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1 rgic, VGAT(+)) or excitatory (glutamatergic, VGLUT2(+)).
2 o expressing nitric oxide synthase (SuM(Nos1/Vglut2)).
3 ents, and vesicular glutamate transporter 2 (VGluT2).
4 ssing the vesicular glutamate transporter 2 (VGluT2).
5 ned using vesicular glutamate transporter 2 (VGLUT2).
6 s, or the vesicular glutamate transporter 2 (vGluT2).
7 y identified as glutamatergic type 2 fibers (vglut2).
8 nst the type 2 vesicular glutamate antibody (vGLUT2).
9 ain vesicular glutamate transporters type 2 (VGluT2).
10 t express vesicular glutamate transporter 2 (VgluT2).
11 cells projecting to several areas expressed VGluT2.
12 edial region, in zones that stain darkly for VGLUT2.
13 form of the vesicular glutamate transporter, VGluT2.
14 erns of the vesicular glutamate transporter, VGLUT2.
15 me location in V2) and positive staining for Vglut2.
16 vesicular glutamate transporters VGLUT1 and VGLUT2.
17 ssion of the vesicular glutamate transporter VGLUT2.
18 vesicular glutamate transporters, VGLUT1 and VGLUT2.
19 munolabeled to reveal the EGFP and VGluT1 or VGluT2.
20 ents were more likely to contain VGluT1 than VGluT2.
21 press the vesicular glutamate transporter 2, VGluT2.
22 evels of the glutamate vesicular transporter vGlut2.
23 sicular glutamate transporter 1 (VGluT1), or VGluT2.
24 nts were equally likely to contain VGluT1 or VGluT2.
25 g calcitonin gene-related peptide (CGRP) and vGluT2.
27 the most widespread expression observed for vglut2.1, and more restricted expression of vglut1 and v
28 el vesicular glutamate transporters (vglut1, vglut2.1, vglut3), glutamate decarboxylases (gad1, gad2)
30 CTb-labeled afferents contained primarily VGLUT2 (83%), whereas IB4-labeled afferents had low leve
32 ei by using in situ hybridization assays for VGluT2 along with three cholinergic markers: the vesicul
34 of transcripts for the glutamatergic marker Vglut2 and for the H1 histamine receptor in neurons exci
35 ent in situ hybridization was used to detect vGlut2 and Gad mRNA in POMC neurons during early postnat
39 urons within this structure that coexpresses Vglut2 and Pitx2, and by conditional targeting of this s
41 the vesicular glutamate receptor transporter vGluT2 and receive inhibitory synapses from striatal neu
44 Approximately 7% of POMC neurons expressed vGlut2 and the highest percentage of vGlut2-positive POM
46 vesicular glutamate transporters (VGLUT1 and VGLUT2) and contacts formed by VGLUT1 terminals which in
47 essed for vesicular glutamate transporter 2 (VGLUT2) and examined for AAS-induced changes in the numb
48 ignaling (vesicular glutamate transporter 2; VGluT2) and GABA signaling (glutamic acid decarboxylase;
49 y for the vesicular glutamate transporter 2 (VGluT2) and performed unbiased disector counts from elec
51 containing both glutamate and GABA (SuM(vgat/vglut2)) and another also expressing nitric oxide syntha
52 press the vesicular glutamate transporter 2 (VGLUT2), and form asymmetrical synapses on their dendrit
53 ker, type 2 vesicular glutamate transporter (VGLUT2), and the GABA synthetic enzyme, glutamic acid de
54 NeuN, and vesicular glutamate transporter 2 (VGlut2)], and cultures exhibited increased action potent
