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1 o expressing nitric oxide synthase (SuM(Nos1/Vglut2)).
2 t express vesicular glutamate transporter 2 (VgluT2).
3 nst the type 2 vesicular glutamate antibody (vGLUT2).
4 ain vesicular glutamate transporters type 2 (VGluT2).
5 ents, and vesicular glutamate transporter 2 (VGluT2).
6 g calcitonin gene-related peptide (CGRP) and vGluT2.
7  cells projecting to several areas expressed VGluT2.
8 edial region, in zones that stain darkly for VGLUT2.
9 form of the vesicular glutamate transporter, VGluT2.
10 erns of the vesicular glutamate transporter, VGLUT2.
11 me location in V2) and positive staining for Vglut2.
12  vesicular glutamate transporters VGLUT1 and VGLUT2.
13 ssion of the vesicular glutamate transporter VGLUT2.
14 vesicular glutamate transporters, VGLUT1 and VGLUT2.
15                                              vglut2.1 is widely expressed in many nuclei from the olf
16  the most widespread expression observed for vglut2.1, and more restricted expression of vglut1 and v
17 el vesicular glutamate transporters (vglut1, vglut2.1, vglut3), glutamate decarboxylases (gad1, gad2)
18 ls of vesicular transporters, VGLUT1 (5%) or VGLUT2 (21%).
19    CTb-labeled afferents contained primarily VGLUT2 (83%), whereas IB4-labeled afferents had low leve
20 e DCN were colabeled with antibodies against VGluT2, a glutamate transporter.
21 (Crh/Vglut2) neurons and found that only Bar(Vglut2) ablation replicates the profound urinary retenti
22 ei by using in situ hybridization assays for VGluT2 along with three cholinergic markers: the vesicul
23 imately 58% of POMC neurons were labeled for VGLUT2 and 37% for GAD67 mRNA.
24  of transcripts for the glutamatergic marker Vglut2 and for the H1 histamine receptor in neurons exci
25      Predominant co-localization of WFA with VGLUT2 and GABA but not with GAD65/67 or glutamate indic
26 ent in situ hybridization was used to detect vGlut2 and Gad mRNA in POMC neurons during early postnat
27 urons within this structure that coexpresses Vglut2 and Pitx2, and by conditional targeting of this s
28 the vesicular glutamate receptor transporter vGluT2 and receive inhibitory synapses from striatal neu
29   Approximately 7% of POMC neurons expressed vGlut2 and the highest percentage of vGlut2-positive POM
30      ChR2-positive RVLM-CA neurons expressed VGLUT2 and their projections were mapped.
31 lly exclusive behavioral effects, such as LH VGLUT2 and VGAT neurons [4-7] and orexin- (ORX) and mela
32 afferents are glutamatergic (express Slc17a6/Vglut2) and are distinct from neuroendocrine PVH neurons
33 t express vesicular glutamate transporter 2 (VGlut2) and are located in subcortical brain regions is
34 ignaling (vesicular glutamate transporter 2; VGluT2) and GABA signaling (glutamic acid decarboxylase;
35 ocytochemistry for glutamatergic (VGlut1 and VGlut2) and GABAergic (VGAT) synapses demonstrated that
36 y for the vesicular glutamate transporter 2 (VGluT2) and performed unbiased disector counts from elec
37 expresses vesicular glutamate transporter 2 (VGluT2) and releases glutamate as a second neurotransmit
38 RNA for the vesicular glutamate transporter (vGlut2) and the GABA synthetic enzyme Gad67.
39 expresses vesicular glutamate transporter 2 (VGluT2) and thus releases glutamate as a second neurotra
40 containing both glutamate and GABA (SuM(vgat/vglut2)) and another also expressing nitric oxide syntha
41 press the vesicular glutamate transporter 2 (VGLUT2), and form asymmetrical synapses on their dendrit
42 ker, type 2 vesicular glutamate transporter (VGLUT2), and the GABA synthetic enzyme, glutamic acid de
43 NeuN, and vesicular glutamate transporter 2 (VGlut2)], and cultures exhibited increased action potent
44                              Noticeably, the VGluT2+ and VIAAT+ varicosity density in Mo7 is 5-fold h
45 ities immunopositive for glutamate (VGluT1+, VGluT2+) and GABA/glycine (known as VIAAT+ or VGAT+) ves
46                                     VGluT1+, VGluT2+, and VIAAT+ varicosities respectively represent:
47  approximately 43% of POMC neurons contained VGLUT2, and 54% contained GAD67 mRNA.
