ライフサイエンスコーパス: dopamine

1 re redox couples (potassium ferrocyanide and dopamine).

2 eases turnover of neurotransmitters, such as dopamine.

3 cost of mental labor by increasing striatal dopamine.

4 nsitivity was significantly reduced when OFF dopamine.

5 gical diseases related to abnormal levels of dopamine.

6 on brain incentive salience systems, such as dopamine.

7 extracellular levels of the neurotransmitter dopamine.

8 n that has been closely linked to mesolimbic dopamine.

9 ous firing of ChINs induces local release of dopamine.

10 ay signal through the release of GABA and/or dopamine.

11 associated with blunted presynaptic striatal dopamine.

12 model to investigate the involvement of the dopamine 1 (D1) receptor on the reward and reinforcement

13 tor (NMDAR) encephalitis alter the levels of dopamine 1 receptor (D1R) and dopamine 2 receptor (D2R)

14 Y is associated with decreased activation of dopamine 1 receptor-expressing medium spiny neurons (D1R

15 the levels of dopamine 1 receptor (D1R) and dopamine 2 receptor (D2R) and cause psychotic-like featu

16 Striatal dopamine activity was assessed as K(i)(cer) value using

17 Although dopamine agonist dose did modulate pupillary responses t

18 n patients with impulse control disorders on dopamine agonists were excluded from the analysis.

19 ctory to the prediction that increased tonic dopamine amplifies reward expectation.

20 involved in cAMP/PKA dynamics in response to dopamine and acetylcholine co-stimulation in living flie

21 a novel form of interaction between striatal dopamine and acetylcholine dynamics.

22 arning and decision-making, is controlled by dopamine and contributes to the pathogenesis of psychosi

23 s long-term effects using dual-probe in vivo dopamine and glutamate microdialysis in nucleus accumben

24 revealed marked decreases in cocaine-induced dopamine and glutamate outflow 4 weeks after VU0364572 t

25 inical evidence for the potential utility of dopamine and L-mimosine in the safer administration of c

26 rate-limiting enzymes for the production of dopamine and melatonin in the brain.

27 ioned urine reduced cholesterol and elevated dopamine and melatonin.

28 e-releasing neurons, extracellular levels of dopamine and net PKA activity in spiny projection neuron

29 These increases in modulation by dopamine and noradrenaline likely indicate changes in be

30 However, the real-time relationship between dopamine and PKA in spiny projection neurons remains unt

31 The dopamine and serotonin systems are impacted by photoperi

32 al sub-division unique to primates-with both dopamine and serotonin tracking decision times.

33 Recent animal research indicates that dopamine and serotonin, neuromodulators traditionally li

34 hat reward-related circuitry is modulated by dopamine and serotonin, we examined, for the first time,

35 While these methods have been applied to dopamine and some other transmitters, estimation of 5-hy

36 Therefore, astrocytes mediate the dopamine- and amphetamine-induced synaptic regulation, r

37 between CHL1 and DRD2 in neurons expressing dopamine- and cAMP-regulated phosphoprotein of 32 kDa (D

38 potential recordings in rodent striatum show dopamine- and reward-dependent transitions between two s

39 Effects of both serotonin and dopamine are mediated largely through their downstream G

40 virtual array of electrochemical sensors for dopamine as a strategy for circumventing sensor fouling,

41 homosynaptic mechanisms-such as presynaptic dopamine autoreceptors and dopamine transporters-as well

42 hat optogenetic stimulation of nigrostriatal dopamine axons rapidly and persistently elevated the exc

43 We show that modulating homoeostatic dopamine balance distinctly alters implicit and explicit

44 under control of the noradrenergic-specific dopamine beta-hydroxylase promoter (DBH-hSNCA).

45 then used dLight fiber photometry to measure dopamine binding across the ventral striatum (medial acc

46 showed complex and heterogeneous profiles of dopamine binding during self-administration and relapse.

47 ns avenues for understanding many aspects of dopamine biology.

48 of the sensor with four reference molecules (dopamine, bovine serum albumin, glucose and elongated pe

49 cordings show that nesfatin-1 hyperpolarizes dopamine, but not GABA, neurons of the VTA by inducing a

50 irect stimulation of VTA or substantia nigra dopamine cell bodies failed to induce food approach or e

51 der range of Parkinson disease features that dopamine cell replacement based on generating neurons fr

52 that flexibly influence the function of the dopamine cells and circuits.

