ライフサイエンスコーパス: DA

1 DA transmission mediates several aspects of reinforced b

2 DA+DCB treatment was effective and safe, but the study w

3 ncreased from none in eyes with less than 10 DA of nonperfusion in total to 14.3% in eyes with 10-30

4 dius centered at the fovea) and more than 10 DA of nonperfusion isolated in the periphery (beyond the

5 posterior pole nonperfusion of more than 10 DA remains the key risk factor for new vessel developmen

6 20.0% for 30-75 DA, and 80% risk with 75-150 DA of nonperfusion.

7 rfusion in total to 14.3% in eyes with 10-30 DA, 20.0% for 30-75 DA, and 80% risk with 75-150 DA of n

8 0.003), larger total lesion size (3.3 vs 2.4 DA; p <0.001), greater total foveal thickness (522microm

9 14.3% in eyes with 10-30 DA, 20.0% for 30-75 DA, and 80% risk with 75-150 DA of nonperfusion.

10 nalyses to identify differentially abundant (DA) proteins among the 4 sample groups.

11 The use of definitive abutments (DAs) at time of implant placement has been introduced to

12 at an organic semiconductor donor-acceptor (DA) interface, as a means to control the magnitude and s

13 increase in extracellular nucleus accumbens DA, locomotion, and brain-stimulation reward.

14 foragers, BA and (E)-dec-2-en-1-yl acetate (DA) generated the strongest antennal electrophysiologica

15 Oxytocin release directly activates DA neurons and indirectly inhibits them through local GA

16 their performance on focal dark adaptation (DA) testing and with choroidal thickness.

17 secondary neurons) confirms that these added DA clusters are primary neurons born in the embryo, rath

18 ontributes to the rhythmic activity of adult DA neurons in the substantia nigra region.

19 The AlN/GaN digital alloy (DA) is a superlattice-like nanostructure formed by stack

20 The III-Nitride digital alloy (DA) is comprehensively studied as a short-period superla

21 n, food reward, and DA neuronal activity and DA neuron expression of FA-handling proteins and FA upta

22 urons to control food-motivated behavior and DA neurotransmission.

23 er the circuit connecting amygdala, CEA, and DA cells follows CEA intrinsic organization, or a more d

24 ecular interaction between TC-TC, TC-DA, and DA-DA enables the construction of strategic sensor for d

25 was observed with ibrutinib monotherapy and DA-TEDDi-R.

26 VTA on feeding, locomotion, food reward, and DA neuronal activity and DA neuron expression of FA-hand

27 ial of adult NSCs and identify alpha-SYN and DA as potential targets to ameliorate neurogenic defects

28 The resulting compounds, MMC(IR800)-TOC and DA(IR800)-TOC, were labeled with Cu and (64)Cu and teste

29 2,3-dimethylmaleic anhydride (DA) is used to convert the TAT's amines to carboxylic ac

30 ted in the ventral wall of the dorsal aorta (DA).

31 neurons with shorter dendritic arborization (DA) and reduced complexity, diminished larval peristalti

32 etinal nonperfusion (measured in disc areas, DA) were determined using the validated concentric rings

33 As DA and GABA work in concert to shape and synchronize neu

34 se OTR-expressing neurons were identified as DA neurons (defined by tyrosine hydroxylase colocalizati

35 asty, stenting, and directional atherectomy (DA) have provided new options for the treatment of super

36 el preparation with directional atherectomy (DA) potentially improves outcomes of DCB.

37 pport reward, most likely through augmenting DA release.

38 larval stages, whereas others do not become DA positive until early pupa.

39 We analyzed the association between DA neuron clusters and specific brain lineages, developm

40 ationship underlying the association between DA production and PCC and PGL behavior needs further cla

41 lowing the initial competition phase between DA and radiotracer for binding to D2R.

42 ells coexpress TH2 and TPH1 and contain both DA and 5-HT, a dual neurotransmitter phenotype hitherto

43 Focusing initially on a single pentacene-C60 DA interface, we confirm that the charge transfer transi

44 atal subregions specifically involved in CEA-DA-striatal loops.

45 ucleus divisions; (2) CRF content of the CEA-DA path; and (3) striatal subregions specifically involv

46 , when incorporated in a non-centrosymmetric DA multilayer stack.

47 apy followed by ibrutinib plus chemotherapy (DA-TEDDi-R).