48 in second-order neurons as well as increased VGlut2- and PSD95-positive puncta, indicative of increas
49 cle hyperacidification and its dependence on VGLUT2 are seen in ventral midbrain dopamine neurons in
50 ing corticotropin releasing hormone (Bar(Crh/Vglut2)) are implicated in bladder control.
51                     Two isoforms, VGLUT1 and VGLUT2, are found in most glutamatergic projections acro
52 he cryo-electron microscopy structure of rat VGLUT2 at 3.8-angstrom resolution and propose structure-
53 sed in Q140 striata, as was the abundance of VGLUT2(+) axodendritic terminals making synaptic contact
54 odynorphin (PPD) was only present in 4-7% of VGLUT2 boutons in laminae I-IV, it was found in 58% of t
55  in laminae I-IV, it was found in 58% of the VGLUT2 boutons that contacted these cells.
56                      Densities of VGluT1 and VGluT2 boutons were on average higher in matrix than in
57                                              VGluT2(+) boutons in M1 were smaller and formed fewer sy
58 howed extensive direct projections from MnPO(VGluT2) but few from MnPO(Vgat) neurons to a key site fo
59                             Ablation of MnPO(VGluT2) but not MnPO(Vgat) neurons abolished fever respo
60 kephalin and vesicular glutamate transporter VGLUT2, but not for GABAergic marker vGAT.Nerve ligation
61  ICSS in VgluT2-cre control mice, but not in VgluT2-CB1 (-/-) mice.
62  in VgluT2-expressing glutamatergic neurons (VgluT2-CB1 (-/-)) and Cre-dependent viral vector to expr
63                    Optogenetic excitation of vGluT2 cells evoked EPSCs in neighbouring neurons, indic
64 ther these data support the perspective that vGluT2 cells may be more prevalent in the ARC than previ
65 e caudal ARC showed a far greater density of vGluT2 cells than the rostral ARC, as seen in transgenic
66 y active with a spike frequency around 2 Hz. vGluT2 cells were responsive to a number of neuropeptide
67 ential projection from VMHvl(vGlut2) to lPAG(vGlut2) cells, and inactivation of downstream lPAG(vGlut
68 teral deafness leads to increased numbers of VGLUT2-colabeled Sp5 and Cu projections to the ventral a
69                         Our findings using a VGLUT2 conditional-null mouse model indicate that glutam
70 VGLUT1 contacts was relatively high although VGLUT2 contacts likewise dominated, while the proportion
71 LUT1 contacts and remarkably high numbers of VGLUT2 contacts.
72  the identity and function of glutamatergic (Vglut2) control of the LHb, comparing the role of inputs
73  by optotagging after Chrimson expression in VGLUT2-cre and GAD-cre mice, respectively.
74 and a reduction in the above optical ICSS in VgluT2-cre control mice, but not in VgluT2-CB1 (-/-) mic
75                                         Male Vglut2-Cre mice were injected with an AAV-DIO-ChR2-mCher
76 e, we trained wild-type, D1-Cre, A2A-Cre, or vGluT2-Cre:Ai9 male and female mice in a cocaine conditi
77                                 In contrast, Vglut2-Cre;Lepr(lox/lox) females exhibited reproductive
78        Female Vgat-Cre;Lepr(lox/lox) but not Vglut2-Cre;Lepr(lox/lox) mice were obese.
79 ronal population: Vgat-Cre;Lepr(lox/lox) and Vglut2-Cre;Lepr(lox/lox) mice, respectively.
80 of NDUFS4 protein within the optic nerves of Vglut2-Cre;ndufs4(loxP/loxP) mice.
81 e rapidly-developing optic atrophy makes the Vglut2-Cre;ndufs4(loxP/loxP) mouse line a promising prec
82                          RGC degeneration in Vglut2-Cre;ndufs4(loxP/loxP) retinas commenced around po
83 as expressed in VTA glutamatergic neurons of VGluT2::Cre mice.
84 d channelrhodopsin2 to VTA VGluT2 neurons of VGluT2::Cre mice.
85                                 We show that VGLUT2 deficiency in corticolimbic circuits results in r
86 r induced vesicular glutamate transporter 2 (Vglut2) deficiency in Trpv1-Cre expressing neurons and i
87  inducing vesicular glutamate transporter 2 (VGLUT2) deficiency in Trpv1-Cre-expressing neurons.