53 zophrenia and test approaches to reverse the dopamine changes.

54 We examined dopamine circuit activity at various stages, including s

55 oward understanding the impact of mesolimbic dopamine circuitry in acute and chronic pain.

56 In this study, we used a simple dopamine coating method to load FGF on the surface of PX

57 um signals at somata and axons, and striatal dopamine concentrations.

58 We hypothesized that the dopamine D(1) receptor (D(1) R) contains structural feat

59 on's disease (HD) include over-activation of dopamine D(1) receptors (D(1)R), producing an imbalance

60 piny striatal neurons of the direct pathway, dopamine D(1)- and adenosine A(1)-receptors are coexpres

61 ctive conformations of the highly homologous dopamine D(2) and D(3) receptors (D(2)R and D(3)R), we f

62 serotonin 5-HT(2A) receptor (5-HT(2A)R), the dopamine D(2) receptor (D(2)R) is a key therapeutic targ

63 colocalization of dopamine D(3) receptor and dopamine D(2) receptor in HCs.

64 of dopamine synthesis or release capacities, dopamine D(2/3) receptor (D2/3R) or dopamine transporter

65 sion tomography in rats to quantify regional dopamine D(2/3) receptors and metabotropic glutamate rec

66 istochemistry demonstrated colocalization of dopamine D(3) receptor and dopamine D(2) receptor in HCs

67 ndicate that NCS-Rapgef2 signaling to ERK in dopamine D1 receptor-expressing neurons in the NAc, but

68 ignaling to ERK that underlies plasticity in dopamine D1 receptor-expressing neurons leading to acqui

69 Here, we demonstrate that dopamine D1 receptors in the dentate gyrus act as a pivo

70 y delays healing, whereas the stimulation of dopamine D1 receptors promotes angiogenesis and expedite

71 )-coupled dopamine receptor belonging to the dopamine D1-like receptor family.

72 mory, and Ca(v)1.2 is a downstream target of dopamine D1-receptor (D1R) signaling, we next generated

73 d in mice with cell-specific ablation of the dopamine D2 receptor (D2R) in the striatal medium spiny

74 The dopamine D2 receptor (D2R) is a G protein-coupled recept

75 henotype is supported by decreased available dopamine D2 receptor (D2R) levels and the failure of ant

76 We hypothesized that striatopallidal dopamine D2 receptor (D2R)-expressing neurons promote av

77 We have previously identified a dopamine D2 receptor (DRD2) coexpression module enriched

78 tal dopamine levels rather than insufficient dopamine D2 receptor occupancy.

79 These results indicate that ALK regulates dopamine D2 receptor trafficking, which has implications

80 ceptors, voltage-gated calcium channels, the dopamine D2 receptor, and complement glycoproteins.

81 Striatal dopamine D2 receptors (D2Rs) are important for motor out

82 l compound, SEP-363856, that does not act on dopamine D2 receptors but has agonist activity at trace

83 The stimulation of dopamine D2 receptors negatively regulates the angiogeni

84 stric rhythm using domperidone, a peripheral dopamine D2/D3 antagonist and common anti-emetic, at a d

85 Preclinical studies show that the dopamine D3 receptor (D3R) is involved in the reinstatem

86 The dopamine D5 receptor (D5R) is a Galpha(s)-coupled dopami

87 n that depression is associated with altered dopamine (DA) and serotonin (5-HT) functioning, the curr

88 Drugs of abuse increase dopamine (DA) concentration in these brain areas, includ

89 own that mGluR2/3 agonists have no effect on dopamine (DA) in wild type rats, we used the methylzoxym

90 d disorder caused by the progressive loss of dopamine (DA) neurons in the substantia nigra pars compa

91 basis of the effects of the neurotransmitter dopamine (DA) on inflammation remain unclear.

92 g the prefrontal cortex (PFC) and mesolimbic dopamine (DA) pathway are particularly susceptible to TH

93 Dopamine (DA) plays a critical role in the brain, and th

94 These dopamine (DA) replacement-resistant symptoms are associa

95 Dysfunctional dopamine (DA) signaling has been associated with a broad

96 ations in [(18)F]DOPA uptake, an estimate of dopamine (DA) synthesis capacity, in the striatum predic

97 cifically, electrochemical polymerization of dopamine (DA) was employed to modify a gold electrode fo

98 onoamine oxidase (MAO) metabolizes cytosolic dopamine (DA), thereby limiting auto-oxidation, but is a

99 ured by the detection of ascorbic acid (AA), dopamine (DA), uric acid (UA), and serotonin (5-HT) in 0

100 est-bed for rapid and sensitive detection of dopamine (DA).

