ライフサイエンスコーパス: glutamate release

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

2 equency of optogenetic stimulation to induce glutamate release).

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

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

5 synapses, accompanied by strongly increased glutamate release.

6 peptides, indicating a presynaptic action on glutamate release.

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

8 naptic efficacy that correlated with reduced glutamate release.

9 d in virtually complete absence of vesicular glutamate release.

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

11 predicts a paradoxical increase in synaptic glutamate release.

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

13 mobilization of calcium and the induction of glutamate release.

14 induced astrocytic Ca(2+) signaling triggers glutamate release.

15 m) media-conditions that suppress endogenous glutamate release.

16 o neuronal viability by inducing excitotoxic glutamate release.

17 d occluded forskolin-induced potentiation of glutamate release.

18 e receptor subtype 3 (mGluR3) and suppresses glutamate release.

19 tes MLIs based on their location relative to glutamate release.

20 r expression, and augmented cocaine-elicited glutamate release.

21 aptic 5-HT1B receptor-mediated inhibition of glutamate release.

22 resynaptic kappa-opioid receptors to inhibit glutamate release.

23 activity of downstream neurons via GABA and glutamate release.

24 esynaptic effects of nicotine is to increase glutamate release.

25 f presynaptic calcium influx, which controls glutamate release.

26 unctional spines are independent of synaptic glutamate release.

27 cient to suppress food intake independent of glutamate release.

28 icantly counteracted optogenetically induced glutamate release.

29 ntly enhanced the action potential-dependent glutamate release.

30 f downstream structures through dopamine and glutamate release.

31 ate glutamate receptor antagonist, increases glutamate release.

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

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

34 calcium channels (LTCCs) become involved in glutamate release after fear learning and LTP induction.

35 We hypothesize that glutamate released after ketamine administration moderat

36 The kinetics of glutamate release allows proper transfer of sound inform

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

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

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

40 that is independent of neuronal activity and glutamate release and another that depends on neuronal a

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

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

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

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

45 self-administration establishes de novo VTA glutamate release and dopaminergic activation in respons

46 nistration of heroin would establish similar glutamate release and dopaminergic activation.

47 el (VRAC) inhibitor, suppresses pathological glutamate release and excitatory neurotoxicity in revers

48 functions in the brain, adenosine regulates glutamate release and has an essential role in ethanol s

49 that offer a remarkably high probability of glutamate release and high safety factor for ST afferent

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

69 ential vanilloid 1 (TRPV1) channels regulate glutamate release at central and peripheral synapses.

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

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

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

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

74 dications to explain how mGluR4 can modulate glutamate release at parallel fiber-Purkinje cell synaps

75 nts for approximately 50% of all spontaneous glutamate release at rat cultured hippocampal synapses,

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

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

78 inic receptors on TC projections and sustain glutamate release at TC synapses via negative regulation

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

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

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

82 VGLUT3) are congenitally deaf due to loss of glutamate release at the inner hair cell afferent synaps

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

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

85 of glutamate neurons, attenuated K(+)-evoked glutamate release but did not alter resting glutamate le

86 ave presynaptic GABA(B) receptors that limit glutamate release, but how these receptors are activated

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

88 How and when glutamate release by DA neurons might play this role rem

89 Moreover, the potentiation of glutamate release by Epac was independent of protein kin

90 ropeptide in the CNS, suppresses presynaptic glutamate release by its action at the mGluR3 (a group I

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 Conversely, blocking glutamate release by targeting tetanus toxin to individu

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

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

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

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

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

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

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

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

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

107 istration of heroin itself did not cause VTA glutamate release, conditioned glutamate release was see

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

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

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

111 Spontaneous glutamate release-driven NMDA receptor activity exerts a

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

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

114 ent that is activated, in part, by excessive glutamate release during exposure to anoxia/ischemia.

115 y feedback mechanism that prevents excessive glutamate release during high-frequency stimulation.

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 ptors under the nonequilibrium conditions of glutamate release during synaptic transmission.

122 kedly to the unfailing, large amplitudes for glutamate released during ST-EPCSs recorded from the sam

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

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

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

126 d with a significant increase in presynaptic glutamate release, evidenced by a transient increase in

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

128 lthough D2 receptors paradoxically increased glutamate release following PCE, normal corticostriatal

129 that increases the magnitude and duration of glutamate release following TBI.

130 reports suggesting increased mPFC levels of glutamate release, following the administration of suban

131 of the absolute dependence of mGlu5 PAMs on glutamate release for their activity can lead to severe

132 opening as a result of increased spontaneous glutamate release from BCs.

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

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

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

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

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

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

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

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

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

142 Glutamate release from midbrain afferents evoked an NMDA

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

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

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

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

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

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

149 help to dynamically shape the time course of glutamate release from ON-type BC terminals.

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

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

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

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

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

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

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

157 root ganglion neurons, enhanced dorsal horn glutamate release from primary afferents, enhanced gluta

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

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

160 nses results from a presynaptic reduction in glutamate release from retinogeniculate terminals.