88 nin gene-related peptide (CGRP) signaling in Vglut2-deficient mice, we also evaluated the contributio
89 nin gene-related peptide (CGRP) signaling in Vglut2-deficient mice, we evaluated the contribution of
90                                              Vglut2 deletions that included the external lateral and
91    In contrast to VGLUT1, the trafficking of VGLUT2 depends almost entirely on the conserved C-termin
92       Bar neurons express a GFP reporter for Vglut2, develop from a Math1/Atoh1 lineage, and exhibit
93 in trafficking signals, wild-type VGLUT1 and VGLUT2 differ in their response to stimulation.
94 Pax6 (CoP); Foxp1 and Six3 (JcP); and Xiro1, VGlut2, Ebf1, and Ebf3 (PcP).
95 UT1-3 knock-out, VGLUT1(Venus) knock-in, and VGLUT2-EGFP transgenic mice.
96 leus pars muralis, which contains a class of vGluT2+ excitatory projection neurons involved in vibris
97  dopamine clearance in vivo, suggesting that Vglut2-expressing cells in the STN regulate dopaminergic
98 findings suggest that activation of CB1Rs in VgluT2-expressing glutamate neurons produces aversive ef
99 ic technology to selectively delete CB1Rs in VgluT2-expressing glutamatergic neurons (VgluT2-CB1 (-/-
100                       Ndufs4 inactivation in Vglut2-expressing glutamatergic neurons leads to decreas
101 xpression in either the larger population of VGlut2-expressing glutamatergic neurons or the smaller p
102                    Approximately half of the vGlut2-expressing POMC cells also expressed Gad65.
103 Moreover, we demonstrate that glutamatergic (VGLUT2-expressing) neurons in the lateral hypothalamus r
104 graphically-organized anatomical pathway via VGlut2-expressing, bursty neurons in the subiculum.
105 ompatible with the possibility that enhanced VGluT2 expression in DA neurons promotes axonal outgrowt
106              Here we show that this enhanced VGluT2 expression in dopamine neurons drives axonal outg
107           The seed-similar miR-137 regulated VGluT2 expression in mouse neurons.
108  Parkinson's disease pathophysiology, boosts VGluT2 expression in surviving dopamine neurons.
109                       Our data indicate that VGLUT2 expression is pivotal to the proper development o
110 l targeting of this subpopulation we reduced Vglut2 expression levels in the STN by 40%, leaving Pitx
111 lopment there is a switch from predominantly VGLUT2 expression to high VGLUT1 and low VGLUT2, raising
112                                 In contrast, VGluT2 expression was restricted to varicosities, some o
113 he PB to permanently and selectively disrupt Vglut2 expression while labeling the affected neurons.
114                 The LM neurons showed strong VGluT2 expression.
115 ated with vesicular glutamate transporter 2 (Vglut2) expression, in the dorsomedial striatum (DMS), a
116  the site of injection, coexpressed NeuN and VGlut2, extended neurites >5 mm, and formed putative syn
117                    Moreover, the use of EYFP(Vglut2) , EYFP(Vgat) , and GFP(Gad67) transgenic mouse l
118  was injected into the RVLM of DbetaH(Cre/0);VGLUT2(flox/flox) mice, into the caudal VLM (A1 noradren
119 al genetic strategy combining Chat(Cre) with Vglut2(Flp) to show that these neurons adopt a glutamate
120 e for the vesicular glutamate transporter 2 (Vglut2) from neurons in the PB.
121                             Here, we analyze vglut2, gad1b and gad2 expression in combination with ty
122 nock-out approach to selectively disrupt the Vglut2 gene in mouse DA neurons, we obtained in vitro an
123 e with lox P sequences flanking exon2 of the Vglut2 gene, in which adeno-associated viral vectors con
124 on of the vesicular glutamate transporter 2 (Vglut2) gene, coupled with immunofluorescence experiment
125  than the rostral ARC, as seen in transgenic vGluT2-GFP mice and mRNA analysis.
126 s, and the two principal isoforms VGLUT1 and VGLUT2 have been suggested to influence the properties o
127 ngs provide further evidence that VGLUT1 and VGLUT2 identify distinct populations of excitatory neuro
128 amic axodendritic terminals, we examined the VGLUT2-immunolabeled thalamic input to striatal choliner
129 minated, while the proportions of VGLUT1 and VGLUT2 immunoreactive terminals were the reverse on the
130  proximally on PC dendrites, as indicated by VGLUT2(+) immunoreactive puncta, and computational model
131 rom previous studies and the distribution of VGluT2-immunoreactive (-ir) puncta.
