ライフサイエンスコーパス: glutamate release

1 equency of optogenetic stimulation to induce glutamate release).

2 ed with the EPSC amplitude (or the amount of glutamate release).

3 myloid-beta (Abeta)(42), elicits presynaptic glutamate release.

4 MDA receptors (NMDARs), and does not require glutamate release.

5 peptides, indicating a presynaptic action on glutamate release.

6 d in virtually complete absence of vesicular glutamate release.

7 mobilization of calcium and the induction of glutamate release.

8 on NMDAR function and disinhibition-mediated glutamate release.

9 unctional spines are independent of synaptic glutamate release.

10 ve can be associated with ~50% inhibition of glutamate release.

11 cient to suppress food intake independent of glutamate release.

12 icantly counteracted optogenetically induced glutamate release.

13 ntly enhanced the action potential-dependent glutamate release.

14 f downstream structures through dopamine and glutamate release.

15 ransporter (VGlut) and increased spontaneous glutamate release.

16 ate glutamate receptor antagonist, increases glutamate release.

17 ncreases in presynaptic Ca(2+) and vesicular glutamate release.

18 g a morphologic explanation for the enhanced glutamate release.

19 synapses, accompanied by strongly increased glutamate release.

20 terminals, abnormally contributes to evoked glutamate release.

21 tic alpha1-ARs but mediated by a decrease in glutamate release.

22 naptic efficacy that correlated with reduced glutamate release.

23 e; visual deprivation enhances both tLTD and glutamate release.

24 predicts a paradoxical increase in synaptic glutamate release.

25 vent the acute stress-induced enhancement of glutamate release.

26 egative modulator of spontaneous presynaptic glutamate release.

27 ses, suggestive of a decrease in presynaptic glutamate release.

28 may inactivate the ISVAID, thereby enhancing glutamate release.

29 h controls, indicating increased presynaptic glutamate release.

30 ng with the function of this domain promotes glutamate release.

31 d compared to WT rods, indicating diminished glutamate release.

32 , demonstrating its dependence on vesicular glutamate release.

33 ues is accompanied by a rapid suppression of glutamate release.

34 activity but is independent of the amount of glutamate released.

35 ts following agonist application or synaptic glutamate release, a feature of astrocyte-neuron communi

36 y, we imaged visually evoked and spontaneous glutamate release across hundreds of dendritic spines in

37 This has been attributed to glutamate release activating Ca(2+)-permeable N-methyl-D

38 We hypothesize that glutamate released after ketamine administration moderat

39 afferents displayed a higher probability of glutamate release, although short-term synaptic plastici

40 s is a crucial mechanism leading to enhanced glutamate release and activation of non-NMDA receptors i

41 ansmission during high frequency firing when glutamate release and AMPA-R responses are reduced.

42 show that in both mutant lines, spontaneous glutamate release and AMPAR-mediated responses are decre

43 er CA3 + CA1 Itm2b inactivation, spontaneous glutamate release and AMPAR-mediated responses are decre

44 anisms of action could correct the defect in glutamate release and associated behavioral abnormalitie

45 and VAMP7 impairs spontaneous high-frequency glutamate release and augments unitary event amplitudes

46 In this study, glutamate release and behavioral responses to tail suspe

47 e glutamate sensor to identify the source of glutamate release and determined the extent of neuronal

48 ersed the reduction in depolarization-evoked glutamate release and in the expression of synaptic vesi

49 re mGluR2/3 have been shown to reduce axonal glutamate release and increase glial glutamate uptake.

50 GTCs) were induced by photolytic or synaptic glutamate release and isolated pharmacologically.

51 nhanced GABA(A) currents, and inhibited both glutamate release and N-methyl-d-aspartate receptors.

52 c machinery requires simultaneous readout of glutamate release and nanomolar presynaptic Ca(2+) in si

53 fied both gamma-aminobutyric acid (GABA) and glutamate release and phospho-cFos expression in the NAc

54 e identified changes in proteins controlling glutamate release and postsynaptic signaling and discove

55 Repetitive glutamate release and reversal behavior require the glut

56 ibited normalized action potential duration, glutamate release and short-term dynamics during natural

57 malized action potential duration, excessive glutamate release and short-term synaptic plasticity dur

58 BDNF-evoked glutamate release and synapsin phosphorylation was atten

59 t has been shown that antidepressants reduce glutamate release and synaptic transmission; in particul

60 MPAR/NMDAR ratio, an increase in presynaptic glutamate release, and a postsynaptic change in AMPAR nu

61 silencer hM4Di-DREADD suppresses presynaptic glutamate release, and by generating an axon-targeted hM

62 changes in intrinsic cellular excitability, glutamate release, and glutamate uptake.

