 n inherited disease that causes depletion of neurotransmitters and severe motor dysfunction in infant

42 (ACh) is the most important parasympathetic neurotransmitter, and increasing evidence indicates that

43 ich diverse moieties from lipid, amino acid, neurotransmitter, and nucleoside metabolism are attached

44 promise not only information about origins, neurotransmitters, and connectivity of related networks,

45 nt loss of dopaminergic neurons and striatal neurotransmitters, and continuous impairment of motor fu

46 dulate physiologic responses to hormones and neurotransmitters, and may therefore have fewer adverse

47 ome profiles, serum markers of inflammation, neurotransmitters, and neurotrophin levels.

48 m, resulting from its complex interplay with neurotransmitters, and pro-insulin processing products.

49 homeostasis by redistributing ions, removing neurotransmitters, and releasing factors to influence bl

50 prised of a brain tissue mimic modified with neurotransmitters, and to determine if each individual n

51 Monoamine neurotransmitters are among the hundreds of signaling sm

52 Hormones and neurotransmitters are released through fluctuating exocy

53 d inhibitory motor neurons released the same neurotransmitters as endogenous motor neurons-acetylchol

54 s, with pathology resulting in disruption to neurotransmitter balance, increases in chronic inflammat

55 However, a purely neurotransmitter-based explanation for antidepressant dr

56 e also found that l-Glu and other activating neurotransmitters bind to the same site on the CYP46A1 s

57 of the beta8-beta9 loop occur in response to neurotransmitter binding.

58 receptors (AChRs) having only one functional neurotransmitter-binding site and single-channel electro

59 in (THB), an essential cofactor in monoamine neurotransmitter biosynthesis.

60 ve molecules such as peptides, hormones, and neurotransmitters, but relatively little is known about

61 nflammation, and levels of neurotrophins and neurotransmitters, but the BL group had reduced urine le

62 inhibitory (gamma aminobutyric acid (GABA)) neurotransmitter circuits in anxiety disorders, the stre

63 s of ion homeostasis, calcium signaling, and neurotransmitter clearance, as well as on the use of tra

64 The data thus implicate neurotransmitter co-transmission in the basal forebrain

65 g of subsecond fluctuations in electroactive neurotransmitter concentrations.

66 mitters, and to determine if each individual neurotransmitter could be accurately identified.

67 tal delay, dystonia, and a unique profile of neurotransmitter deficiencies without mutations in PAH o

68 itro application for extracellular monoamine neurotransmitters detection in living cells.

69 ectroelectrochemical method was proposed for neurotransmitters detection.

70 Many neurotransmitters directly inhibit neurons by activating

71 The neurotransmitter distributions described here in the bra

72 tion.SIGNIFICANCE STATEMENT Signaling by the neurotransmitter dopamine (DA) is tightly regulated by t

73 The neurotransmitter dopamine (DA) regulates multiple behavi

74 striatum that likely mediates effects of the neurotransmitter dopamine acting on these cells.

75 n region important for the production of the neurotransmitter dopamine.

76 il to produce normal levels of the monoamine neurotransmitters dopamine and serotonin, and suffer a m

77 robiopterin (BH4) deficiency with additional neurotransmitter (dopamine and serotonin) deficiency.

78 assess the modulatory influences of a major neurotransmitter, dopamine, on hemispheric lateralizatio

79 ds to behavioral alterations probably due to neurotransmitter dysbalance on the level of the striatum

80 els for neurological diseases connected with neurotransmitter dysregulation, e.g. attention deficit h

81 tive disorders are characterized by dopamine neurotransmitter dysregulation.

82 for physiological responses to the hormones/neurotransmitters epinephrine and norepinephrine which a

83 ers on the sensor slides were optimized, and neurotransmitter exocytosis was evoked by injecting solu

84 ructures and synaptic ribbons, photoreceptor neurotransmitter expression, and membrane conductances a

85 can be activated by protons (coreleased with neurotransmitter from acidified synaptic vesicles).

86 nociceptor neurons release neuropeptides and neurotransmitters from nerve terminals that regulate vas

87 ssion is mediated by the exocytic release of neurotransmitters from readily releasable synaptic vesic

88 c transmission is mediated by the release of neurotransmitters from synaptic vesicles in response to

89 roteins mediating sodium-dependent uptake of neurotransmitters from the extracellular space.

90 roteins that are responsible for reuptake of neurotransmitters from the synaptic cleft to terminate a

91 sodium-dependent reuptake of small-molecule neurotransmitters from the synaptic cleft.

92 Neurotransmitter function in behavioral addictions is po

93 y available antidepressants target monoamine neurotransmitter function.

