ライフサイエンスコーパス: neurotransmission

1 ative strengths of excitatory and inhibitory neurotransmission.

2 rojection co-expresses markers for GABAergic neurotransmission.

3 effect on glutamate release or AMPA-mediated neurotransmission.

4 and particularly in glutamate metabolism and neurotransmission.

5 ased ratio of excitatory to inhibitory (E/I) neurotransmission.

6 sorting, cell growth, hormone secretion, and neurotransmission.

7 s, disrupting synaptic vesicle recycling and neurotransmission.

8 mine efflux without affecting basal dopamine neurotransmission.

9 e different synaptic vesicle pools mediating neurotransmission.

10 demands of neuronal activity is critical to neurotransmission.

11 ion buffering along axons to synapses during neurotransmission.

12 ng relationship between intracellular pH and neurotransmission.

13 um (VS) and are thought to modulate striatal neurotransmission.

14 essential for the homeostatic modulation of neurotransmission.

15 ation of the synaptic cleft that accompanies neurotransmission.

16 ligands that are selective for noradrenergic neurotransmission.

17 s a function of dopaminergic and opioidergic neurotransmission.

18 y through oxidized metabolites that regulate neurotransmission.

19 biographical memories enhances noradrenergic neurotransmission.

20 rneurons and further reduction in inhibitory neurotransmission.

21 pre- and postsynaptic inhibitory effects on neurotransmission.

22 was reported to be dependent on dopaminergic neurotransmission.

23 tinic or glutamatergic) mediated cholinergic neurotransmission.

24 morphology, neural physiology, and modes of neurotransmission.

25 ty of i5HT neurons for studying serotonergic neurotransmission.

26 rk phenotype that is veiled by NMDA-mediated neurotransmission.

27 determining the efficacy of fast inhibitory neurotransmission.

28 vasodilation, antimicrobial, anticancer, and neurotransmission.

29 l intracellular calcium handling and cardiac neurotransmission.

30 ocking, demonstrating its essential roles in neurotransmission.

31 t sodium currents and abnormal glutamatergic neurotransmission.

32 caine use and related to changes in dopamine neurotransmission.

33 is a central mediator of SV availability for neurotransmission.

34 f various cell surface receptors to regulate neurotransmission.

35 d usually involves dysfunctional glycinergic neurotransmission.

36 ification of the synaptic cleft accompanying neurotransmission.

37 rotonin) after its exocytotic release during neurotransmission.

38 methyl-D-aspartate receptor (NMDAR)-mediated neurotransmission.

39 d that this would require intact cholinergic neurotransmission.

40 eedback for the homeostatic stabilization of neurotransmission.

41 y is more complex than a direct action on DA neurotransmission.

42 tsynaptic densities, a feature of excitatory neurotransmission.

43 y play key roles in neuronal development and neurotransmission.

44 ns to control food-motivated behavior and DA neurotransmission.

45 in the central nervous system by modulating neurotransmission.

46 and the role of AMPA receptors in excitatory neurotransmission.

47 cts on cellular processes being studied like neurotransmission.

48 lateral SNc neurons modulated by cholinergic neurotransmission.

49 t traditionally associated with VTA dopamine neurotransmission.

50 unction was used as a direct marker of brain neurotransmission abnormalities in complex mental phenom

51 al alterations in layer 3 glutamate and GABA neurotransmission across cortical regions may contribute

52 but action potential-independent spontaneous neurotransmission also contributes to the collection of

53 n important role in excitatory glutamatergic neurotransmission, although its precise mechanism of act

54 DA) transporter (hDAT) is a key regulator of neurotransmission and a target for antidepressants and a

55 glutamate receptors mediate fast excitatory neurotransmission and are implicated in numerous neurolo

56 e receptors (AMPARs) mediate fast excitatory neurotransmission and are selectively recruited during a

57 A expression levels of some genes related to neurotransmission and cell adhesion were altered in the

58 It has been suggested that DBN modulates neurotransmission and changes in dendritic spine morphol

59 marked impairments related to glutamatergic neurotransmission and chromatin remodeling in the human

60 effects of stress-level corticosterone on PL neurotransmission and cocaine seeking were determined us

61 unexpectedly leads to enhanced steady-state neurotransmission and consequently less synaptic depress