63 te receptor (VGLUT) 3 machinery orchestrates glutamate release, and its distribution overlaps with me

64 shields the auditory synapse from excessive glutamate release, and its loss of function increases th

65 bine with AMPARs to encode rapidly modulated glutamate release, and NMDAR kinetics do not limit tempo

66 volved astrocyte GABAB receptors, astrocytic glutamate release, and presynaptic metabotropic glutamat

67 Here we show that glutamate-releasing ARC neurons expressing oxytocin rece

68 However, the mechanisms of this increased glutamate release are not fully understood.

69 napse and their respective activation during glutamate release are still unclear.

70 fied local interneuron loss and excess glial glutamate release as chief contributors to network disin

71 ther, I compile evidence regarding astrocyte glutamate release as well as astrocyte association with

72 , presynaptic mGlu2 receptors, which inhibit glutamate release, as a stress-sensitive marker of indiv

73 ic delay, increased time to peak, and severe glutamate release asynchrony, distinct from previously d

74 Our results show that N-type VGCCs control glutamate release at a limited number of release sites t

75 binoid signaling as a key mechanism limiting glutamate release at BLA-plPFC synapses and the function

76 Munc13/Rab3/RIM-dependent pathway to enhance glutamate release at cerebrocortical nerve terminals.

77 ir cell development, and genes essential for glutamate release at hair cell ribbon synapses, suggesti

78 /Q-type calcium channel-mediated presynaptic glutamate release at layer VI pyramidal neuron terminals

79 ctivating its type 2, 3 receptors, increased glutamate release at nerve terminals in some LHb neurons

80 Furthermore, experimentally facilitating glutamate release at rBLAp-vlNAc synapses suppressed suc

81 nant autoreceptor responsible for regulating glutamate release at SC terminals.

82 (NVC) implies that activity-dependent axonal glutamate release at synapses evokes the production and

83 ory nociceptor sensitization is dependent on glutamate release at the DRG and subsequent NMDAR activa

84 that modulate neurite outgrowth and regulate glutamate release at the DRG-dorsal horn synapse.

85 otion of neurite outgrowth and modulation of glutamate release at the DRG-dorsal horn synapse.

86 It selectively reduced glutamate release at the rostral BLAp (rBLAp) onto ventr

87 er miR-1000 acts presynaptically to regulate glutamate release at the synapse by controlling expressi

88 nist (JWH133 or GP1a) for 7-10 days, quantal glutamate release became more frequent and spine density

89 ercalated cells, we found that inhibition of glutamate release by a submaximal concentration of enkep

90 primarily by AMPA-type glutamate receptors, glutamate release by cholinergic interneurons activates

91 and we validated its utility for visualizing glutamate release by neurons and astrocytes in increasin

92 Local blockade of glutamate release by perfusion of an adenosine A2A recep

93 y by selectively impairing the inhibition of glutamate release by presynaptic Group III metabotropic

94 of synaptic Zn(2+): synaptic Zn(2+) inhibits glutamate release by promoting 2-AG synthesis.

95 llows independent and opposite modulation of glutamate release by single lipid metabolites.

96 Finally, inhibition of corticostriatal glutamate release by TAAR1 showed mechanistic similariti

97 Importantly, reducing glutamate release by the group 2 metabotropic glutamate

98 nvestigated the roles that acetylcholine and glutamate released by cholinergic interneurons play in h

99 al ganglion neurons (SGNs), which respond to glutamate released by hair cells and transmit auditory i

100 of glucose is oxidized for every molecule of glutamate released by neurons and recycled through astro

101 Furthermore, glutamate released by the cystine/glutamate antiporter a

102 rdings suggested that spontaneous and evoked glutamate release can activate separate groups of postsy

103 Because ischemic glutamate release can be mediated by a plethora of mecha

104 During this time, glutamate release can spill outside the synaptic cleft a

105 a7-nAChRs by antibody crosslinking increases glutamate release capacity as seen in the frequency of s