48 In the circulation, DA is primarily stored in and transported by blood plate

49 uptake for (64)Cu-MMC(IR800)-TOC than (64)Cu-DA(IR800)-TOC (5.2 +/- 0.2 vs. 3.6 +/- 0.4 percentage in

50 through the liver and spleen whereas (64)Cu-DA(IR800)-TOC was cleared through the kidneys.

51 (64)Cu-MMC(IR800)-TOC uptake whereas (64)Cu-DA(IR800)-TOC was not affected.

52 ory effect of GABAB receptor (GABABR) and D2 DA receptor (D2R) activation in VTA DA neurons.

53 Also, activation of D2 DA receptors in these cells significantly inhibited thei

54 DCFH2-DA (2',7'-dichlorodihydrofluorescein diacetate) is the m

55 However, the use of DCFH2-DA, as many other fluorogenic redox probes, is mainly co

56 ) subunits bind directly to DAT and decrease DA clearance.

57 a distinct functional role for brain-derived DA in the direct and indirect modulation of the peripher

58 human induced pluripotent stem cells-derived DA neurons.

59 oated electrodes rapidly and robustly detect DA, both in solution and in the rat dorsal striatum.

60 hosphorescence sensor is developed to detect DA based on l-cysteine capped Mn doped ZnS quantum dots

61 layer, while retaining the ability to detect DA.

62 The influences of diacetylene (DA) monomer, and the TC chemical structure and concentra

63 e a previously unappreciated role for direct DA input to the master circadian clock and highlight the

64 e behaviors across phylogeny, with disrupted DA signaling in humans associated with addiction, attent

65 Light caused a similar increase in DOPAC/DA ratio but interindividual variation was significantly

66 retinae a significant increase in the DOPAC/DA ratio is observed following in vivo light stimulation

67 Dopamine (DA) is one of the most important catecholamine neurotran

68 Dopamine (DA) neurotransmission controls behaviors important for s

69 Dopamine (DA) transmission mediates numerous aspects of behavior.

70 selves, are unable to induce acute dopamine (DA) neurodegeneration.

71 xcitatory/inhibitory imbalance and dopamine (DA) dysfunction.

72 ells containing monoamines such as dopamine (DA) and serotonin (5-HT) occur in the periventricular zo

73 We report here an atypical dopamine (DA) transporter (DAT) inhibitor, CTDP-32476, that may ha

74 choices is known to be mediated by dopamine (DA) neurons.

75 e first time high expression of D2 dopamine (DA) receptors in CD133+ve adenocarcinoma NSCLC cells.

76 eurons, but not 5-HT2CR expressing dopamine (DA) neurons.

77 trochemical fouling is typical for dopamine (DA) as its oxidation products are very reactive and the

78 Using induced human dopamine (DA) neurons, a study by Burbulla and colleagues demonstr

79 The increase in dopamine (DA) neurotransmission stimulated by in vivo cocaine expo

80 bility and methylphenidate-induced dopamine (DA) release, we retrospectively analyzed D2R availabilit

81 Mesocortical dopamine (DA) regulates a variety of cognitive functions via actio

82 The mesolimbic dopamine (DA) circuitry determines which behaviors are positively

83 rresponding inhibition of midbrain dopamine (DA) neurons.

84 hlights the importance of midbrain dopamine (DA).

85 The neurotransmitter dopamine (DA) regulates multiple behaviors across phylogeny, with

86 TATEMENT The high vulnerability of dopamine (DA) neurons in the substantia nigra (SN) to neurodegener

87 The release of dopamine (DA) regulates rewarding behavior and motor actions throu

88 ater solutions, and in ESSI MS, of dopamine (DA), tyrosine (Tyr) and N,N-dimethyl-p-phenylenediamine

89 kin odorants changes the number of dopamine (DA)- or gamma aminobutyric acid (GABA)-expressing neuron

90 This may be due to age-related dopamine (DA) decline affecting neural processing in striatum, pre

91 l behavioral process that requires dopamine (DA) release.

92 specific roles of phasic and tonic dopamine (DA) in action learning and selection, respectively.

93 ormone, exerting its functions via dopamine (DA) receptors that are present in a broad variety of org

94 ory drive onto reward-specific VTA dopamine (DA) neurons.

95 ed by ventral tegmental area (VTA) dopamine (DA) neurons to control food-motivated behavior and DA ne

96 th in ventral tegmental area (VTA) dopamine (DA) neurons.