56 ities immunopositive for glutamate (VGluT1+, VGluT2+) and GABA/glycine (known as VIAAT+ or VGAT+) ves
59 in second-order neurons as well as increased VGlut2- and PSD95-positive puncta, indicative of increas
60 cle hyperacidification and its dependence on VGLUT2 are seen in ventral midbrain dopamine neurons in
62 sed in Q140 striata, as was the abundance of VGLUT2(+) axodendritic terminals making synaptic contact
63 ssue, we found that double-labeled PHA-L (+)/VGluT2 (+) axon terminals formed synaptic contacts on de
64 r, the density of paired association between VGLUT2 boutons and PSD-95 was approximately 2-fold highe
65 odynorphin (PPD) was only present in 4-7% of VGLUT2 boutons in laminae I-IV, it was found in 58% of t
69 on: (1) a major subpopulation that expresses VGluT2 but lacks tyrosine hydroxylase (TH; VGluT2-only n
70 kephalin and vesicular glutamate transporter VGLUT2, but not for GABAergic marker vGAT.Nerve ligation
71 GluT2-immunoreactive boutons; 2) a subset of vGluT2-, but not vGluT1-immunoreactive, terminals displa
75 in VgluT2-expressing glutamatergic neurons (VgluT2-CB1 (-/-)) and Cre-dependent viral vector to expr
76 amined for AAS-induced changes in the number VGLUT2 cells containing retrograde tracer (VGLUT2/tracer
78 teral deafness leads to increased numbers of VGLUT2-colabeled Sp5 and Cu projections to the ventral a
80 VGLUT1 contacts was relatively high although VGLUT2 contacts likewise dominated, while the proportion
82 ) cortex, but does not support expression in VGLUT2-containing glutamatergic neurons in the ventral m
84 and a reduction in the above optical ICSS in VgluT2-cre control mice, but not in VgluT2-CB1 (-/-) mic
91 r induced vesicular glutamate transporter 2 (Vglut2) deficiency in Trpv1-Cre expressing neurons and i
93 nin gene-related peptide (CGRP) signaling in Vglut2-deficient mice, we also evaluated the contributio
94 nin gene-related peptide (CGRP) signaling in Vglut2-deficient mice, we evaluated the contribution of
96 duced by peripheral injury rely on distinct (VGLUT2 dependent and VGLUT2 independent, respectively) p
97 hich vesicular glutamate transporter type 2 (VGLUT2)-dependent synaptic glutamate release from mainly
98 In contrast to VGLUT1, the trafficking of VGLUT2 depends almost entirely on the conserved C-termin
103 porter 2-enhanced green fluorescent protein [vGluT2-eGFP], glutamic acid decarboxylase [GAD]67-eGFP,
104 leus pars muralis, which contains a class of vGluT2+ excitatory projection neurons involved in vibris
105 dopamine clearance in vivo, suggesting that Vglut2-expressing cells in the STN regulate dopaminergic
106 findings suggest that activation of CB1Rs in VgluT2-expressing glutamate neurons produces aversive ef
107 ic technology to selectively delete CB1Rs in VgluT2-expressing glutamatergic neurons (VgluT2-CB1 (-/-
108 es in release efficiency between VGLUT1- and VGLUT2-expressing neurons are due to VGLUT1's ability to
113 l targeting of this subpopulation we reduced Vglut2 expression levels in the STN by 40%, leaving Pitx
114 lopment there is a switch from predominantly VGLUT2 expression to high VGLUT1 and low VGLUT2, raising
116 he PB to permanently and selectively disrupt Vglut2 expression while labeling the affected neurons.