106 aptic voltage-gated Ca(2+) channel directing glutamate release (CaV1.4) with postsynaptic mGluR6 rece

107 pe of associative learning where presynaptic glutamate release coincides with postsynaptic depolariza

108 e relationship between cupula deflection and glutamate release demonstrated maximum sensitivity at di

109 is modulated separately from TRPV1-mediated glutamate release despite coexistence in the same centra

110 itatory amino acid transporters or vesicular glutamate release did not inhibit ischemia-gated current

111 mpal neurons although spontaneous and evoked glutamate release driven NMDA receptor mediated Ca2+ tra

112 Spontaneous glutamate release-driven NMDA receptor activity exerts a

113 cells and later accentuated at the level of glutamate release driving retinal networks.

114 ional release sites act together to increase glutamate release during burst activity.

115 cyte Ca(2+)signals were mediated by neuronal glutamate release during cortical stimulation, accompani

116 ponses and mechanisms of increased vesicular glutamate release during in vitro ischaemia in the calyx

117 naptic responses and mechanisms of increased glutamate release during in vitro ischaemia, using pre-

118 A major source of glutamate release during oxidative stress is the system

119 adequate mitochondrial function to maintain glutamate release during physiologically relevant activi

120 acrine cells (SACs) and DS acetylcholine and glutamate release during preferred direction motion from

121 the level of Vglut3 protein or the level of glutamate release during the recovery period.

122 n our previous studies, we hypothesized that glutamate released during seizures activates cytosolic p

123 fied alcohol-sensitive proteins that control glutamate release (e.g., SV2A, synaptogyrin-1) and posts

124 s in identified axonal circuits reveals that glutamate release efficacy, but not its short-term plast

125 nergy metabolism in which activity-dependent glutamate release enhances oligodendroglial glucose upta

126 new molecular mechanism for channel-mediated glutamate release establishes a role for astrocyte-neuro

127 luSnFR detected single field stimulus-evoked glutamate release events.

128 Further, we examined optically evoked glutamate release ex vivo in BNST from mice with virally

129 tive, however, recent evidence suggests that glutamate release from bipolar cells is not directional,

130 nsient and sustained OFF layers, cone-driven glutamate release from bipolar cells was blocked by anta

131 inhibiting NKCC1 with BMN greatly increased glutamate release from both rod and cone terminals.

132 naptic proteins RIM1alphabeta in controlling glutamate release from cortical inputs to the dorsolater

133 nd cortico-amygdala plasticity by inhibiting glutamate release from cortical neurons, but mechanisms

134 We evaluated the in vivo effects of enhanced glutamate release from corticostriatal axons and postsyn

135 known about the properties and modulation of glutamate release from DA midbrain terminals and the eff

136 osensory modules are separate and redundant; glutamate release from either module can drive the full

137 These effects range from dampening of glutamate release from excitatory terminals to depolariz

138 pproach allowed us to demonstrate that local glutamate release from glutamatergic terminals from the

139 pula to rest: a large and transient burst of glutamate release from hair cells unresponsive to the in

140 y tissue-damaging noise and does not require glutamate release from IHCs.

141 ltage-dependent Ca(2+) channels that mediate glutamate release from IHCs.

142 Moreover, optogenetically-induced glutamate release from M2 cortex terminals in the dorsol

143 Similarly, nAChR-driven glutamate release from MHb axons was enhanced by cNIC.

144 Glutamate release from midbrain afferents evoked an NMDA

145 monstrate that acute cocaine inhibits DA and glutamate release from midbrain DA neurons via presynapt

146 Here, by imaging light-driven glutamate release from more than 13,000 bipolar cell axo

147 ACh also reduces glutamate release from mossy fibers by acting on presyna

148 Here, we measured glutamate release from mouse bipolar cells by two-photon

149 crossover circuits, in which ON CBCs control glutamate release from OFF CBCs via diffusely stratified

150 tive to sound and only weakly depolarized by glutamate release from OHCs.

151 The properties of presynaptic glutamate release from olfactory receptor neurons are si

152 acts, glycine centrifugal feedback increases glutamate release from photoreceptors and suppresses the

153 ise and the consequent increase in vesicular glutamate release from presynaptic terminals in the earl

154 ise and the consequent increase in vesicular glutamate release from presynaptic terminals in the earl

155 that accelerates axon outgrowth and enhances glutamate release from presynaptic terminals.