132               These terminals were generally VGLUT2-immunoreactive and formed numerous close appositi
133 that the PVH is preferentially innervated by VGLUT2-immunoreactive terminals/boutons.
134  phenylethanolamine N-methyl transferase and VGLUT2 immunoreactivities were highly colocalized in DMV
135           Immunohistochemistry assays showed VGluT2 immunoreactivity in the TeO codistributing with a
136 important changes in the pattern of cortical VGluT2 immunostaining that may be related to evolutionar
137 se here that the developmental expression of VGluT2 in DA neurons can be reactivated at postnatal sta
138 ined with immunohistochemistry for VGLUT1 or VGLUT2 in medial NTS and evaluated with confocal microsc
139 ization of OPCs with the presynaptic protein VGluT2 in MS lesions implies that this mechanism may pro
140 ergy balance regulation, genetic deletion of vGlut2 in POMC neurons was accomplished using Cre-lox te
141           Male, but not female, mice lacking vGlut2 in POMC neurons were unable to maintain energy ba
142      To assess a neurodevelopmental role for VGLUT2 in pyramidal neuron maturation, we generated reco
143 as MPTP and 6-hydroxydopamine can upregulate VGluT2 in surviving DA neurons, suggesting the possibili
144 nd protein expression patterns of VGLUT1 and VGLUT2 in the lateral geniculate nucleus (LGN), superior
145 th c-Fos analyses, showed that glutamate via VGLUT2 in the Trpv1-Cre population together with substan
146 vesicular glutamate transporters (vGLUT1 and vGLUT2) in postmortem human SN in schizophrenia subjects
147 er, after cocaine CPP and abstinence, the VP(VGluT2) input to the aversion-related structures is pote
148 ral complexity compared with those receiving VGLUT2 inputs, suggesting pathway-specific diversity.
149 gative dopaminergic groups, however, express vglut2 instead and use glutamate as a second transmitter
150 tion were vesicular glutamate transporter 2 (VGLUT2)-ir.
151 dence between cytochrome oxidase density and VGluT2-ir puncta distribution.
152   First, we investigated the distribution of VGluT2-ir puncta in all layers of macaque monkey primary
153         In many aspects, the distribution of VGluT2-ir puncta in human was qualitatively similar to t
154 r study was to determine the distribution of VGluT2-ir puncta in macaque and human visual cortex.
155 aque: high densities in layer 4C, patches of VGluT2-ir puncta in the supragranular layer (2/3), lower
156 of human, there was a sparse distribution of VGluT2-ir puncta, whereas in macaque, there was a dense
157                              Using Vgat- and Vglut2-ires-Cre knock-in mice and ESR1 immunohistochemis
158 isspeptin neurons expressed Cre in Vgat- and Vglut2-ires-Cre lines, approximately 70% of arcuate kiss
159                         We crossed Vgat- and Vglut2-ires-Cre mice with an Esr1(lox/lox) line to gener
160  EP3R conditional knock-out mice with either VGluT2-IRES-cre or Vgat-IRES-cre mice and used both male
161                                              Vglut2-ires-Cre;Esr1(lox/lox) mice were also infertile b
162  arcuate kisspeptin neurons were targeted in Vglut2-ires-Cre;Esr1(lox/lox) mice, possibly contributin
163                Our results also uncover that Vglut2 is expressed at some point during cell lifetime i
164                               In conclusion, VGLUT2 is expressed by RVLM-CA (C1) neurons in rats and
165                                              VGLUT2 is predominantly expressed in the granule cell do
166 ificantly decreased in ipsilateral VCN while VGLUT2 is significantly increased in the ipsilateral GCD
167  bladder pressure, while activity of Bar(Crh/Vglut2) is phase delayed.
168 hown that vesicular glutamate transporter 2 (VGLUT2) is the predominant VGLUT isoform expressed in th
169  neuron maturation, we generated recombinant VGLUT2 knock-out mice and inactivated VGLUT2 throughout
170                                  Conditional VGLUT2 knock-out mice exhibit increased open-field explo
171                            Numerous VGAT and VGLUT2 labeled varicosities were observed apposed to dDp
172 nmedicated schizophrenia subjects had higher vGLUT2 levels than controls (an increase of 28.7%, P=0.0
173 ontrols (an increase of 28.7%, P=0.041), but vGLUT2 levels were similar between medicated schizophren
174 , GAD67, Lhx1, and Nkx2.2) and caudal (Gbx2, VGlut2, Lhx2, Lhx9, and Sox2) domains.