120 the site of injection, coexpressed NeuN and VGlut2, extended neurites >5 mm, and formed putative syn
122 was injected into the RVLM of DbetaH(Cre/0);VGLUT2(flox/flox) mice, into the caudal VLM (A1 noradren
123 knockout (cKO) of the Slc17a6 gene encoding VGLUT2 from the great majority of nociceptors profoundly
126 nock-out approach to selectively disrupt the Vglut2 gene in mouse DA neurons, we obtained in vitro an
127 e with lox P sequences flanking exon2 of the Vglut2 gene, in which adeno-associated viral vectors con
128 s, and the two principal isoforms VGLUT1 and VGLUT2 have been suggested to influence the properties o
129 ngs provide further evidence that VGLUT1 and VGLUT2 identify distinct populations of excitatory neuro
130 amic axodendritic terminals, we examined the VGLUT2-immunolabeled thalamic input to striatal choliner
131 Anterograde tract tracing combined with VGluT2 immunolabeling showed that 1) ventromedial nucleu
132 PTH2R and vesicular glutamate transporter 2 (VGlut2) immunolabeling in animals with retrograde tracer
133 minated, while the proportions of VGLUT1 and VGLUT2 immunoreactive terminals were the reverse on the
137 tic densities (PSDs) than those contacted by vGluT2-immunoreactive boutons; 2) a subset of vGluT2-, b
138 ound on excitatory and inhibitory cells, but VGLUT2-immunoreactive terminals originating from intrasp
140 phenylethanolamine N-methyl transferase and VGLUT2 immunoreactivities were highly colocalized in DMV
143 important changes in the pattern of cortical VGluT2 immunostaining that may be related to evolutionar
145 ined with immunohistochemistry for VGLUT1 or VGLUT2 in medial NTS and evaluated with confocal microsc
146 ization of OPCs with the presynaptic protein VGluT2 in MS lesions implies that this mechanism may pro
148 ergy balance regulation, genetic deletion of vGlut2 in POMC neurons was accomplished using Cre-lox te
150 To assess a neurodevelopmental role for VGLUT2 in pyramidal neuron maturation, we generated reco
151 nd protein expression patterns of VGLUT1 and VGLUT2 in the lateral geniculate nucleus (LGN), superior
152 th c-Fos analyses, showed that glutamate via VGLUT2 in the Trpv1-Cre population together with substan
154 vesicular glutamate transporters (vGLUT1 and vGLUT2) in postmortem human SN in schizophrenia subjects
155 njury rely on distinct (VGLUT2 dependent and VGLUT2 independent, respectively) primary afferent mecha
156 d related thalamic regions, and the enhanced VGluT2 input ventromedially with input from ventral medi
157 gative dopaminergic groups, however, express vglut2 instead and use glutamate as a second transmitter
159 a lesser extent, VGLUT(1) ; 2) abundance of VGLUT2-IR fibers innervating colorectum; and 3) a subpop
161 First, we investigated the distribution of VGluT2-ir puncta in all layers of macaque monkey primary
163 r study was to determine the distribution of VGluT2-ir puncta in macaque and human visual cortex.
164 aque: high densities in layer 4C, patches of VGluT2-ir puncta in the supragranular layer (2/3), lower
165 of human, there was a sparse distribution of VGluT2-ir puncta, whereas in macaque, there was a dense
167 isspeptin neurons expressed Cre in Vgat- and Vglut2-ires-Cre lines, approximately 70% of arcuate kiss
170 arcuate kisspeptin neurons were targeted in Vglut2-ires-Cre;Esr1(lox/lox) mice, possibly contributin
174 ificantly decreased in ipsilateral VCN while VGLUT2 is significantly increased in the ipsilateral GCD
176 hown that vesicular glutamate transporter 2 (VGLUT2) is the predominant VGLUT isoform expressed in th
177 neuron maturation, we generated recombinant VGLUT2 knock-out mice and inactivated VGLUT2 throughout
180 nmedicated schizophrenia subjects had higher vGLUT2 levels than controls (an increase of 28.7%, P=0.0
181 ontrols (an increase of 28.7%, P=0.041), but vGLUT2 levels were similar between medicated schizophren