156 suggesting that ischaemia enhances vesicular glutamate release from presynaptic terminals.

157 brain ischaemia is an increase in vesicular glutamate release from presynaptic terminals.

158 inhibitory effect of the opioid on synaptic glutamate release from primary afferent nerves.

159 on of presynaptic M2 and M4 subtypes reduces glutamate release from primary afferents.

160 ast, DCPIB had no direct effect on vesicular glutamate release from rat brain synaptosomes or the cys

161 These data demonstrate how glutamate release from single CFs modulates excitability

162 cord sub-millisecond spikes, which represent glutamate release from single vesicles that burst open.

163 Here, we generate transgenic mice in which glutamate release from specific sets of retinal bipolar

164 ed following selective genetic disruption of glutamate release from SuM(vglut2) neurons.

165 KV1.3 channel-dependent signaling stimulates glutamate release from Th17 cells upon direct cell-cell

166 high signal-to-noise ratios in recordings of glutamate release from thalamocortical axons and calcium

167 In contrast, glutamate release from the primary afferents in sham-ope

168 s governing the properties and plasticity of glutamate release from these inputs are not fully unders

169 acilitates the feedback inhibition of DA and glutamate release from these terminals.

170 These findings suggest the possibility that glutamate release from unmyelinated vagal afferents may

171 ation curve that is based on measurements of glutamate release from vesicles pre-filled with various

172 Here, we report calcium-dependent glutamate release from vGluT3-expressing amacrine cells

173 These results suggest that glutamate release from VTA is sufficient to promote rein

174 Here, we show that glutamate released from climbing fibers activates ionotr

175 This, together with glutamate released from damaged phloem, activates GLRs,

176 release, and transporters are used to clear glutamate released from excitatory synapses.

177 y pathway (activation of type-I afferents by glutamate released from inner hair cells) is silenced [5

178 In the retina, glutamate released from photoreceptors in the dark activ

179 Together, these results suggest that glutamate released from the IHCs activates group I mGluR

180 Moreover, endogenous glutamate released from the IHCs also enhances IHC effer

181 revealed transient decreases in spontaneous glutamate release, glutamate release probability, and th

182 However, evidence for DS acetylcholine and glutamate release has been inconsistent and at least one

183 However, the mechanisms of astrocytic glutamate release have been debated.

184 However, CA1 evoked glutamate release in AbetaPP/PS1 mice was elevated at 2-

185 inked to a cell-penetrating peptide, reduces glutamate release in acute hippocampal slices from wild-

186 omparable to the measured exocytotic quantal glutamate release in amperometric glutamate sensing in t

187 pic glutamate receptors enhanced spontaneous glutamate release in an auditory brainstem nucleus, whil

188 onally expressed in On-Off DSGCs showed that glutamate release in both On- and Off-layer dendrites la

189 in treatment dampened tail suspension-evoked glutamate release in CA3.

190 isolation of a PKA-independent component of glutamate release in cerebrocortical nerve terminals aft

191 nabinoid receptors (CB1R) decreases GABA and glutamate release in cortical and subcortical regions, w

192 al glutamate and that increasing hippocampal glutamate release in high-trait-anxious monkeys normaliz

193 nit, regulates action potential waveform and glutamate release in hippocampal and cortical pyramidal

194 suspension stress evoked a rapid increase in glutamate release in hippocampal field CA3, which declin

195 ustly increases firing, and also potentiates glutamate release in LHb.

196 tance P to induce a long-lasting increase in glutamate release in LIPN neurons.

197 current at -60 mV and increased spontaneous glutamate release in MNTB neurons.

198 In addition, the effect of d-amphetamine on glutamate release in mPFC and OFC of EC and IC rats was

199 dependent mechanism, as well as differential glutamate release in mPFC and OFC.