97 Dopaminergic (DA) neurons in the ventral tegmental area (VTA) mediate

98 -)) mice develop age-dependent dopaminergic (DA) neuronal loss in the substantia nigra (SN) and ventr

99 t and maintenance of embryonic dopaminergic (DA) neurons in the midbrain.

100 ted into mature and functional dopaminergic (DA) neurons.

101 sion of RGMa in midbrain human dopaminergic (DA) neurons.

102 Loss of dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc)

103 drogenase 1 (ALDH1A1)-positive dopaminergic (DA) neurons at the ventral substantia nigra pars compact

104 En1 microdomain gives rise to dopaminergic (DA) neurons, whereas the Dbx1 microdomain gives rise to

105 eated dorsal raphe nucleus dopaminergic (DRN(DA)) activity upon exposure to arousal-evoking salient c

106 (DA) activity and optogenetically driven DRN(DA) activity were associated with waking from sleep, wit

107 Both endogenous DRN(DA) activity and optogenetically driven DRN(DA) activity

108 We also observed broader fluctuations of DRN(DA) activity across sleep-wake cycles with highest activ

109 Therefore, the DRN(DA) population is a critical contributor to wake-promoti

110 By supplying lineage information for each DA cluster, our analysis promotes further developmental

111 te progenitors (mFPPs) that retain efficient DA neurogenic potential over multiple passages and can b

112 g VTA neurons did not colocalize with either DA or GLU phenotypic markers.

113 For excess DA levels, a failure in energy metabolism is indicated.

114 seeking, and cocaine-enhanced extracellular DA in the nucleus accumbens.

115 c axonal projections regulates extracellular DA levels and relevant behaviors.

116 target lesion revascularization was 7.3% for DA+DCB and 8.0% for DCB (P=0.90).

117 major adverse events at 1 year was 89.3% for DA+DCB and 90.0% for DCB (P=0.86).

118 4.1% for DCB; postdilation rate was 6.3% for DA+DCB versus 33.3% for DCB.

119 rcent diameter stenosis was 33.6+/-17.7% for DA+DCB versus 36.4+/-17.6% for DCB (P=0.48), and clinica

120 Predilation rate was 16.7% for DA+DCB versus 74.1% for DCB; postdilation rate was 6.3%

121 findings underscore that DAT is critical for DA neurotransmission and homeostasis.

122 itivity and lower the limit of detection for DA compared to bare CFEs.

123 Technical success was superior for DA+DCB (89.6% versus 64.2%; P=0.004).

124 across the ME and consists of high-frequency DA discharges that are coordinated within the minutes ra

125 st the potential of implementing the AlN/GaN DA as a promising active region design for high efficien

126 nificant miniband engineering in the AlN/GaN DA by tuning the thicknesses of AlN barriers and GaN wel

127 nd optoelectronics properties of the AlN/GaN DA for mid- and deep-ultraviolet (UV) applications.

128 ows that the valence subbands of the AlN/GaN DA is properly rearranged leading to the heavy-hole (HH)

129 on-hole wavefunction overlaps in the AlN/GaN DA structure can be remarkably enhanced up to 97% showin

130 First, locally generated DA release signals are organized over more than four ord

131 epsilon-caprolactone) (PEG-PCL, PECL) to get DA-TAT-PECL.

132 crease (30%) in IC50 for inhibition of [(3)H]DA uptake by cocaine in WT hDAT.

133 RD2, and DRD4 alleles associated with higher DA tone.

134 In contrast, in the hindbrain, DA terminals form traditional synaptic contacts with aud

135 However, it is unclear how DA mediates opposing patterns of behavior by acting on d

136 Mice lacking GIRK channels in DA neurons exhibited increased locomotor activation in r

137 -dependent inhibitory feedback mechanisms in DA neurons of the ventral tegmental area (VTA).

138 CHL1 in the VM, corresponding with roles in DA progenitor migration and differentiation.

139 ene therapy by expressing DAT selectively in DA neurons and terminals, resulting in the rescue of abe

140 This study examined whether variation in DA-related genes moderated APZ effects on reward-related

141 monstrate that expanded mFPPs have increased DA neuron potential and differentiate more efficiently a

142 binding/activating peptide, mSIRK, increases DA efflux through DAT in heterologous cells and primary

143 Increasing DA sensitivity without compromising electrode kinetics i

144 f DAT blocked the ability of mSIRK to induce DA efflux, consistent with a direct interaction of Gbeta

145 uring fear extinction, and Gq-DREADD-induced DA potentiated activity of D1-expressing neurons in both

146 e carried out numerical studies on the InGaN DA showing the tunable optoelectronic properties of the

147 n overlaps are remarkably large in the InGaN DA structure despite the existence of strain effect and

148 ive and therapeutic psychostimulants inhibit DA reuptake and multiple DAT coding variants have been r

149 d by GABA and ACh corelease, which inhibited DA neurons.