62 e (DA) transporter (DAT), terminates DAergic neurotransmission and constrains extracellular DA levels

63 rs, which mediate the majority of excitatory neurotransmission and contribute to seizure generation a

64 interventions for augmenting corticothalamic neurotransmission and enhancing IC during the course of

65 ondrial pyruvate metabolism to glutamatergic neurotransmission and establishes the MPC as a therapeut

66 GABA-mediated neurotransmission and fast-spiking (FS) GABAergic intern

67 paminergic or GABAergic markers for synaptic neurotransmission and harboring the ability to engage in

68 ortical and striatal dysfunction in dopamine neurotransmission and hence have the potential to correc

69 dings underscore that DAT is critical for DA neurotransmission and homeostasis.

70 ecting not only mitochondrial ATP output but neurotransmission and integrity of synaptic structures i

71 t function for NeuroD2 in balancing synaptic neurotransmission and intrinsic excitability and offer i

72 t function for NeuroD2 in balancing synaptic neurotransmission and intrinsic excitability.

73 ability would lead to increased dopaminergic neurotransmission and mania, whilst increased striatal d

74 la Piccolo-RIM-related Fife, which regulates neurotransmission and motor behavior through an unknown

75 sts the involvement of abnormal glutamateric neurotransmission and N-methyl-D-aspartate receptor hypo

76 l code for ion channels, factors influencing neurotransmission and neuromodulation, and proteins invo

77 a key cellular mechanism underlying impaired neurotransmission and neuromuscular junction maintenance

78 d metabolic alterations are likely to affect neurotransmission and neuronal homeostasis and in turn c

79 bnormalities in excitatory and/or inhibitory neurotransmission and neuronal plasticity may lead to ab

80 a distinctive feature that is essential for neurotransmission and neuronal survival.

81 ines, induce synapse formation, and regulate neurotransmission and plasticity.

82 rheumatoid arthritis, normalizes hippocampal neurotransmission and reduces seizure susceptibility in

83 mechanisms by which inflammation affects DA neurotransmission and relevance to novel therapeutic str

84 Thus, METH modulation of dopamine neurotransmission and resulting behavioral responses is,

85 Neurotransmission and secretion of hormones involve a se

86 evidence for sigma1R regulation of dopamine neurotransmission and support the sigma1R as a putative

87 that altered expression of MOCOS results in neurotransmission and synaptic defects.

88 MPARs), which are central mediators of rapid neurotransmission and synaptic plasticity, predominantly

89 or of neuronal physiology by contributing to neurotransmission and synaptic plasticity.

90 cation channels that mediate fast excitatory neurotransmission and synaptic plasticity.

91 a nigra pars compacta, a deficit in dopamine neurotransmission and the development of motor and non-m

92 results link neuroinflammation to defective neurotransmission and the enhanced susceptibility to sei

93 on spontaneous neurotransmission from evoked neurotransmission and vice versa.

94 recaptures released DA and modulates DAergic neurotransmission, and a number of DAT coding variants h

95 nslatome with strong links to axon survival, neurotransmission, and neurodegenerative disease.

96 central oxytocin, vasopressin, and serotonin neurotransmission, and neuroinflammation.

97 differentiation, regulation of glutamatergic neurotransmission, and oxytocin receptor expression in b

98 crucial to balance excitatory and inhibitory neurotransmission, and perturbations are linked with neu

99 Deficits in GABAergic inhibitory neurotransmission are a reliable finding in schizophreni

100 d extracellular proton concentrations during neurotransmission are converted to excitatory sodium inf

101 y still remains about whether these forms of neurotransmission are regulated independently on a molec

102 at inflammation and alterations in glutamate neurotransmission are two novel pathways to pathophysiol

103 d essential role for Parkin in glutamatergic neurotransmission, as a stabilizer of postsynaptic Homer

104 to dieldrin (Rdl), genes vital for GABAergic neurotransmission, as well as cacophony (cac) and paraly

105 the effects of drugs on endogenous dopamine neurotransmission, as well as to evaluate the long-term

106 Aberrant excitatory neurotransmission associated with overproduction of glut

107 pecialized presynaptic proteins that support neurotransmission at active zone structures known as rib

108 Stronger inhibitory neurotransmission at baseline may reflect the integrity

109 line transporter in sustaining acetylcholine neurotransmission at both central and neuromuscular syna

110 Neurotransmission at dopaminergic synapses has been stud

111 was conservation of underlying mechanisms of neurotransmission at excitatory and inhibitory synapses.