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

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

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

164 genous IL-1beta in neuropathic rats enhances glutamate release from the primary afferent terminals an

165 We showed that increased glutamate release from the primary afferents contributed

166 s used by the endogenous IL-1beta to enhance glutamate release from the primary afferents in neuropat

167 s activation of presynaptic NMDARs increased glutamate release from the primary afferents in neuropat

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

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

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

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

174 injured and the normal adult brain, and that glutamate released from neurons, via neuron-OPC synapses

175 hotoreceptor's signal via a cascade in which glutamate released from photoreceptors closes the TRPM1

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

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

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

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

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

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

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

183 luK1-containing KARs caused an inhibition of glutamate release in both OT and VP neurons, revealing t

184 nels increases presynaptic calcium-dependent glutamate release in CA1 pyramidal neurons.

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

186 nd was found to potently suppress pathologic glutamate release in cerebral ischemia.

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

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

189 ecordings, we found that preGlyRs facilitate glutamate release in developing, but not adult, visual c

190 Mild footshock stress also caused glutamate release in heroin-trained animals.

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

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

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

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

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

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

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

198 By visualizing glutamate release in real time, iGluSnFR provides a powe

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

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

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

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

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

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

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

206 ABA has the capacity to presynaptically gate glutamate release in the DR through a combination of GAB

207 ransmission to DR 5-HT neurons by inhibiting glutamate release in the DR.

208 atergic afferents, the effect of nicotine on glutamate release in the DRN has not been studied in det

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

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

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

212 PRS, and that strategies aimed at enhancing glutamate release in the ventral hippocampus correct the

213 hese findings indicate that an impairment of glutamate release in the ventral hippocampus is a key co

214 lated to the extent of depolarization-evoked glutamate release in the ventral hippocampus.

215 GluK1-mediated inhibition of glutamate release in VP neurons was also blocked by a ka

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

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

218 nt processes in astrocytes (i.e., exocytotic glutamate release, in vitro wound closure, and prolifera

219 The overall facilitatory effect of CICR on glutamate release induced during trains of action potent

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

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

222 However, because glutamate release is concentrated between glomeruli, whe

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

224 Thus, tight regulation of glutamate release is critical to neuronal function and s

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

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

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

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

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

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

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

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

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

234 We thus postulated that the inhibition of glutamate release observed with exogenous applications o

235 When glutamate release occurs, it decreases Pr by activating

236 n unexpectedly dynamic impact of spontaneous glutamate release on synaptic efficacy and provide new i

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

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

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

240 presynaptic inhibition of the probability of glutamate release onto VTA dopamine neurons.

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

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

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

244 NPY does not affect evoked synaptic glutamate release, paired synaptic facilitation, or syna

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

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

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

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

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

250 However, glutamate release probability is negatively regulated by

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

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

253 ppears to be secondary to an overall reduced glutamate release probability.

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

255 As a consequence of reduced glutamate release, PRS rats were also highly resistant t

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

257 We used a genetic approach to reduce glutamate release selectively from ipsilateral-projectin

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

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

260 ailability can provoke persistent changes in glutamate release that contribute to neuropsychiatric di

261 ed a chronic presynaptic depression (CPD) in glutamate release that was most pronounced in corticostr

262 oth nicotine and endogenous ACh can increase glutamate release through activation of presynaptic alph

263 Increasing glutamate release through infusions of the mGluR7 presyn

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

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

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

267 l frequencies, dopamine D1 receptors promote glutamate release to both D1 and D2 receptor-expressing

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

269 Enhancement of glutamate release/transmission, in turn induced by stres

270 coincidence between a postsynaptic spike and glutamate release triggers a lasting enhancement of syna

271 -acting GlyRs (preGlyRs) can also facilitate glutamate release under certain circumstances, although

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

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

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

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

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

277 In addition, cAMP also increases glutamate release via PKA-independent mechanisms, althou

278 lutamate transporter GLAST, nor did it block glutamate release via the P2X(7)/pannexin permeability p

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

280 In each case, the VTA glutamate release was accompanied by elevations in VTA d

281 tween anxiety-like behavior and reduction in glutamate release was demonstrated using a mixture of th

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

283 This Epac-mediated increase in glutamate release was dependent on phospholipase C, and

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

285 Whereas glutamate release was facilitated in oxytocin (OT) neuro

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

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

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

289 not cause VTA glutamate release, conditioned glutamate release was seen when rats expecting rewarding

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

291 Potentiation of glutamate release was triggered by the orexigenic hormon

292 Abnormalities of glutamate release were associated with large reductions

293 Ectopic vesicle exocytosis and glutamate release were detected in acute preparations of

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

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

296 Although immature RBCs elevate their glutamate release when GABA synthesis is impaired, homeo

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

298 consequence, a protocol pairing presynaptic glutamate release with somatic hyperpolarization, to inc

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