150 ard system, directly and indirectly inhibits DA neurons in the VTA.

151 tegies for the conversion of stem cells into DA neurons.

152 with significant increases in intracellular DA and noraderenaline levels.

153 rgic AOB interneurons or locally introducing DA or GABA receptor antagonists alters kinship preferenc

154 onditions to accurately and reliably measure DA turnover in the mammalian retina.

155 Medial DA neurons received predominantly GABAergic currents med

156 These findings reveal that mesocortical DA can facilitate dissociable components of reward seeki

157 inals within the NAc that inhibit mesolimbic DA release and constrain reward-driven behavior.

158 analog prepared using conventional methods (DA-TOC).

159 component of a pathway that enables midbrain DA neurons to encode the negative valence associated wit

160 oter control to ablate Cnr2 gene in midbrain DA neurons of DAT-Cnr2 conditional knockout (cKO) mice.

161 Our results connect changes in midbrain DA neurons to menthol-induced enhancements of nicotine r

162 sessed on LHb-induced inhibition of midbrain DA cell firing in anesthetized rats.

163 ental area stimulates activation of midbrain DA cells and promotes DA release in terminal regions suc

164 However, NRG has also been shown to modulate DA levels, suggesting a role for ErbB4 signaling in dopa

165 Oxytocin-modulated DA neurons give rise to canonical striatal projections.

166 ave attracted great attention for monitoring DA and APD levels but none of the methods developed so f

167 ed virus-mediated targeting of RGMa to mouse DA neurons showed that overexpression of this repulsive

168 erial specification, was decreased in mutant DA endothelial cells (ECs), which ectopically expressed

169 The mutant DA and CV were abnormally connected.

170 an acid-active tumor targeting nanoplatform DA-TAT-PECL is developed to inhibit the nonspecific inte

171 Unlike other neurons, DA neurons depend on Cav1.3 channels for their rhythmic

172 re we investigated the role of nigrostriatal DA in fear extinction.

173 optoelectronic properties of the III-Nitride DA.

174 , we investigated how the firing activity of DA neurons should behave if they were coding the error i

175 w the biochemical and physiologic aspects of DA with a focus on its relations with VEGF and hypoxia i

176 These findings highlight the capacity of DA neurons to act as metabolic sensors by responding not

177 e the origin and synaptic characteristics of DA fibers innervating the inner ear and the hindbrain au

178 Previous work shows that clusters of DA neurons innervate different brain compartments, which

179 The degree of DA fouling of different carbon electrodes with different

180 en successfully applied for the detection of DA in urine samples, yielding recoveries as high as 93%.

181 In vivo detection of DA poses a challenge due to the low concentration and hi

182 review evidence suggesting that low doses of DA agonists that effectively treat TS decrease both phas

183 zed trial designed to estimate the effect of DA before DCB to facilitate the development of future en

184 ions of the SNc regulate the excitability of DA neurons differentially, resulting in different patter

185 aled persistent changes in the expression of DA-related proteins, including reductions in the express

186 eved using unilateral intra-PFC infusions of DA antagonists combined with contralateral inactivation

187 ribute directly to LHb-induced inhibition of DA cell activity and support the widely held proposition

188 eved to underlie the transient inhibition of DA neurons attributed to activation of the LHb.

189 ntributes to the use-dependent inhibition of DA release through muscarinic receptors only in the shel

190 g of behaviour, fMRI and PET measurements of DA D1 availability.

191 e properties of this disynaptic mechanism of DA transmission are not well understood in the NAc shell

192 sions of the RMTg reduced both the number of DA neurons inhibited by, and the duration of inhibition

193 e SNpc of LRRK(-/-) mice before the onset of DA neuron loss.

194 n mutants, we observed ectopic production of DA neurons derived from the Dbx1 microdomain, at the exp

195 UHPLC-MS/MS method for the quantification of DA and its primary metabolite 3,4-dihydroxyphenylacetic

196 neuroanatomical evidence of OT regulation of DA neurons within the VTA is sparse.

197 show that Gbetagamma induces the release of DA through DAT.