112 eover, functional ribbon synapses and active neurotransmission at foveal cone pedicles are possibly p

113 sting fundamental differences in spontaneous neurotransmission at GABAergic and glutamatergic synapse

114 ic deficits, by promoting synaptogenesis and neurotransmission at glutamatergic terminals.

115 integration in relation to catecholaminergic neurotransmission at the behavioral and neural level.

116 se, evidence for abnormalities in functional neurotransmission at the level of specific interneuron p

117 otropic glutamate receptors (iGluRs) mediate neurotransmission at the majority of excitatory synapses

118 ated ion channels that mediate fast chemical neurotransmission at the neuromuscular junction and have

119 ormation by helping to terminate cholinergic neurotransmission at the Pn:MBn synapse.

120 neuritic process increasing the fidelity of neurotransmission at those synapses as well.

121 al role of CHT for multisystemic cholinergic neurotransmission, autonomic dysfunctions were reported

122 receptor function and excitatory-inhibitory neurotransmission balance.

123 to understand how alpha-syn mutations impair neurotransmission before neurodegeneration.

124 he evolutionary conservation in dopaminergic neurotransmission between Drosophila and people, pharmac

125 , optogenetics, and transgenic tetanus toxin neurotransmission block show that elevated PN activity p

126 In Young MAs, capsaicin (to inhibit sensory neurotransmission) blocked dilatation and increased cons

127 id loads is necessary to maintain control of neurotransmission, but neuronal acid clearance mechanism

128 We find that inhibitory neurotransmission, but not excitatory neurotransmission,

129 c ligand-gated ion channels control synaptic neurotransmission by converting chemical signals into el

130 ne transporter (DAT) regulates dopamine (DA) neurotransmission by recapturing DA into the presynaptic

131 ansmitter:sodium symporters (NSSs) terminate neurotransmission by the reuptake of released neurotrans

132 ot ganglion (DRG) neuronal cell survival and neurotransmission by transporting mitochondria from the

133 syt1 function in suppression of spontaneous neurotransmission can be acutely dissociated from syt1 f

134 and action potential-evoked and spontaneous neurotransmission can be segregated at least partially o

135 cleave neuronal SNARE proteins required for neurotransmission, causing flaccid paralysis and death b

136 J whereby persistent but incoherent opposite neurotransmission changes have been reported to take pla

137 Dysfunction of dopaminergic neurotransmission contributes to the genesis of psychoti

138 loss of synaptic fidelity and specificity of neurotransmission, contributing to circuit dysfunction a

139 Dopamine (DA) neurotransmission controls behaviors important for survi

140 receptors) and 'fast' (ionotropic receptors) neurotransmission converging on the protein DARPP-32.

141 eceptors or biphasic GABAergic and nicotinic neurotransmission conveyed by GABA and ACh corelease, wh

142 els of FGFs/FGFRs by excessive glutamatergic neurotransmission could lead to abnormal neuronal circui

143 of SDB in which hypoxia-mediated inhibitory neurotransmission deficit in DLPFC could lead to hyperex

144 indicating alpha-syn overexpression-mediated neurotransmission deficits.

145 (A240V, V244A) was not sufficient to rescue neurotransmission despite full recovery of vesicle docki

146 t at some synapses, to sustain high-fidelity neurotransmission driven by synchronous release during h

147 f synapsin I and causes defects in sustained neurotransmission due to defective SV replenishment.

148 To sustain neurotransmission during periods of elevated activity, r

149 emerging mechanisms that modulate GABAergic neurotransmission dynamically from either the presynapti

150 We show that cholinergic neurotransmission encodes the oscillatory sensory respon

151 le yet important addition to the paradigm of neurotransmission, essentially dividing it into membrane

152 imbalances between excitatory and inhibitory neurotransmission evident in Fmr1-KO mice.