101 e, we show that the octopamine-Octbeta1R and dopamine-dDA1 signals together drive both aversive and a

102 substantia nigra, which is the root cause of dopamine deficit in the striatum in Parkinson's disease.

103 daptive molecular and motor responses in the dopamine-denervated striatum may prompt the development

104 aberrant and baseline reach kinematics in a dopamine-dependent manner.

105 Here, by mapping a dopamine-dependent transcriptional activation marker in

106 decision-making and reward learning are both dopamine-dependent, but preclinical research suggests th

107 h recent studies, these data suggest that in dopamine-depleted mice abnormally correlated and tempora

108 We found that, in dopamine-depleted mice, (1) the firing rate of D2-SPNs w

109 critically involved in the motor deficits of dopamine-depleted mouse models of Parkinson's disease, w

110 fic transcriptomic and epigenetic effects of dopamine depletion on PV(+) and PV(-) cells within three

111 tance of about 20 Omega, high sensitivity of dopamine detection (7.8 muA/muM), which is about 312 fol

112 tein (GFP) enable high-resolution imaging of dopamine dynamics in behaving animals.

113 review these and summarize the evidence for dopamine dysfunction, reward processing, and salience ab

114 In this context, dopamine dysregulation may be transdiagnostic of the pat

115 Goal-trackers do not rely on dopamine for learning and are thought to use model-based

116 omotor activity, and anxiety-like behavior], dopamine function [striatal expression of tyrosine hydro

117 Most evidence for these aspects of dopamine function comes from simple tasks (e.g. lever pr

118 Aberrant dopamine function in the dorsal striatum and aberrant in

119 MRI (NM-MRI) as a novel tool to investigate dopamine function in the human brain.

120 Because dopamine has been implicated in contextual fear memory,

121 s been shown that reward signals mediated by dopamine help guide the prioritization of events for lon

122 These findings indicate [(18)F]FDOPA PET dopamine imaging has potential as biomarker to guide tre

123 GC dopamine immunoreactivity was increased in BPA- and BPS-

124 extension of the prediction error theory of dopamine, imported from artificial intelligence, represe

125 ntists have tried to define the functions of dopamine in concise conceptual terms(2), but the practic

126 calcium imaging, we identify a new role for dopamine in coupling locomotion and egg-laying together

127 However, the contribution of dopamine in dynamic, ecological situations where reward

128 in, as well as increased basal extracellular dopamine in prefrontal cortex and 5-hydroxytryptamine in

129 Involvement of dopamine in regulating exploration during decision-makin

130 l manipulation, we show that the activity of dopamine in the brain modulates decisions to move on, wi

131 T1 limited the accumulation of serotonin and dopamine in the brain upon sleep deprivation (SD).

132 ychotic symptoms, consistent with a role for dopamine in the development of psychotic symptoms, but i

133 were required for half-maximum inhibition of dopamine-induced cAMP accumulation in cells coexpressing

134 T cells showed phase-dependent IPSPs during dopamine-induced fictive crawling, whereas P cells were

135 periments, we found that fibers positive for dopamine innervate reticulospinal neurons in the four re

136 Brain dopamine is critical for normal motor control, as eviden

137 The neurotransmitter dopamine is implicated in diverse functions, including r

138 g in a low excitability state, we found that dopamine is primarily inhibitory.

139 e-induced elevations of c-Fos expression and dopamine level in the striatum were greater in Het mice

140 of striatum is accompanied by restoration of dopamine levels and rescue of motor deficits.

141 Voltammetry recordings of mesolimbic dopamine levels demonstrated that acute stress selective

142 ransporter (DAT) availabilities, or synaptic dopamine levels in 983 patients and 968 control subjects

143 Psychomotor stimulants increase dopamine levels in the striatum and promote locomotion;

144 Dopamine levels in the ventral striatum are elevated fol

145 lines in concert with extracellular striatal dopamine levels rather than insufficient dopamine D2 rec

146 ible for the molecular adaptation of ChIs to dopamine loss and chronic L-DOPA treatment.