198 ne formation, indicating a prominent role of DA in effective bone regeneration.

199 onal extension and repulsion, selectively of DA neurons, suggestive of a role in guidance towards for

200 an essential role of LRRK in the survival of DA neurons and in the regulation of the autophagy-lysoso

201 idence is presented for the selective use of DA-class drugs in obesity treatment.

202 implant failure rate associated with use of DAs and PAs.

203 s were searched for studies comparing use of DAs and PAs.

204 t marginal bone level associated with use of DAs should be viewed with caution as its clinical signif

205 itry is more complex than a direct action on DA neurotransmission.

206 ionally examined the effect of anesthesia on DA and DOPAC levels in the retina in vivo and find that

207 tentiate the inhibitory effect of cocaine on DA uptake and attenuate the effects of SRI-compounds on

208 iogenesis pathways, with special emphasis on DA producing PCC and PGL.

209 ence-dependent synaptic plasticity occurs on DA neurons while an organism is engaged in aversive expe

210 ipulate glutamatergic synaptic plasticity on DA neurons.

211 causal link between synaptic plasticity onto DA neurons and fear learning.

212 However, whether synaptic plasticity onto DA neurons is causally involved in aversion learning is

213 OPLS-DA was used to discriminate RA patients from controls.

214 iate (ANOVA) and multivariate analyses (OPLS-DA) allowed us to identify new potential volatile marker

215 atent structures-discriminant analysis (OPLS-DA) was applied successfully to predict the origin of th

216 ial last-squares discriminant analysis (OPLS-DA), multivariate models were created for both modes of

217 When the training set used to build the OPLS-DA models contained samples representative of each harve

218 ioplasty and stenting (56+/-29%, P=0.009) or DA (55+/-29%, P=0.007).

219 stenting (n=48), BA and stenting (n=52), or DA with distal protection and bailout stenting (n=55).

220 stenting as compared with BA and stenting or DA.

221 its reinforced by aberrant, increased phasic DA responses.

222 PLS-DA model was able to correctly classify samples with nea

223 PLS-DA models based on spectroscopic data were able to class

224 geneity, a robust, reliable and accurate PLS-DA model was generated and validated, which was able to

225 al Least Square Discrimination Analysis "PLS-DA" and Support Vectors Machines "SVM"), was able to dis

226 tial Least Square Discriminant Analysis (PLS-DA) and Partial Least Square Regression (PLS-R) have bee

227 ial least-squares discriminant analysis (PLS-DA) model built to discriminate healthy from adenomatous

228 ial least squares discriminant analysis (PLS-DA) models were developed and validated with an independ

229 ial least-squares discriminant analysis (PLS-DA) to compare results between platforms, a 92% overlap

230 ial least-squared discriminant analysis (PLS-DA) with double leave-one-patient-out cross-validation w

231 least squares for discriminant analysis (PLS-DA).

232 ial Least Squares Discriminant Analysis (PLS-DA).

233 tial least square discriminant analysis, PLS-DA) was developed and applied to the discrimination of a

234 A two-level PLS-DA Hierarchical strategy was employed, with coffee being

235 multivariate modeling by PCA and partial PLS-DA on the Workflow4Metabolomics infrastructure.

236 release characteristics of ALDH1A1-positive DA fibers, supporting a regional specific function of AL

237 racer binding is measured when postchallenge DA levels have returned to baseline, following the initi

238 larval brain contains six groups of primary DA neurons (born in the embryo), which we assign to six

239 hat Gbetagamma interacts with DAT to promote DA efflux.

240 activation of midbrain DA cells and promotes DA release in terminal regions such as the nucleus accum

241 Pt-DA showed photocytotoxicity against cisplatin-resistant

242 njugated platinum(IV) anticancer complex (Pt-DA) has been incorporated into G-quadruplex G4K(+) borat

243 Most notably, Pt-DA and Pt-G4K(+)B hydrogels show selective phototoxicity

244 to discrete flakes after incorporation of Pt-DA.

245 The endocannabinoid (eCB) system regulates DA release and is a canonical gatekeeper of goal-directe

246 ErbB4 expression in DAergic neurons, rescues DA dysfunction and ameliorates behavioral deficits.

247 T's amines to carboxylic acid; the resulting DA-TAT is conjugated to poly(ethylene glycol)-poly(epsil

248 Within the limitations of this review, DAs appear to be a viable alternative to PAs at time of

249 SN DA-like burst activity increased integrated ICa during (

250 ological properties of human LTCCs during SN DA-like and arterial smooth muscle (aSM)-like activity p

251 wer sensitivity to Cav1.3 variants during SN DA-like pacemaking compared with Cav1.2 during aSM-like

252 a likely target mediating the effects of SN DA activation.