153 on rates to meet the demanding timescales of neurotransmission, exploiting the large number of v-SNAR

154 transmission, this work has implications for neurotransmission, extrasynaptic receptor activation, an

155 cular free radical generation on spontaneous neurotransmission from evoked neurotransmission and vice

156 erve responses elicited by afferent chemical neurotransmission from hair cells and modulated by effer

157 t genetically attenuating synaptic glutamate neurotransmission from retinal ganglion cells phenocopie

158 Neurotransmission from these synapses is characterized b

159 Glutamatergic neurotransmission governs excitatory signaling in the ma

160 tive synaptic vesicle pool heterogeneity and neurotransmission has been difficult.

161 atory synapses, but their role in inhibitory neurotransmission has been less well characterized.

162 The septohippocampal cholinergic neurotransmission has long been implicated in seizures,

163 MENT Action potential-evoked and spontaneous neurotransmission have been observed in nervous system c

164 es investigating the role of ICC-IM in motor neurotransmission have used indiscriminate electric fiel

165 of increasing inhibitory spinal glycinergic neurotransmission hold in providing new and transformati

166 ity, lower glucose oxidation, and attenuated neurotransmission (hypofrontality).

167 rotein alpha-synuclein (alpha-SYN) modulates neurotransmission in a complex and poorly understood man

168 gion is necessary for modulating spontaneous neurotransmission in an activity-dependent manner, but n

169 at mediate cell-to-cell communication during neurotransmission in animals, but their functional role

170 identification of VGCC agonists that rescue neurotransmission in BoNT/A-intoxicated synapses provide

171 rted the importance of pallidal dopaminergic neurotransmission in both the early compensatory mechani

172 diaminopyridine (3,4-DAP)-mediated rescue of neurotransmission in central nervous system synapses and

173 Recent reports indicate enhanced excitatory neurotransmission in cortical neurons expressing mutant

174 ein family to selectively reduce spontaneous neurotransmission in cultured mouse and rat neurons.

175 findings positively implicate NMDAR-mediated neurotransmission in developmental synapse maturation an

176 to drug seeking via beta-adrenergic and 5-HT neurotransmission in DH.

177 uring the last 20 years implicated glutamate neurotransmission in different brain regions in drug sel

178 n the well-established role of glutamatergic neurotransmission in drug addiction, novel medication de

179 vesicle mobility and release rate, lowering neurotransmission in fly and rat neurons.

180 a novel tool for studying human serotonergic neurotransmission in health and disease.

181 ry effect on excitatory, but not inhibitory, neurotransmission in hippocampal slices.

182 Previous work has implicated spontaneous neurotransmission in homeostatic synaptic scaling, but f

183 otential evolutionary shift in basal ganglia neurotransmission in humans that may favor increased syn

184 pedunculopontine tegmental nucleus glutamate neurotransmission in modulating VTA dopamine neuron acti

185 oints to a regulatory role for noradrenergic neurotransmission in perceptual metacognition.

186 el that increased synaptic Complexin reduces neurotransmission in response to insulin signaling.

187 mechanism for sigma1R regulation of dopamine neurotransmission in response to methamphetamine.

188 GABAergic neurotransmission in the amygdala contributes to the reg

189 ed oxidative stress and altered dopaminergic neurotransmission in the brain.

190 uRs) play key roles in modulating excitatory neurotransmission in the brain.

191 d ion channels that contribute to excitatory neurotransmission in the central nervous system (CNS).

192 ropic glutamate receptors mediate excitatory neurotransmission in the central nervous system and are

193 receptors, mediate a majority of excitatory neurotransmission in the central nervous system.

194 ificantly alter the maturation of inhibitory neurotransmission in the cingulate region of the mouse m

195 ght into the genetic network regulating 5-HT neurotransmission in the CNS that is also associated wit

196 eking behavior continued to require dopamine neurotransmission in the core of the nucleus accumbens (

197 Dopamine neurotransmission in the dorsal hippocampus is critical

198 tment drives an early increase in inhibitory neurotransmission in the frontal cortex, but not the som

199 AMPA receptors mediate fast excitatory neurotransmission in the mammalian brain and transduce t

200 ted gamma-aminobutyric acidergic (GABAergic) neurotransmission in the medial CeA and the sensitivity

201 ethyl-D-aspartate receptor and glutamatergic neurotransmission in the pathophysiology of the acute ea

202 dence indicates the involvement of GABAergic neurotransmission in the physiopathology of AD.