147 The effect of dopamine loss on ChIs was due to decreased currents of b

148 MAOB, a crucial monoamine oxidase for dopamine metabolism, triggers oxidative stress in dopami

149 hese regions in exploration and suggest that dopamine modulates how this circuit tracks accumulating

150 erneurons, which drive dopamine release from dopamine neuron axons by activation of nicotinic acetylc

151 ne signals evoked by stimulation of midbrain dopamine neuron axons.

152 nce in this trade-off, and identify a single dopamine neuron called DAN-i1 that can do so.

153 Antipsychotic failure coincided with reduced dopamine neuron firing, which was not observed during an

154 signaling and not recapitulated by NAcSh or dopamine neuron photostimulation.

155 t into behavioral reinforcement via midbrain dopamine neuron responses.

156 gs provide a circuit framework through which dopamine neuronal activation shifts from reward delivery

157 Independent discharges of dopamine neurons (tonic or pacemaker firing) determine t

158 ine system, which may be utilized to protect dopamine neurons against Parkinson's disease pathology.

159 n severe motor impairment, selective loss of dopamine neurons and increased astrocyte activation, whe

160 ficantly attenuated the MPTP-induced loss of dopamine neurons and motor behavioral deficits.

161 in vivo firing patterns of ventral midbrain dopamine neurons are controlled by afferent and intrinsi

162 These dopamine neurons are especially susceptible to Parkinson

163 of cell-replacement therapies that comprise dopamine neurons derived from human pluripotent stem cel

164 ENT This project serves to determine whether dopamine neurons encode differences in cued approach beh

165 in Parkinson disease (PD) is not uniform, as dopamine neurons from the ventral tier are lost more rap

166 ncentive cues, support an important role for dopamine neurons in the attribution of incentive salienc

167 ced striatal dopamine signaling, and loss of dopamine neurons in the substantia nigra.

168 Here we show that dopamine neurons in the VTA that project to the basal am

169 The activity of VTA dopamine neurons increases significantly after administr

170 Dopamine neurons of the ventral tegmental area (VTA) reg

171 used with optofluidic delivery to stimulate dopamine neurons of the ventral tegmental area of freely

172 Dopamine neurons played a causal role only after outcome

173 show for the first time that the activity of dopamine neurons precisely represents the impulse vector

174 However, the way dopamine neurons receive information about reward outcom

175 This suggests that dopamine neurons specifically in the VTA encode motivati

176 onin neurons activate ventral tegmental area dopamine neurons via glutamate co-transmission and that

177 echanism of manganese-induced dysfunction of dopamine neurons, and reveal a potential therapeutic tar

178 d that many VTA neurons, among them putative dopamine neurons, are excited by footshocks, and acquire

179 gic input to NAc shell arising from midbrain dopamine neurons, it alters fundamental properties of th

180 Finally, silencing VTA dopamine neurons, or their axon terminals in the BA duri

181 duces DCC cleavage and a significant loss of dopamine neurons, resulting in motor deficits.

182 ion leading to disinhibition of mesostriatal dopamine neurons.

183 tablished that RPEs are signaled by midbrain dopamine neurons.

184 ice in which Synaptotagmin-1 is removed from dopamine neurons.

185 regions or how it regulates the activity of dopamine neurons.

186 euron subtypes locally inhibited neighboring dopamine neurons.

187 Cerebral dopamine neurotrophic factor (CDNF) is expressed in the

188 been extensively studied(3), the effects of dopamine on larger-scale neural activity profiles are le

189 al subtypes selectively expressing either D1-dopamine or D2-dopamine receptors.

190 e observed reduced levels of norepinephrine, dopamine or serotonin, mainly in the brainstem.

191 e develop a translational mouse model of the dopamine pathophysiology seen in schizophrenia and test

192 ne hydroxylase, a biosynthetic enzyme in the dopamine pathway.

193 flexibility observed in disorders linked to dopamine perturbations may be attributable to specific D

194 In some cases, for example Dopamine-PKA-CREB and GABA-PKC-CREB signaling pathways,

195 The neuromodulator dopamine plays a key role in motivation, reward-related

196 L88-A, and Tb(2)(BDC)(3)-were coated on poly(dopamine) precoated stainless steel needles and used to

197 n under three drug conditions: 150 mg of the dopamine precursor L-dopa, 2 mg of the D2 receptor antag

198 We posit that dopamine promotes goal-directed motivation, but dampens

199 zing the reduction of ortho-quinones such as dopamine quinone.