175 oach, we find that >98% of DA neurons have a VGluT2(+) lineage.
176 ate that the vesicular glutamate transporter VGLUT2 may be exploited to drive robust Cre recombinase
177       To determine whether the expression of vGlut2 may play a role in energy balance regulation, gen
178                                              VGLUT2-mCherry colocalization was virtually absent when
179 esence of vesicular glutamate transporter 2 (VGLUT2)-mediated glutamatergic transmission in Trpv1-Cre
180 n, together with c-Fos analyses, showed that VGLUT2-mediated glutamatergic transmission in Trpv1-Cre
181 modulations, with or without the presence of VGLUT2-mediated glutamatergic transmission in Trpv1-Cre
182                Additionally, SP-, CGRP-, and VGLUT2-mediated transmission together were found to play
183  We further show that itch, regulated by the VGLUT2-mediated transmission via the Trpv1-Cre populatio
184 significantly less time in the chamber where VGluT2 mesohabenular fiber stimulation occurred.
185 ptor antagonists in LHb were unresponsive to VGluT2-mesohabenular fiber stimulation, demonstrating th
186  chamber that was previously associated with VGluT2-mesohabenular fiber stimulation.
187 hat there is a glutamatergic signal from VTA VGluT2-mesohabenular neurons that plays a role in aversi
188                                  Here, using VGLUT2 mice from both sexes, we report the existence of
189 ates and humans by simultaneous detection of VGluT2 mRNA and tyrosine hydroxylase (TH; for identifica
190 is caused an average 2.5-fold enhancement of Vglut2 mRNA in DA neurons.
191    The percentage of POMC neurons expressing vGlut2 mRNA in POMC neurons progressively decreased from
192 ro-Gold (FG), with in situ hybridization for VGLUT2 mRNA, to map the brainstem and caudal forebrain d
193 Ipc neurons exhibited a strong expression of VGluT2 mRNA.
194 on of the vesicular glutamate transporter 2 (VGluT2) mRNA in Ipc neurons, have raised doubts about th
195 r Phox2b, vesicular glutamate transporter 2 (VGLUT2) mRNA, and a subset contains preprogalanin mRNA.
196 express the vesicular glutamate transporter (VGluT2) mRNA, indicating a glutamatergic identity.
197  and type 2 vesicular glutamate transporter (VGLUT2) mRNAs, respectively.
198  Fiber photometry recordings reveal that Bar(Vglut2) neuron activity precedes increased bladder press
199         We found that the LHb-projecting LHA Vglut2 neurons encode negative valence and rapidly devel
200 we test whether local photoactivation of VTA VGluT2 neurons expressing Channelrhodopsin-2 (ChR2) unde
201                                          LHA Vglut2 neurons formed activity clusters representing dis
202 tral linear nuclei have a high prevalence of VGluT2 neurons lacking TH; their paranigral and parabrac
203 eurons, we targeted channelrhodopsin2 to VTA VGluT2 neurons of VGluT2::Cre mice.
204  vast majority of neurons are TH neurons but VGluT2 neurons were detected in the pars lateralis subdi
205 recording electrophysiology in brain slices, vGluT2 neurons were spontaneously active with a spike fr
206                            Here, we revealed VGluT2 neurons within the VTA and SNC of nonhuman primat
207      We further recorded the activity of LHA Vglut2 neurons, by imaging calcium dynamics in response
208 termine the behavioral role of mesohabenular VGluT2 neurons, we targeted channelrhodopsin2 to VTA VGl
209 vealed a predominantly limbic input onto LHA Vglut2 neurons, while sensorimotor inputs were more prom
210 c aspect of enhancing food intake, inhibited vGluT2 neurons.