94 from neuronal subpopulations expressing the neurotransmitters GABA or glutamate within this circuit

95 We imaged the distribution of neurotransmitters-gamma-aminobutyric acid, dopamine and

96 are ion channels activated by the excitatory neurotransmitter glutamate and are essential to all aspe

97 ted ion channels activated by the excitatory neurotransmitter glutamate and have well-characterized r

98 ansporters are essential for recovery of the neurotransmitter glutamate from the synaptic cleft.

99 triggers the calcium-induced release of the neurotransmitter glutamate that activates the postsynapt

100 Gated by the neurotransmitter glutamate, AMPA receptors are critical

101 regulate GABA synthesis from the excitatory neurotransmitter glutamate, are direct transcriptional t

102 isplayed increased hippocampal levels of the neurotransmitters glutamate and N-acetyl-aspartyl-glutam

103 organic molecules, including the amino acid neurotransmitters glutamate, aspartate and taurine.

104 presynaptic structures for the three primary neurotransmitters (glutamate, glycine, and GABA) in the

105 t these channels decrease the release of the neurotransmitter, glutamate.

106 ropic and metabotropic receptors for various neurotransmitters-glutamate, gamma-aminobutyric acid (GA

107 nges range from neuronal integrity losses to neurotransmitter imbalance and metabolite dysregulation,

108 f PD, rigidity and bradykinesia, result from neurotransmitter imbalance, particularly the catecholami

109 sis, glutaminolysis and lactic acidosis, and neurotransmitter imbalances.

110 Dopamine is the key neurotransmitter implicated in PD, and although electroc

111 GABA is the primary inhibitory neurotransmitter in human brain.

112 CANCE STATEMENT GABA, the primary inhibitory neurotransmitter in human visual system, varies substant

113 creases in amino acids glutamate (excitatory neurotransmitter in learning and memory) and phenylalani

114 utyric acid (GABA) is the primary inhibitory neurotransmitter in the brain and is increasingly recogn

115 Glutamate is the dominant excitatory neurotransmitter in the brain, but under conditions of m

116 in coupled receptors for the main inhibitory neurotransmitter in the brain, GABA.

117 CANCE STATEMENT GABA is the major inhibitory neurotransmitter in the brain.

118 GABA is the key inhibitory neurotransmitter in the cortex but regulation of its syn

119 inobutyric acid (GABA), the major inhibitory neurotransmitter in the mammalian brain, plays a vital r

120 that [Pyr(1) ]apelin-13 acts as a modulating neurotransmitter in the normotensive RVLM to affect vasc

121 The requirement for both neurotransmitters in both the feeding and fasting states

122 Both inhibitory and excitatory neurotransmitters in dACC were predictive of the strengt

123 ficant progress in understanding the role of neurotransmitters in normal and pathologic brain functio

124 th reduced recruitment of glycine and serine neurotransmitters in the ventromedial prefrontal cortex

125 Caged neurotransmitters, in combination with focused light bea

126 ce the interference from other catecholamine neurotransmitters, including L-DOPA, epinephrine, and no

127 of serotonin (5-hydroxytryptamine, 5-HT), a neurotransmitter involved in both sleep-wake and satiety

128 Glycine and GABA are both inhibitory neurotransmitters involved in fast synaptic transmission

129 ased immensely as the detection of the level neurotransmitter is first priority for patients sufferin

130 eostasis.SIGNIFICANCE STATEMENT Corelease of neurotransmitters is a common feature of the brain.

131 site of SULT1A3, which sulfonates monoamine neurotransmitters, is modeled on that of 1A1 and used to

132 When neurons use this neurotransmitter, its concentration drops, thus protecti

133 itochondrial glutamate metabolism to control neurotransmitter levels.

134 etection results of other negatively-charged neurotransmitters like acetylcholine demonstrated the se

135 st pharmacological studies focus on a single neurotransmitter, many neuromodulators can have related

136 discoveries of the single gain or loss of a neurotransmitter may have been harbingers of neurotransm

137 icate that vagal nerves that release several neurotransmitters may allow simultaneous activation of m

138 We therefore conclude that the two neurotransmitters may be functionally interchangeable an

139 Here we present SERS measurements of neurotransmitters (melatonin, serotonin, and epinephrine

140 arboxylase 1 (GAD1), a regulator of the GABA neurotransmitter metabolic pathway.

141 an essential role in the evolution of simian neurotransmitter metabolism.