203 g evidence shows that glycinergic inhibitory neurotransmission in the spinal cord dorsal horn gates n

204 were to understand the role of glutamatergic neurotransmission in the ventromedial hypothalamus (VMH)

205 expression of genes involved in dopaminergic neurotransmission in the zebrafish brain.

206 at is triggered after blockade of spiking or neurotransmission in which the strengths of all synaptic

207 eurocognitive disorders (HAND) by disrupting neurotransmission including dopamine uptake by human dop

208 bitory neurotransmission, but not excitatory neurotransmission, increases onto cingulate pyramidal ne

209 ogether, these data suggest that spontaneous neurotransmission independently contributes to the regul

210 prefrontal cortical neurons known to mediate neurotransmission interrogated by our behavioral tasks.

211 naptic strength, suggesting that spontaneous neurotransmission is able to communicate independently w

212 red gamma-aminobutyric acidergic (GABAergic) neurotransmission is believed to cause muscle stiffness

213 Neurotransmission is ensured by a high concentration of

214 Dopamine neurotransmission is highly dysregulated by the psychost

215 Fast excitatory neurotransmission is mediated by AMPA-subtype ionotropic

216 Neurotransmission is mediated by the exocytic release of

217 variants in the AKT1 gene influence dopamine neurotransmission is not well understood.

218 Further, neurotransmission is similarly reduced at these synapses

219 dritic spines, suggesting that glutamatergic neurotransmission is unnecessary for synapse assembly an

220 role of the protein kinase Akt1 in dopamine neurotransmission is well recognized and has been implic

221 fects on dendritic morphology and excitatory neurotransmission its role in regulating neuronal inhibi

222 How such rapid hypothalamic neurotransmission leads to slowly evolving hormonal sign

223 nutrient for cell structure, cell signaling, neurotransmission, lipid transport, and bone formation.

224 Alterations in glutamatergic neurotransmission may be fundamental to the pathophysiol

225 aling pathways, can regulate fast inhibitory neurotransmission mediated by GABA receptors in the nerv

226 ed neuroplasticity, and changes in glutamate neurotransmission might be relevant etiological factors.

227 processes and genetic variants affecting its neurotransmission might control the unique balance betwe

228 el or whether they are simply a continuum of neurotransmission modes.

229 ptic disruption, dysfunction of dopaminergic neurotransmission, motor impairment, and measurable chan

230 here drugs are combined to influence several neurotransmission networks.

231 ical increases or decreases in glutamatergic neurotransmission observed in animal models of ASD, we f

232 e cultures to study plasticity of inhibitory neurotransmission on CA1 pyramidal neurons.

233 AR channel opening, but which cannot mediate neurotransmission on its own.

234 ased on either disruption of the orexinergic neurotransmission or neurons, do not allow study of the

235 And, neurotransmission outputs from these MBONs are all requi

236 ity to obesity is linked to genes regulating neurotransmission, pancreatic beta-cell function and ene

237 s growing evidence that defects in GABAergic neurotransmission participate in the pathogenesis of gen

238 These effects were not due to cholinergic neurotransmission, persisted during partial blockade of

239 g gene pickpocket 29 contributes to baseline neurotransmission, possibly via the modulation of postsy

240 sium ion action on HCN channels can modulate neurotransmission, preserving the fidelity of high-speed

241 ic properties remain intact, including basal neurotransmission, presynaptic Ca(2+) influx, initial re

242 een shown to alter hippocampal glutamatergic neurotransmission, providing a potential explanation for

243 hypothalamus in vitro, reduced glutamatergic neurotransmission recapitulated the repressive effects o

244 Synaptic neurotransmission relies on maintenance of the synapse a

245 ABSTRACT: Neurotransmission relies on membrane endocytosis to main

246 tic circuitry and functional advantage of co-neurotransmission remain poorly understood in general.

247 he molecular mechanism by which S1P promotes neurotransmission remained largely undefined.

248 ransmission, whereas action potential-evoked neurotransmission remained relatively normal.

249 protein receptor (SNARE) interactions during neurotransmission remains unclear.