200 r findings suggest that the combination of a dopamine receptor antagonist with radiation enhances the

201 ine D5 receptor (D5R) is a Galpha(s)-coupled dopamine receptor belonging to the dopamine D1-like rece

202 Here we developed a neurochemical model of dopamine receptor binding taking into account the differ

203 molecule close homolog of L1 (CHL1) and the dopamine receptor D2 (DRD2) are associated with psychiat

204 the saccharin-exposed fathers, especially at dopamine receptor promoter regions, suggesting that epig

205 f spiny projection neurons (SPNs) expressing dopamine receptor type 1 (D1-SPNs) or 2 (D2-SPNs) in mic

206 ls in adult mammals, that is required for D1 dopamine receptor-dependent ERK phosphorylation in mouse

207 to identify and interrupt the activity of D2 dopamine receptor-expressing striatal projection neurons

208 y neurons expressing either the D1 or the D2 dopamine receptor.

209 ructures of the A(2A) adenosine and the D(4) dopamine receptors were carried out, and 53 top-ranked m

210 dence of robust alterations in glutamate and dopamine receptors within brain regions that are known t

211 ectively expressing either D1-dopamine or D2-dopamine receptors.

212 The spinal cord also expresses all dopamine receptors; however, how the specific receptors

213 Thus, dopamine related sex-differences are likely mediated by

214 ne D2/3 receptor availability (P = 0.02) and dopamine release (P = 0.05) also predicted improvements

215 RNP H with decreased methamphetamine-induced dopamine release and behaviors, synaptosomal proteomic a

216 ChIN synchronization and its interplay with dopamine release are not fully understood.

217 ngs confirmed that presynaptic inhibition of dopamine release by the KOR agonist U69,593 was not bloc

218 terms(2), but the practical implications of dopamine release depend on its diverse brain-wide conseq

219 engage cholinergic interneurons, which drive dopamine release from dopamine neuron axons by activatio

220 n tonic VTA activity and associated accumbal dopamine release help regulate motivational behavior.

221 expand the toolkit for measuring endogenous dopamine release in Drosophila, introducing chemogenetic

222 Interestingly, VAChTcKO mice had reduced dopamine release in the dorsomedial striatum but not in

223 Dual-color photometry revealed that dopamine release in the nucleus accumbens evoked by rewa

224 e stress selectively increased reward-evoked dopamine release in the ventral lateral striatum (VLS),

225 Remarkably, dopamine release induced by strong depolarization and as

226 ct signaling through the NAcc and subsequent dopamine release is still not well known.

227 ing performance was not predictive of phasic dopamine release or dopamine supply.

228 recordings and optogenetics, they show that dopamine release persistently enhances the intrinsic exc

229 h lower D2/3 receptor availability and lower dopamine release predicting greater improvements.

230 resonance imaging to determine how striatal dopamine release shapes local and global responses to re

231 cts were found to demonstrate greater phasic dopamine release than "risk-averse" subjects.

232 However, with CsChrimson, dopamine release was significantly higher in the heel th

233 shown that striatal GABA tonically inhibits dopamine release, but whether GABA-A receptors directly

234 nant of MSN activity and local regulation of dopamine release.

235 ynaptotagmin-1 is the Ca(2+) sensor for fast dopamine release.

236 ring adolescence decreased nucleus accumbens dopamine release.

237 Here we monitor the activity of dopamine-releasing neurons, extracellular levels of dopa

238 , leaving open questions about the effect of dopamine replacement on the prioritization of memories b

239 ssociated risk for falls do not benefit from dopamine replacement therapy and often result in long-te

240 precipitated in Parkinson's disease (PD) by dopamine replacement therapy, often with detrimental con

241 (2020) show that stimulus-evoked dopamine responses are enhanced by novelty and increase

242 er than only the average and better explains dopamine responses.

243 dial prefrontal cortex, and ex vivo striatal dopamine reuptake.

244 s (NAc), a central component of the midbrain dopamine reward circuit, exhibits disturbed circadian rh

245 sted by theoretical models based on striatal dopamine's topographic modulation of cortico-thalamic co

246 We propose that the molecular machinery for dopamine secretion has evolved to support fast and slow

247 We find that synchronous dopamine secretion is abolished in acute brain slices of

248 Here we combine dynamic dopamine-sensitive molecular imaging(4) and functional m

249 Genetically encoded dopamine sensors based on green fluorescent protein (GFP

250 is a persistent problem for electrochemical dopamine sensors.