200 , as well as increased d-amphetamine-induced glutamate release in nucleus accumbens compared to rats

201 aring-induced modulation of DAT function and glutamate release in prefrontal cortical subregions may

202 h directions from rest, either by increasing glutamate release in response to a deflection in the pos

203 s, with some hair cells generating sustained glutamate release in response to a steady deflection of

204 activation upon light-induced suppression of glutamate release in rod photoreceptors, thereby driving

205 hat the lack of NMDAR-mediated regulation of glutamate release in sham-operated rats was not attribut

206 rt [corrected] the hypothesis that transient glutamate release in the BLA can encode the outcome-spec

207 We found that glutamate release in the brain was impaired in mice lack

208 iature EPSCs (s/mEPSCs) by mainly decreasing glutamate release in the CeA of naive rats.

209 rked inhibitory control over corticostriatal glutamate release in the DLS, yet the signalling pathway

210 The VGLUT1-targeting vector attenuated tonic glutamate release in the dorsal hippocampus without affe

211 ion of MCH projections evoked a monosynaptic glutamate release in the LS.

212 by group I mGluRs (mGluR Is) on spontaneous glutamate release in the medial nucleus of the trapezoid

213 changes in Gpr39 and Bdnf expression, and in glutamate release in the NAcc.

214 als and horizontal cell dendrites as well as glutamate release in the outer plexiform layer.

215 we found that both TCP and tyramine reduced glutamate release in the substantia nigra in wild-type b

216 rated a causal link between the reduction of glutamate release in the ventral hippocampus and anxiety

217 ioning causes an increase of evoked striatal glutamate release in wild type, but not in global p11KO

218 ical analysis of ERK1/2 phosphorylation) and glutamate release (in vivo microdialysis) upon ILC elect

219 antane-2-carboxylic acid derived P2X7-evoked glutamate release inhibitor and 4-amino-tetrahydropyrany

220 naptic action potential can retard escape of glutamate released into the cleft.

221 e presynaptic level and that the NMDA-evoked glutamate release is controlled by presynaptic JNK-JIP1

222 In contrast, the probability of spontaneous glutamate release is decreased, while short-term synapti

223 The data suggest that glutamate release is important for proper activation of

224 ate that action potential-evoked synchronous glutamate release is modulated separately from TRPV1-med

225 Importantly, presynaptic glutamate release is sufficient to drive tau release.

226 t alter the duration of the EPSP or increase glutamate release lack efficacy.

227 urrent seizures and the associated excessive glutamate release lead to increased vascular permeabilit

228 esent data support the notion that APP tunes glutamate release, likely through intravesicular and ext

229 by reductions in probability of presynaptic glutamate release, long-term synaptic plasticity and int

230 luR5 signaling is under the tight control of glutamate release machinery mediated through vesicular g

231 aving only one functional copy suggests that glutamate release may promote synapse regeneration.

232 f mGluRs, either of which can inhibit evoked glutamate release, may be suitable for testing in humans

233 so compared speed of feedback to feedforward glutamate release measured at the same cone/HC synapses

234 zed by enhanced synchronous and asynchronous glutamate release mechanisms.

235 Here we report that glutamate-releasing neurons of the supramammillary regio

236 errant GLT-I activity, increased presynaptic glutamate release, NMDA-R 2B subunit upregulation, and i

237 These results suggest that, without glutamate release, noise-induced presynaptic Ca(2+) infl

238 When glutamate release occurs, it decreases Pr by activating

239 We found that M5 mAChRs potentiate DA and glutamate release only from DA and DA/glutamate projecti

240 stimulation of 5-HT terminals did not evoke glutamate release onto BA principal neurons, but inhibit

241 one corticotropin releasing factor (CRF) and glutamate release onto dopamine neurons in the ventral t

242 hese lamina terminalis AT1aR neurons induced glutamate release onto magnocellular neurons and was suf

243 Notably, acute ethanol decreased presynaptic glutamate release onto parvocellular PVN neurons in both

244 Using inhibition of glutamate release onto the intercalated cells of the amy

245 ation of d-serine has no immediate effect on glutamate release or AMPA-mediated neurotransmission.