250 not been sufficient to explain how GABAergic neurotransmission sculpts principal cell activity in a r

251 expression of markers of glutamate and GABA neurotransmission selectively in layer 3 of four cortica

252 nce of cell membrane and specific lipids for neurotransmission, should to be of interest to neuroscie

253 ', and 'Signalling', while in neurons it is 'Neurotransmission', 'Signalling' and 'Gene expression',

254 , these results demonstrate that spontaneous neurotransmission signals independently of stimulus-evok

255 in the postsynaptic regulation of excitatory neurotransmission.SIGNIFICANCE STATEMENT Members of the

256 The increase in dopamine (DA) neurotransmission stimulated by in vivo cocaine exposure

257 cern and cannabis is known to act on central neurotransmission, studying the retinal ganglion cells i

258 e NMDARs contribute to overall glutamatergic neurotransmission, such loss-of-function experiments fai

259 on proteomic measures related to presynaptic neurotransmission, synaptic function, cytoskeletal rearr

260 During neurotransmission, synaptic vesicles undergo multiple ro

261 Also, structural distribution maps of major neurotransmission systems in the brain were generated.

262 associated with the deregulation of several neurotransmission systems.

263 ubstrates by system, focusing on elements of neurotransmission, targets in white matter-associated co

264 xhibits 11-fold higher efficacy in blocking neurotransmission than wild-type botulinum neurotoxin B

265 oltage-gated Ca(2+) channels are fulcrums of neurotransmission that convert electrical inputs into ch

266 l auditory thresholds but defective cochlear neurotransmission, that is, reduced suprathreshold ampli

267 ations in MECP2, display impaired excitatory neurotransmission, the RTT phenotype can be largely repr

268 e been proposed, including the modulation of neurotransmission, the upregulation of neurogenesis and

269 demonstrated polySia at sites that influence neurotransmission: the extracellular space, fine astrocy

270 is a fundamental and essential mechanism for neurotransmission, this work has implications for neurot

271 Normalization of altered glutamate neurotransmission through activation of the mGluR2 has e

272 he spatial and temporal dynamics of dopamine neurotransmission through reuptake of extracellular tran

273 y lowered IIS rescues age-related decline in neurotransmission through the Drosophila giant fiber sys

274 glutamate receptors mediate fast excitatory neurotransmission throughout the central nervous system.

275 ulating physiological processes ranging from neurotransmission to cardiovascular function.

276 First, clostridial neurotoxins block neurotransmission to or from neurons by targeting the SN

277 ission without substantial changes in evoked neurotransmission to study this function in detail.

278 avering binary pulse over its arbor, driving neurotransmission uniformly at release sites.

279 f diminished serotonin (5-hydroxytryptamine) neurotransmission using dietary tryptophan depletion (TD

280 nonhuman primates influences serotoninergic neurotransmission via at least two ways: (1) by provokin

281 males but not in females, striatal dopamine neurotransmission was elevated after hearing songs.

282 tsynaptic maturation, terminal branching and neurotransmission was exaggerated in the Col13a1tm/tm mi

283 The involvement of central neurotransmission was explored by administering caffeine

284 ate's song, although their striatal dopamine neurotransmission was only slightly elevated.

285 loid type 1-dependent increase of excitatory neurotransmission was reduced in liver-related PVN neuro

286 Clinically, the striking depression of neurotransmission we found may help explain the motor im

287 By blocking olivocerebellar excitatory neurotransmission, we eliminated Purkinje cell complex s

288 Considering its modulating effect on neurotransmission, we hypothesized that cerebral mGluR5

289 The beneficial effects of CBD on inhibitory neurotransmission were mimicked and occluded by an antag

290 ted, which caused a reduction in spontaneous neurotransmission, whereas action potential-evoked neuro

291 f the neocortex is an increase in inhibitory neurotransmission, which alters the balance of excitatio

292 Our study reveals how cholinergic neurotransmission, which can represent sensory and motor

293 unctions of Stx1 in neuronal maintenance and neurotransmission, with the latter explored further into

294 ked vesicle fusion comprises the majority of neurotransmission within chemical synapses, but action p

295 terize in vivo changes in GABA and glutamate neurotransmission within M1 and determine their contribu

296 These findings suggest that HCRT neurotransmission within the CeA is implicated in compul

297 siological data indicated enhanced GABAergic neurotransmission within the medial CeA in LgA rats, whi

298 he balance between excitatory and inhibitory neurotransmission within the prefrontal cortex.

299 ies have selectively manipulated spontaneous neurotransmission without substantial changes in evoked

300 ellular population in the CNS that regulates neurotransmission, yet the role of astrocytes in mediati