142 oamine oxidases are all capable of affecting neurotransmitter modulation in brain, we consider dual t

143 Tyramine is an important neurotransmitter, neuromodulator, and neurohormone in in

144 Acting as neurotransmitters, neuromodulators, hormones, or growth

145 The neurotransmitters/neuromodulators involved in sleep cont

146 1) showed that the truncated cleaved form of neurotransmitter neuropeptide Y (NPY) actively promotes

147 26 (DPP4/CD26), an enzyme that truncates the neurotransmitter neuropeptide Y (NPY).

148 he effects of olfactory system activation on neurotransmitter (NT) expression in accessory olfactory

149 ase delays and advances, indicating that the neurotransmitter of the compound eyes participates in bo

150 ) is one of the most important catecholamine neurotransmitters of the human central nervous system, a

151 bility may be pivotal in determining whether neurotransmitters or hormones are released through a tra

152 nd TPH1 and contain both DA and 5-HT, a dual neurotransmitter phenotype hitherto undescribed in the b

153 e at which cells are isolated influences the neurotransmitter phenotype of interneurons that are gene

154 hes in mice, the authors reveal the lineage, neurotransmitter phenotype, and connectivity patterns of

155 lfactory bulb (OB) interneurons with varying neurotransmitter phenotypes and positions.

156 Dopamine, one of catecholamine neurotransmitters, plays an important role in many brain

157 es for presynaptic DA recycling to replenish neurotransmitter pools.

158 r in learning and memory) and phenylalanine (neurotransmitter precursor) after alpha-HBCD and gamma-H

159 Early treatment with BH4 and/or neurotransmitter precursors had dramatic beneficial effe

160 Conversely, levels of the neurotransmitter precursors phenylalanine and tryptophan

161 Finally, analysis of neurotransmitters profile showed a significant effect on

162 d on the proper assembly of the postsynaptic neurotransmitter receptor apparatus.

163 ing the cell adhesion molecule L1/NgCAM, the neurotransmitter receptor GluA2, and beta-APP.

164 c, titratable Arg analog, canavanine, into a neurotransmitter receptor in a living cell, utilizing a

165 alpha, encoded by Gnas, mediates hormone and neurotransmitter receptor-stimulated cAMP generation.

166 on the activation dynamics of this important neurotransmitter receptor.

167 n deletions decreased the synaptic levels of neurotransmitter receptors and had no effect on presynap

168 te to spine-specific compartmentalization of neurotransmitter receptors and signaling molecules and t

169 annels (ASICs), a small family of excitatory neurotransmitter receptors implicated in pain and neuroi

170 quired for the physiological organization of neurotransmitter receptors in postsynaptic specializatio

171 ticity in which perturbation to postsynaptic neurotransmitter receptors leads to a retrograde enhance

172 Ionotropic neurotransmitter receptors mediate fast synaptic transmi

173 Glutamate recognition by neurotransmitter receptors often relies on Arg residues

174 Neurotransmitter receptors on postsynaptic cells change

175 Neurotransmitter receptors previously implicated in C. e

176 t, to a decrease in synaptic distribution of neurotransmitter receptors upon deletion of neuroligins.

177 s mitochondria, synaptic vesicle precursors, neurotransmitter receptors, cell signaling and adhesion

178 late to investigate the gating of eukaryotic neurotransmitter receptors, for which intermediate state

179 hesis that all iGluRs, and potentially other neurotransmitter receptors, rely on the cooperative bind

180 reciate the function and regulation of these neurotransmitter receptors, we must understand their int

181 interact with ion channels and cytokine and neurotransmitter receptors.

182 le of VACCs in the regulation of spontaneous neurotransmitter release (in the absence of a synchroniz

183 ulation and support an ultrafast recovery of neurotransmitter release after low-frequency depression.

184 effector protein that decreases spontaneous neurotransmitter release and enhances evoked release.

185 sary for normal postsynaptic responsivity to neurotransmitter release and for normal coordinated larv

186 d protein of 25kDa (SNAP-25B), which disrupt neurotransmitter release and have been implicated in neu

187 utamatergic synapses of CH and SR supporting neurotransmitter release and synaptic plasticity.

188 cal role of presynaptic ER in the control of neurotransmitter release and will help frame future inve

189 t increase in presynaptic calcium levels and neurotransmitter release at individual glutamatergic ter

190 Munc13 proteins are essential regulators of neurotransmitter release at nerve cell synapses.

191 pled G protein-coupled receptors can inhibit neurotransmitter release at synapses via multiple mechan

192 trograde, homeostatic control of presynaptic neurotransmitter release at the neuromuscular junction i

193 er segment, metabolism in the cell body, and neurotransmitter release at the synaptic terminal.