251 protein corona dynamics on ssDNA-SWCNT-based dopamine sensors.

252 cuit components, where fluctuating levels of dopamine shift the balance of compartment-specific stria

253 These changes in phasic dopamine signaling correspond with increases in the rate

254 l research suggests they depend on different dopamine signaling dynamics.

255 reely moving rats to test for differences in dopamine signaling in the nucleus accumbens core at base

256 This novel component in dopamine signaling provides a potential new target for i

257 Elucidation of the mechanism of dopamine signaling to ERK that underlies plasticity in d

258 otor and nonmotor symptoms, reduced striatal dopamine signaling, and loss of dopamine neurons in the

259 psychiatric disorders involving dysregulated dopamine signaling.

260 amatergic afferents to the striatum triggers dopamine signals both in vivo and in vitro These afferen

261 and sensitivity to temperature changes than dopamine signals evoked by stimulation of midbrain dopam

262 recent studies describing slowly increasing dopamine signals have instead proposed that they represe

263 Further, these input-specific dopamine signals have only been studied in separate anim

264 We also show that cortically evoked dopamine signals have other unique properties, including

265 behavioral relevance.SIGNIFICANCE STATEMENT Dopamine signals in the striatum play a critical role in

266 ferent afferents to the striatum can trigger dopamine signals, but their release properties are not w

267 mpartment selective action helps explain how dopamine somatic, but not terminally expressed, KORs are

268 We hypothesized that dopamine specifically modulates the influence of backgro

269 We propose the dopamine stabilizer (-)-OSU6162 may serve as an adjunct

270 untary abstinence and determined whether the dopamine stabilizer (-)-OSU6162 would decrease this new

271 Thus, in the high dopamine state, packets of FSI gamma and SPN beta altern

272 not predictive of phasic dopamine release or dopamine supply.

273 Mean dopamine synthesis (g = 0.65, p = .004) and release (g =

274 Striatal dopamine synthesis capacity at presentation predicts the

275 Results demonstrate that reduced striatal dopamine synthesis capacity links topographically with c

276 Striatal dopamine synthesis capacity predicted the worsening of p

277 reater for participants with higher striatal dopamine synthesis capacity, whereas methylphenidate and

278 an [(18)F]DOPA PET scan to quantify striatal dopamine synthesis capacity.

279 that reported molecular imaging measures of dopamine synthesis or release capacities, dopamine D(2/3

280 practical imaging tool for interrogating the dopamine system in addiction.

281 al information about basic properties of the dopamine system in males and females.

282 A dysfunctional dopamine system is implicated in most psychiatric disord

283 ctional importance of O-GlcNAcylation in the dopamine system, which may be utilized to protect dopami

284 y of neuronal alterations in addition to the dopamine system.

285 static properties related to the mesolimbic dopamine system.

286 el than the medial tip, and females had more dopamine than males.

287 distinct neuromodulatory actions of striatal dopamine that extend well beyond its sites of peak relea

288 Reward-evoked dopamine transients are well established as prediction e

289 to attenuate manganese-induced impairment of dopamine transmission.SIGNIFICANCE STATEMENT Manganese i

290 tic polymorphisms reducing expression of the dopamine transporter (DAT) are associated with some cond

291 acities, dopamine D(2/3) receptor (D2/3R) or dopamine transporter (DAT) availabilities, or synaptic d

292 Atypical dopamine transporter (DAT) inhibitors have shown therape

293 ly determined by its capacity to inhibit the dopamine transporter (DAT), and emerging evidence sugges

294 riments against tyrosine hydroxylase (TH) or dopamine transporter (DAT).

295 Dopamine transporter single-photon emission computed tom

296 ch as presynaptic dopamine autoreceptors and dopamine transporters-as well as heterosynaptic mechanis

297 72 treatment, without significant changes in dopamine uptake function.

298 o assessed the ability of cocaine to inhibit dopamine uptake in the nucleus accumbens core using fast

299 form for in situ monitoring of cell-secreted dopamine using Au-coated arrays of micropyramid structur

300 By enabling multiplexed imaging of dopamine with other circuit components in vivo, RdLight1