184 esence of vesicular glutamate transporter 2 (VGLUT2)-mediated glutamatergic transmission in Trpv1-Cre
185 rovide definitive physiological evidence for VGLUT2-mediated glutamate release by mature dopamine neu
186 n, together with c-Fos analyses, showed that VGLUT2-mediated glutamatergic transmission in Trpv1-Cre
187 modulations, with or without the presence of VGLUT2-mediated glutamatergic transmission in Trpv1-Cre
189 We further show that itch, regulated by the VGLUT2-mediated transmission via the Trpv1-Cre populatio
191 ptor antagonists in LHb were unresponsive to VGluT2-mesohabenular fiber stimulation, demonstrating th
193 hat there is a glutamatergic signal from VTA VGluT2-mesohabenular neurons that plays a role in aversi
194 majority of nociceptors profoundly decreased VGLUT2 mRNA and protein in these neurons, and reduced fi
195 Here, we report that a striking induction of VGLUT2 mRNA and synaptic protein is triggered by a prolo
196 ates and humans by simultaneous detection of VGluT2 mRNA and tyrosine hydroxylase (TH; for identifica
197 high level of coexpression between PTH2R and VGlut2 mRNA by cells located in the PVN and nearby brain
199 The percentage of POMC neurons expressing vGlut2 mRNA in POMC neurons progressively decreased from
200 are two subpopulations of neurons expressing VGluT2 mRNA in the A10 region: (1) a major subpopulation
201 ion and from mRNA quantification showed that VGluT2 mRNA is not present in every TH-IR neuron, but re
202 ro-Gold (FG), with in situ hybridization for VGLUT2 mRNA, to map the brainstem and caudal forebrain d
204 on of the vesicular glutamate transporter 2 (VGluT2) mRNA in Ipc neurons, have raised doubts about th
205 r Phox2b, vesicular glutamate transporter 2 (VGLUT2) mRNA, and a subset contains preprogalanin mRNA.
207 ed with in situ hybridization for VGluT1 and VGluT2 mRNAs to identify forebrain regions that provide
210 we test whether local photoactivation of VTA VGluT2 neurons expressing Channelrhodopsin-2 (ChR2) unde
211 tral linear nuclei have a high prevalence of VGluT2 neurons lacking TH; their paranigral and parabrac
213 vast majority of neurons are TH neurons but VGluT2 neurons were detected in the pars lateralis subdi
215 termine the behavioral role of mesohabenular VGluT2 neurons, we targeted channelrhodopsin2 to VTA VGl
223 istribution of antibodies against VGLUT1 and VGLUT2 on SB neurons (which have dominating inhibitory i
224 ion, and immunohistochemistry, we found that VGluT2-only neurons and VGluT2-TH neurons each innervate
225 s VGluT2 but lacks tyrosine hydroxylase (TH; VGluT2-only neurons), present in each nucleus of the A10
226 we determined the mRNA copy numbers encoding VGluT2 or TH in samples of individual microdissected TH
227 ption of the vesicular glutamate transporter VGLUT2 or the obligatory NMDA receptor subunit NR1 promo
232 l and mid levels of the POMC cell group with VGLUT2-POMC neurons dominating in lateral portions and G
234 vGluT1-positive (i.e., corticostriatal) and vGluT2-positive (i.e., mostly thalamostriatal) axo-spino
236 and MPTP-treated monkeys; and 3) VGluT1- and vGluT2-positive axo-spinous synapses undergo ultrastruct
237 pressed vGlut2 and the highest percentage of vGlut2-positive POMC cells were located in the rostral a
238 nuclei) or the presence of both vGLUT1- and vGLUT2-positive terminals, which were significantly smal
239 reticulospinal fibers exhibited excitatory, vGLUT2-positive varicosities, indicating their synaptic
240 minal brainstem nuclei, the effectiveness of vGluT2 preparations in revealing septa in VP likely refl
241 ChE), and vesicular glutamate transporter-2 (VGluT2) preparations, received widespread projections fr
242 g neurons of the supramammillary region (SuM(vglut2)) produce sustained behavioral and EEG arousal wh