194 superficial layers consistent with enhanced neurotransmitter release at these synapses.

195 te calcium-dependent cellular events such as neurotransmitter release by limiting calcium influx.

196 inding contributes to enabling regulation of neurotransmitter release by Munc13-1.

197 naptotagmins (Syts) act as Ca(2+) sensors in neurotransmitter release by virtue of Ca(2+)-binding to

198 Neurotransmitter release depends on the SNARE complex fo

199 eract with presynaptic proteins and regulate neurotransmitter release downstream of Ca(2+) influx.

200 Fast neurotransmitter release from ribbon synapses via Ca(2+)

201 ne potential fluctuations at the soma affect neurotransmitter release from synaptic boutons.

202 nate a neuronal signal and enable subsequent neurotransmitter release from the presynaptic neuron.

203 ecular understanding of CaV2.1 regulation of neurotransmitter release in mammalian CNS synapses.

204 SIGNIFICANCE STATEMENT: Neurotransmitter release involves fusion of synaptic ves

205 IFICANCE STATEMENT In presynaptic terminals, neurotransmitter release is dynamically regulated by the

206 Neurotransmitter release is orchestrated by synaptic pro

207 stem (CNS) synapses, action potential-evoked neurotransmitter release is principally mediated by CaV2

208 ribes reconstitution assays to study how the neurotransmitter release machinery triggers Ca(2+)-depen

209 esicles that maintain spontaneous and evoked neurotransmitter release preserve their identity during

210 studies suggest that spontaneous and evoked neurotransmitter release processes are maintained by syn

211 ant of syntaxin could only minimally restore neurotransmitter release relative to Munc13-1 rescue.

212 Although synchronous neurotransmitter release relies on both P/Q- and N-type

213 release, and rendered evoked and spontaneous neurotransmitter release sensitive to the slow Ca(2+) bu

214 ty of presynaptic dopamine terminals to tune neurotransmitter release to meet the demands of neuronal

215 ommunication at chemical synapses occurs via neurotransmitter release whereas electrical synapses uti

216 luR agonists act presynaptically to increase neurotransmitter release without affecting postsynaptic

217 lo-1 gain-of-function mutants in locomotion, neurotransmitter release, and calcium-mediated asymmetri

218 Gi/o, they limit cAMP accumulation, diminish neurotransmitter release, and induce neuronal hyperpolar

219 ion to the nerve terminal suggests a role in neurotransmitter release, and overexpression inhibits re

220 hannels, decreased and desynchronized evoked neurotransmitter release, and rendered evoked and sponta

221 c contribution of VGCCs to calcium dynamics, neurotransmitter release, and short-term facilitation re

222 ene expression and protein levels, glutamate neurotransmitter release, and, consequently, reduced spo

223 vity inhibits presynaptic calcium signal and neurotransmitter release, assigning synaptic defects to

224 Prior to entering neurons and blocking neurotransmitter release, BoNT/A recognizes motoneurons

225 eceptor) proteins mediate evoked synchronous neurotransmitter release, but the molecular mechanisms m

226 oregulates synapse number and probability of neurotransmitter release, emerging as a potential therap

227 ing a previously unrecognized role of 5RK in neurotransmitter release.

228 action potential (AP) has a strong impact on neurotransmitter release.

229 channel clusters for reliable and modifiable neurotransmitter release.

230 ut affecting normal fluctuations of synaptic neurotransmitter release.

231 minant of the functions of Syt C2 domains in neurotransmitter release.

232 ncluding axonal elongation and branching and neurotransmitter release.

233 n within the approximately 1-ms timescale of neurotransmitter release.

234 ity, intracellular [Ca(2+) ] regulation, and neurotransmitter release.

235 x assembly together with Munc13-1 to mediate neurotransmitter release.

236 synaptic plasticity consistent with enhanced neurotransmitter release.

237 ial widening that could account for enhanced neurotransmitter release.

238 ponent of the SNARE complex, which underlies neurotransmitter release.

239 rough local estrogen synthesis or inhibitory neurotransmitter release.

240 h regulation of cell firing and heterologous neurotransmitter release.

241 +) influx to trigger action potential-evoked neurotransmitter release.

242 ed contribution of P/Q- and N-types VGCCs to neurotransmitter release.SIGNIFICANCE STATEMENT In presy

243 chanism controlling vesicle availability and neurotransmitter release.SIGNIFICANCE STATEMENT Mechanis

244 ive zone (AZ) are critical factors governing neurotransmitter release; yet, these fundamental synapti

245 aptic vesicle exocytosis and thereby enhance neurotransmitter release?