253 d by weaker state-dependent inhibition of SN DA LTCCs compared with aSM Cav1.2.SIGNIFICANCE STATEMENT

254 These data suggest that activation of SN DA neurons and DS D1 receptors during fear extinction re

255 lly relevant isradipine levels to protect SN DA neurons can be explained by weaker state-dependent in

256 Using sorted DA neuron preparations from TH-eGFP mice we found that D

257 various arms of the circuit through specific DA subpopulations to assess: (1) whether the circuit con

258 Striatal DA D2 receptors (D2Rs) also regulate reinforcement learn

259 resulting in the rescue of aberrant striatal DA dynamics, reversal of characteristic phenotypic and b

260 e I (GCH1) transcription; increases striatal DA in vivo; and has symptomatic efficacy in two postneur

261 s in SN, neuritic swelling, reduced striatal DA release, and impaired motor behavior.

262 intermolecular interaction between TC-TC, TC-DA, and DA-DA enables the construction of strategic sens

263 preparations from TH-eGFP mice we found that DA neurons express FA transporter and binding proteins,

264 Finallly, we found that DA-induced expression of core circadian clock genes Peri

265 We explored the possibility that DA may act on separate networks of PFC neurons that are

266 We show that DA terminals in the saccule contain vesicles but transmi

267 In vitro and in vivo studies have shown that DA inhibits angiogenesis through activation of the DA re

268 ntify a novel, direct connection between the DA neurons of the ventral tegmental area (VTA) and the s

269 lation at the tumor site and deshielding the DA group.

270 rphism in DAT1/SLC6A3 (the gene encoding the DA transporter (DAT)) were tested.

271 est that flow has essential functions in the DA by promoting arterial and suppressing venous marker e

272 s of dopaminergic medications, including the DA partial agonist aripiprazole (APZ), have been inconsi

273 gnificantly improve our understanding of the DA function in vivo.

274 ibits angiogenesis through activation of the DA receptor type 2.

275 art accounts for functional diversity of the DA system.

276 Current treatments replenish the DA deficit and improve symptoms but induce dyskinesias o

277 and the loss of either TRPC1 or STIM1 led to DA cell death, which was prevented by inhibiting L-type

278 vely treat TS decrease both phasic and tonic DA, thereby also reducing the propensity for both tic le

279 Increased tonic DA amplifies the tendency to execute learned tics and al

280 the surfaces as well as the response toward DA was recovered close to the original performance level

281 velopment of clinical interventions to treat DA-related brain disorders.

282 may provide new insights into understanding DA developmental conditions such as autism spectrum diso

283 wered the LLQ on the same day they underwent DA testing using a focal dark adaptometer measuring rod

284 mic CSF-c cells have been thought to take up DA from the ventricle instead of synthesizing it.

285 erature regarding the effectiveness of using DAs, the aim of this systematic review is to examine mar

286 two prosthetic techniques in favor of using DAs.

287 ffective method to monitor real-time in vivo DA signaling, however the sensitivity is somewhat limite

288 , these findings enhance our knowledge of VM DA pathways development, and may provide new insights in

289 ugmented excitatory synaptic strength in VTA DA neurons and increased addiction risk after PE.SIGNIFI

290 ncreased excitatory synaptic strength in VTA DA neurons is a critical cellular mechanism for addictio

291 enhanced excitatory synaptic strength in VTA DA neurons, which in turn contributes to PE-induced incr

292 ) and D2 DA receptor (D2R) activation in VTA DA neurons.

293 ed eCB-LTD at the excitatory synapses of VTA DA neurons primarily due to CB1 receptor downregulation.

294 ocial behavior through direct effects on VTA DA neurons, thus providing mechanistic insight into how

295 data suggest that feedback inhibition to VTA DA neurons, mediated by GIRK channel activation, tempers

296 using increased ventral tegmental area (VTA) DA neurons' activity and stress-related behaviors, such

297 a role in epithelial barrier function, were DA in patients with SAR and control subjects, irrespecti

298 , and that this mechanism is associated with DA D1 receptor availability.

299 le patients achieved complete remission with DA-TEDDi-R.

300 were associated with waking from sleep, with DA signal strength predictive of wake duration.