243 xpressing vesicular glutamate transporter-2 (VGluT2)--project to limbic and cortical regions, but als
244 where moving into one chamber stimulated VTA VGluT2 projections within the LHb, and exiting the chamb
246 pressing Channelrhodopsin-2 (ChR2) under the VGluT2 promoter causes place preference and supports ope
247 lation of myenteric plexus neurons expressed VGLUT2 protein and mRNA, but VGLUT1 mRNA was undetectabl
248 from these mesohabenular neurons coexpresses VGluT2 protein and VGaT protein and, surprisingly, estab
250 ls of RTN-Phox2b neurons contain galanin and VGLUT2 proteins, to identify the specific projections of
251 coexpress vesicular glutamate transporter 2 (VGLUT2), providing evidence that excitatory projections
253 tly VGLUT2 expression to high VGLUT1 and low VGLUT2, raising the question of whether the developmenta
254 ithout this motif, a substantial fraction of VGLUT2 redistributes to the plasma membrane and the tran
256 hed to determine whether the upregulation of VGLUT2 represents increases in the number of somatosenso
257 h vesicular glutamate transporters VGLUT1 or VGLUT2, respectively), we compared sources of excitatory
258 ls in the IC: (1) those with both a PN and a VGLUT2 ring; (2) those with only a PN; (3) those with on
260 Functionally, the presence or absence of VGLUT2 rings indicates differences in inputs, whereas th
261 ncluding the vesicular glutamate transporter VGLUT2, several synaptic vesicle marker proteins, glutam
263 le-labeling studies combining CTb, CGRP, and VGluT2 showed that very few corneal afferents contain bo
264 ibers expressing channelrhodopsin2 driven by VGluT2 (Slc17a6) or VGaT (Slc32a1) promoters elicits rel
265 corneal afferents contained either VGluT1 or VGluT2, suggesting that some afferents lack a VGluT.
266 n average (1.3 vs 2.1) than those in S1, but VGluT2(+) synapses in M1 were larger than in S1 (median
268 wake and optogenetic stimulation of SuM(vgat/vglut2) terminals elicits monosynaptic release of both g
269 rse transcriptase-PCR (n = 40) were Phox2b+, VGlut2+, TH-, and ChAT-, the neurochemical phenotype pre
270 istry, we found that VGluT2-only neurons and VGluT2-TH neurons each innervate both the prefrontal cor
273 orneal afferents were more likely to contain VGluT2 than VGluT1, whereas rostral corneal afferents we
275 strated to express the glutamate transporter VGlut2, the projections are presumed to be excitatory.
276 binant VGLUT2 knock-out mice and inactivated VGLUT2 throughout development using Emx1-Cre(+/+) knock-
278 xtent to which the developmental switch from VGLUT2 to VGLUT1 occurs through an increase in VGLUT1 at
279 xpressing vesicular glutamate transporter 2 (VGLUT2)--to subdivide IC GABAergic cells in adult guinea
281 vesicular glutamate transporters VGluT1 and VGluT2, together with boutons immunoreactive for vesicul
282 owed a significant increase in the number of VGLUT2/tracer cells in the LAH when compared with contro
283 wed a significant reduction in the number of VGLUT2/tracer cells in the LAH, aggressive AAS-treated h
287 x genetic targeting of Channelrhodospin 2 in VGluT2 transgenic mice, we examined the effect of glutam
289 ctron microscopy, we determined that mCherry-VGluT2 varicosities correspond to axon terminals, formin
290 The mesoaccumbens axon terminals containing VGluT2 vesicles make asymmetric synapses, commonly assoc
291 d the distribution of five antigens: VGLUT1, VGLUT2, VGLUT3, the postsynaptic protein PSD-95, and a m
294 sic and corticothalamic connections, whereas VGLUT2 was predominantly distributed in subcortical and
297 essed the vesicular glutamate transporter 2 (VGLUT2), which is found in highly efficient "driver" pat
300 ly prominent in brain sections processed for vGluT2, which is expressed in the synaptic terminals of
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