211 tically ablate either Bar(Vglut2) or Bar(Crh/Vglut2) neurons and found that only Bar(Vglut2) ablation
212  influences on GABA input to VP(GABA) and VP(vGluT2) neurons and these influences are affected differ
213                                       PeriLC(VGLUT2) neurons are a hub between hunger and thirst that
214                                       PeriLC(VGLUT2) neurons are scalably inhibited by palatability a
215  in free-moving mice, which show that periLC(VGLUT2) neurons are tuned to ingestive behaviors and res
216                   These results identify SuM(vglut2) neurons as a key node of the wake-sleep regulato
217                 Here, we demonstrate that VP(VGluT2) neurons contact different targets with different
218                            Inhibition of SuM(vglut2) neurons decreases and fragments wake, also suppr
219                           As VP(GABA) and VP(vGluT2) neurons have contrasting effects on drug-seeking
220                                          SuM(vglut2) neurons include a subpopulation containing both
221                         Inhibition of periLC(VGLUT2) neurons is rewarding and increases consumption b
222                       Activation of SuM(Nos1/Vglut2) neurons potently drives wakefulness, whereas inh
223  and female transgenic mice, we show that VP(VGluT2) neurons preferentially contact aversion-related
224                       Activation of SuM(vgat/vglut2) neurons produces minimal wake and optogenetic st
225 tribution to micturition behavior of Bar(Crh/Vglut2) neurons relative to the overall Bar(Vglut2) popu
226 ed signals from the VMHvl to downstream lPAG(vGlut2) neurons that are sensitive to features of ongoin
227 aine CPP followed by abstinence may allow VP(VGluT2) neurons to recruit aversion-related targets more
228    Similarly, optogenetic stimulation of Bar(Vglut2) neurons triggers voiding, whereas stimulating th
229                                         EGFP(Vglut2) neurons were not TH-ir.
230  neurons in the peri-locus coeruleus (periLC(VGLUT2) neurons) as a polysynaptic convergence node from
231 ingly potentiated the inhibitory input on VP(vGluT2) neurons, but this effect was abolished after coc
232 tic disruption of glutamate release from SuM(vglut2) neurons.
233 dolescence many transition into mature (TBR1+VGLUT2+) neurons.
234 d that VP Gad1 and parvalbumin (PV), but not vGlut2, neurons show relapse-associated changes in c-Fos
235 ated with inhibitory (GAD65) and excitatory (VGLUT2) neurotransmission revealed a significant positiv
236 istribution of antibodies against VGLUT1 and VGLUT2 on SB neurons (which have dominating inhibitory i
237 ption of the vesicular glutamate transporter VGLUT2 or the obligatory NMDA receptor subunit NR1 promo
238       Next, we genetically ablate either Bar(Vglut2) or Bar(Crh/Vglut2) neurons and found that only B
239  neurons expressing the vesicular glutamate (vGLUT2) or GABA transporter (vGAT), then determined whet
240 esence of vesicular glutamate transporter 2 (Vglut2) or parvalbumin (PV).
241 r TH-ir neurons colocalized with native EGFP(Vglut2) - or EGFP(Vgat) -fluorescence, respectively.
242  were innervated exclusively by either giant vGLUT2- or vGLUT1-positive boutons.
243 l and mid levels of the POMC cell group with VGLUT2-POMC neurons dominating in lateral portions and G
244 /Vglut2) neurons relative to the overall Bar(Vglut2) population.
245 ) cells, and inactivation of downstream lPAG(vGlut2) populations results in aggression-specific defic
246 solitary tract, or ventrolateral medulla are VGLUT2 positive.
247 uced an increase in phosphorylated Stat-3 in vGluT2-positive neurons, indicating a response to hormon
248 pressed vGlut2 and the highest percentage of vGlut2-positive POMC cells were located in the rostral a
249  nuclei) or the presence of both vGLUT1- and vGLUT2-positive terminals, which were significantly smal
250  reticulospinal fibers exhibited excitatory, vGLUT2-positive varicosities, indicating their synaptic
251 g neurons of the supramammillary region (SuM(vglut2)) produce sustained behavioral and EEG arousal wh
252 xpressing vesicular glutamate transporter-2 (VGluT2)--project to limbic and cortical regions, but als
253 where moving into one chamber stimulated VTA VGluT2 projections within the LHb, and exiting the chamb
254                       Optical stimulation of VGLUT2(+) projections expressing channelrhodopsin-2 furt
255 pressing Channelrhodopsin-2 (ChR2) under the VGluT2 promoter causes place preference and supports ope
256 annelrhodopsin-2 (ChR2) under control of the Vglut2 promoter, optical stimulation of the DMS reinforc
257 ol of the vesicular glutamate transporter 2 (vGluT2) promoter.