246 explained either by presynaptic increases in glutamate release or by direct modification of postsynap

247 llular glutamate concentrations, (c) mediate glutamate release, or (d) control the pH inside insulin

248 oteins in Th17 cells that enable a vesicular glutamate release pathway that induces local intracytopl

249 These changes included increased glutamate release probability (P < 0.001, n = 7-9; consi

250 rough a combination of increased presynaptic glutamate release probability and increased postsynaptic

251 ate-type glutamate receptors (KARs) regulate glutamate release probability and short-term plasticity

252 PARs, we propose a novel method to determine glutamate release probability and uncover an increased h

253 ed that there was selective reduction of the glutamate release probability at the medial prefrontal c

254 ptic currents and an increase in presynaptic glutamate release probability by selectively impairing t

255 1460, we found an increased heterogeneity in glutamate release probability for adult-like calyces (P3

256 However, glutamate release probability is negatively regulated by

257 dependent, and synapse-selective increase in glutamate release probability with no direct actions on

258 rain extracts block hippocampal LTP, augment glutamate release probability, and disrupt the excitator

259 decreases in spontaneous glutamate release, glutamate release probability, and the number of primary

260 ed pulse ratios, and was occluded by raising glutamate release probability.

261 oliferation, while riluzole, an inhibitor of glutamate release, promoted apoptotic cell death in vitr

262 ented the increase of evoked corticostriatal glutamate release provoked by dopamine deficiency after

263 We show that reducing sensory glutamate release results in decreased expression of GAB

264 affects MOR-mediated suppression of GABA and glutamate release, showing weaker efficacy of synaptic r

265 presynaptic Ca(2+) entry with the prevalent glutamate release site, suggesting loose coupling betwee

266 rent terminals are sufficiently close to IHC glutamate release sites to allow activation of mGluRs on

267 precise receptor positioning with respect to glutamate release sites to enable efficient synaptic tra

268 ith action-potential-independent spontaneous glutamate release, suggesting plumes are a consequence o

269 ort has an unappreciated role in maintaining glutamate release synchrony by disturbing axonal signal

270 hort-term plasticity because of an increased glutamate release that results from an anomalous contrib

271 t with a presynaptic origin of the augmented glutamate release, the increased sEPSC frequency was pre

272 Increasing glutamate release through infusions of the mGluR7 presyn

273 Endogenously released opioids inhibit glutamate release through the delta-opioid receptor (DOR

274 e capacity of axonal D-type current to limit glutamate release, thus contributing to epileptogenesis.

275 ulating glucose uptake in response to axonal glutamate release, thus controlling metabolic cooperatio

276 ion contributed to the higher probability of glutamate release, thus facilitating reverberant circuit

277 However, the functional role of glutamate release/transmission in behavioral processes r

278 pool for oxidation decreases the quantity of glutamate released upon depolarization and, in turn, lim

279 the BLA and tonically activated to regulate glutamate release via a G-protein-dependent mechanism.

280 ytes, which then diffusely inhibits neuronal glutamate release via activation of presynaptic adenosin

281 zed effect on VRAC, DCPIB potently inhibited glutamate release via connexin hemichannels and glutamat

282 re it regulates dopamine levels, presynaptic glutamate release via D2-dependent synaptic plasticity a

283 of GABA, suggesting that CRF-R2 may regulate glutamate release via heterosynaptic facilitation of GAB

284 a indicate that mGluR I enhances spontaneous glutamate release via regulation of I (NaP) and subseque

285 e changes in tLTD are mirrored by changes in glutamate release; visual deprivation enhances both tLTD

286 This facilitated glutamate release was absent in transient receptor poten

287 We found that ischaemia-induced vesicular glutamate release was dependent on a rise in basal Ca(2+

288 In contrast, accumbal glutamate release was determined using individual rats.

289 Evoked glutamate release was elevated in all three age groups i

290 minal zones, and confirmed that P/Q-mediated glutamate release was reduced at these synapses.

291 Furthermore, action potential-independent glutamate release was regulated by tonic eCB signaling i

292 Augmentation of OrxA-induced glutamate release was reversed by DynA.

293 The effect on glutamate release was strongly correlated with the impro

294 upled with cNIC-enhanced nicotine-stimulated glutamate release, was associated with stronger depolari

295 statement, the actions of CRF-R2 on GABA and glutamate release were reversed.

296 ficits in the ability of GABABRs to suppress glutamate release were seen in Fmr1-KO mice.

297 ebbian activity, which increases Pr, and (2) glutamate release, which decreases Pr.

298 density and selectively enhances presynaptic glutamate release, which is impaired on alpha2delta1 kno

299 is therefore a major trigger for spontaneous glutamate release, with differential roles for distinct

300 lutamate content and blunted cocaine-induced glutamate release within the mPFC, whereas Homer2b knock