246 ex firing frequencies and tune the amount of neurotransmitter released.

247 own complement of transcription factors and neurotransmitter response profiles.

248 Dopamine (DA) is a monoamine neurotransmitter responsible for regulating a variety of

249 this end, molecular imaging approaches using neurotransmitter-sensitive MRI agents have appeared rece

250 rcuits within the brainstem modulated by the neurotransmitter serotonin (5-HT).

251 ery plays a crucial role in the mechanism of neurotransmitter-sodium symporters, such as the human do

252 he dopamine transporter (DAT) belongs to the neurotransmitter:sodium symporter (NSS) family of membra

253 Neurotransmitter:sodium symporters (NSSs) are integral m

254 The Neurotransmitter:Sodium Symporters (NSSs) represent an i

255 Neurotransmitter:sodium symporters (NSSs) terminate neur

256 Compared with all other neurotransmitter:sodium:symporters, GAT-1 and other memb

257 It is a member of the neurotransmitter:sodium:symporters, which are crucial fo

258 n of ultra-trace concentrations of monoamine neurotransmitter such as noradrenaline (NA) in living ce

259 fferences in the capacity to coexpress other neurotransmitters such as glutamate, GABA, thyrotropin r

260 Monoamine neurotransmitters such as serotonin, dopamine, histamine

261 ith a marked drop in the levels of important neurotransmitters, such as acetylcholine (ACh).

262 These niches serve as sources of enteric neurotransmitters, such as epinephrine and norepinephrin

263 Amine neurotransmitters, such as noradrenaline, mediate arousa

264 there is strong evidence for accumulation of neurotransmitters, such as serotonin and dopamine, in in

265 In these cases, neurotransmitter switching and receptor matching thus ch

266 These findings raise the possibility that neurotransmitter switching contributes to depression, sc

267 Neurotransmitter switching is the gain of one neurotrans

268 Neurotransmitter switching often appears to change the s

269 Neurotransmitter switching produces up or down reversals

270 neurotransmitter may have been harbingers of neurotransmitter switching.

271 ring the ability to engage in task-dependent neurotransmitter switching.

272 biopterin, a critical cofactor for monoamine neurotransmitter synthesis.

273 ng cell type-specific transcription factors, neurotransmitter-synthesizing enzymes and neuropeptides,

274 The serotonergic neurotransmitter system has been widely implicated in th

275 ther challenges in modulating this prevalent neurotransmitter system include potential induction of s

276 ent redundancy may ensure homeostasis if one neurotransmitter system is compromised.

277 brain are among the most carefully analyzed neurotransmitter systems in the brain of most vertebrate

278 quires a detailed knowledge of how different neurotransmitter systems modulate DA neuronal excitabili

279 communication across different slow and fast neurotransmitter systems through intracellular signaling

280 to investigate the potential involvement of neurotransmitter systems through which the apelin presso

281 ms (SNPs) in genes involved in regulation of neurotransmitter systems, nerve growth/death and gene ex

282 Malfunctioning neurotransmitter systems, such as glutamate, are implica

283 obutyric acid (GABA), dopamine and serotonin neurotransmitter systems.

284 ceptors are blocked, confirming that the two neurotransmitters systems are segregated.

285 (5-hydroxytryptamine, 5-HT) is a well-known neurotransmitter that is involved in a growing number of

286 rolonged alcohol exposure to investigate the neurotransmitters that are potentially responsible for d

287 mines, such as like serotonin, are conserved neurotransmitters that regulate behavior and metabolism

288 ndicate that males likely use biogenic amine neurotransmitters through the nervous system to control

289 The ability to noninvasively detect neurotransmitters through the skull would aid in underst

290 s followed by the SESORS measurements of the neurotransmitters to a concentration as low as 100 muM i

291 nel P2X7, allowing the release of excitatory neurotransmitters to sustain spreading depolarization an

292 Thus, we enhanced the neurotransmitter transporter activity of rigid nucleosid

293 roaches for examining the oligomerization of neurotransmitter transporters and sheds light on their d

294 ill focus on technical aspects of performing neurotransmitter uncaging and channelrhodopsin-assisted

295 However, rapid changes of astrocyte neurotransmitter uptake and morphology may also underlie

296 drives and maintains astrocytic maturity and neurotransmitter uptake function, is conserved in human

297 he cellular effects of multiple hormones and neurotransmitters via activation of its main effector, p

298 Levels of 12 neurotransmitters were monitored in the rat vmPFC during

299 nvolve the release of endogenous opiates and neurotransmitters, with the signals mediating through el

300 epends on release and reception of different neurotransmitters within complex circuits that ultimatel