258 from these mesohabenular neurons coexpresses VGluT2 protein and VGaT protein and, surprisingly, estab
259 ls of RTN-Phox2b neurons contain galanin and VGLUT2 proteins, to identify the specific projections of
260 coexpress vesicular glutamate transporter 2 (VGLUT2), providing evidence that excitatory projections
261  neuronal activity as measured by density of VGLUT2(+) puncta and Purkinje cell firing rate respectiv
262 tly VGLUT2 expression to high VGLUT1 and low VGLUT2, raising the question of whether the developmenta
263 ithout this motif, a substantial fraction of VGLUT2 redistributes to the plasma membrane and the tran
264            Vesicular glutamate transporter2 (VGLUT2) represented the largest number of anterogradely
265 hed to determine whether the upregulation of VGLUT2 represents increases in the number of somatosenso
266 h vesicular glutamate transporters VGLUT1 or VGLUT2, respectively), we compared sources of excitatory
267 ls in the IC: (1) those with both a PN and a VGLUT2 ring; (2) those with only a PN; (3) those with on
268  those with only a PN; (3) those with only a VGLUT2 ring; and (4) those with neither marker.
269     Functionally, the presence or absence of VGLUT2 rings indicates differences in inputs, whereas th
270 ncluding the vesicular glutamate transporter VGLUT2, several synaptic vesicle marker proteins, glutam
271                                 In contrast, VGluT2 showed a global increase in density from lateral
272 ibers expressing channelrhodopsin2 driven by VGluT2 (Slc17a6) or VGaT (Slc32a1) promoters elicits rel
273 ers voiding, whereas stimulating the Bar(Crh/Vglut2) subpopulation causes bladder contraction, typica
274                                              VGluT2 synapses show a rather consistent decrease in den
275 n average (1.3 vs 2.1) than those in S1, but VGluT2(+) synapses in M1 were larger than in S1 (median
276 region and whether associated with VGLUT1 or VGLUT2 terminals.
277 wake and optogenetic stimulation of SuM(vgat/vglut2) terminals elicits monosynaptic release of both g
278 rse transcriptase-PCR (n = 40) were Phox2b+, VGlut2+, TH-, and ChAT-, the neurochemical phenotype pre
279 heir parabrachial pigmented nuclei have dual VGluT2-TH neurons.
280 xpressing vesicular glutamate transporter 2 (VGluT2) that also project to LHb.
281 strated to express the glutamate transporter VGlut2, the projections are presumed to be excitatory.
282 binant VGLUT2 knock-out mice and inactivated VGLUT2 throughout development using Emx1-Cre(+/+) knock-
283 reveals a preferential projection from VMHvl(vGlut2) to lPAG(vGlut2) cells, and inactivation of downs
284 xpressing vesicular glutamate transporter 2 (VGLUT2)--to subdivide IC GABAergic cells in adult guinea
285  vesicular glutamate transporters VGluT1 and VGluT2, together with boutons immunoreactive for vesicul
286                                              VGLUT2 transcripts were found in very small, nonpigmente
287 x genetic targeting of Channelrhodospin 2 in VGluT2 transgenic mice, we examined the effect of glutam
288 ization to show coexpression of EP3R and the VGluT2 transporter in MnPO neurons.
289                Here we examined the level of VGluT2 upregulation in response to neurotoxins and its i
290 ctron microscopy, we determined that mCherry-VGluT2 varicosities correspond to axon terminals, formin
291  The mesoaccumbens axon terminals containing VGluT2 vesicles make asymmetric synapses, commonly assoc
292                                  A subset of VGLUT2(+) VTA neurons corelease dopamine with glutamate
293  DA neurons in female and male mice in which VGluT2 was conditionally removed established fewer stria
294                                Expression of VGluT2 was detectable in most DA neurons at embryonic da
295 sic and corticothalamic connections, whereas VGLUT2 was predominantly distributed in subcortical and
296                                   VGLUT1 and VGLUT2 were coexpressed in the LGN and in the pulvinar c
297 essed the vesicular glutamate transporter 2 (VGLUT2), which is found in highly efficient "driver" pat
298 xpressing vesicular glutamate transporter 2; VGluT2), which play roles in reward and aversion.
299  of VGLUT1-positive terminals also expressed VGLUT2, which decreased at these terminals.
300 ng the vesicular glutamate transporter 2 (VP(VGluT2))], whose activation generates aversion.

 
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