ライフサイエンスコーパス: dopamine

1 and the posterior tail of the striatum ('TS dopamine').

2 us IPSCs was increased by quinpirole but not dopamine.

3 eases in pump activity, which is affected by dopamine.

4 of movement despite the continued absence of dopamine.

5 f this dynamic pump potential is enhanced by dopamine.

6 gastric tone and motility via activation of dopamine 1 receptors in the dorsal vagal complex.

7 found that dopamine acts exclusively through Dopamine 2 Receptors to entrain the circadian rhythm in

8 We found that dopamine acts exclusively through Dopamine 2 Receptors t

9 o involve mechanisms other than stimulant or dopamine agonist effects.

10 rate amount of PD treatment and can tolerate dopamine agonist therapy.

11 In summary, our results suggest that dopamine alters the composition of functional OFC circui

12 ignificant elevations in brain extracellular dopamine and 5-HT in vivo.

13 pression of a marker gene in the presence of dopamine and blue-light exposure, both in vitro and in v

14 Learning and memory rely on dopamine and downstream cAMP-dependent plasticity across

15 The combination of dopamine and ketones in a PSR leads to the formation of

16 TFH cells produce high amounts of dopamine and release it upon cognate interaction with B

17 We anticipate that investigation of dopamine and serotonin disturbances will be facilitated

18 s implicated gamma-aminobutyric acid (GABA), dopamine and serotonin neurotransmitter systems.

19 Loss of function in other genes in the dopamine and serotonin synthesis pathways did not alter

20 flavum (TfNCS) can catalyse the PSR between dopamine and unactivated ketones, thus facilitating the

21 ne axon signals in the ventral striatum ('VS dopamine') and the posterior tail of the striatum ('TS d

22 Dopamine- and tyrosine hydroxylase-immunopositive cells

23 preciated for decades that optimal levels of dopamine are essential for dlPFC working memory function

24 an significantly improve sensitivity towards dopamine as well as selectively promote cell viability.

25 nditioning, we observed opposite dynamics in dopamine axon signals in the ventral striatum ('VS dopam

26 We show, for the first time, that dopamine axons continue to grow from the striatum to the

27 The prolonged growth of dopamine axons represents an extraordinary period for ex

28 Here we demonstrate that nigrostriatal dopamine biases ongoing action selection.

29 onjugated to an engineered cysteine near the dopamine binding site.

30 The endogenous agonist dopamine binds with preference to D2/3 HIGH receptors re

31 res we show that (i) the detection limit for dopamine can be improved by two orders of magnitude [fro

32 The main goal of dopamine cell replacement therapy in Parkinson disease (

33 was revealed formed by conspicuous groups of dopamine cells in the midbrain tegmentum and profuse inn

34 Dopamine cells in turn are innervated and regulated by n

35 These neuroendocrine dopamine cells may contribute to the dopaminergic inhibi

36 o the ventral mesencephalon, the location of dopamine cells projecting to the striatum.

37 sed GABA cell activity, therefore downstream dopamine cells will be disinhibited; and thus, this coul

38 entified major projections to the mesolimbic dopamine circuit from the lateral hypothalamus and dorsa

39 y could allow for more precise modulation of dopamine circuit function.

40 c synaptic strength in the mesocorticolimbic dopamine circuitry.

41 nervation for humans, with higher amounts of dopamine compared with acetylcholine in the striatum.

42 The resulting dopamine concentration scales proportionally to the valu

43 A photoactivatable dopamine-conjugated platinum(IV) anticancer complex (Pt-

44 ll depolarization increases synaptic vesicle dopamine content prior to release via vesicular hyperaci

45 o rapidly, reversibly, and selectively block dopamine D1 and D2 receptors (D1R and D2R) when the PTL

46 Finally, conditional knock-out of Cav1.2 in dopamine D1 receptor (D1R)-expressing cells resulted in

47 an be used to reveal potentially therapeutic dopamine D1 receptor and adenosine A2A receptor ligands

48 eversed in the presence of 4 mum SCH23390, a dopamine D1 receptor antagonist.

49 e, the PDE10A radioligand (18)F-MNI-659, the dopamine D1 receptor radioligand (11)C-NNC 112, and the

50 In particular, direct pathway (dopamine D1 receptor-containing; D1R-) spiny projection

51 diacylglycerol lipase alpha (DGLalpha), from dopamine D1 receptor-expressing or adenosine A2a recepto

52 STDP in MSNs expressing dopamine D1 receptors shifted from spike-timing-dependen

53 rther analyzed by their ability to couple to dopamine D1R receptors by real-time bioluminescence reso

54 antipsychotic drugs (APDs) target primarily dopamine D2 or serotonin (5-HT2A) receptors, or both; ho

55 ve previously described a phenomenon whereby dopamine D2 receptor (D2R) activation elicits afterdepol

56 ines and heteroarylhomopiperazines with high dopamine D2 receptor (D2R) affinity.

57 (WT, C57BL/6J) animals were imaged with the dopamine D2 receptor radioligand (11)C-raclopride, the P

58 been ascribed to D2Rs.SIGNIFICANCE STATEMENT Dopamine D2 receptors (D2Rs) in the prefrontal cortex (P

59 Opioid stimulation of JNK also inactivates dopamine D2 receptors in a PRDX6-dependent manner.

60 ture-functional selectivity relationships at dopamine D2 receptors.

61 um, and the latter effect was blocked by the dopamine D2-like receptor antagonist haloperidol.

62 the dorsal striatum, an effect mediated via dopamine D2-like receptors.

63 served in rats following administration of a dopamine D2/3 receptor antagonist.

64 In the absence of dopamine D2/3 receptor occupancy data to inform antipsyc

65 How an optimal level of human dopamine D4 receptor (hD4R) is maintained in synaptic me

66 The dopamine D4 receptor garnered a great deal of interest i

67 rized by excitatory/inhibitory imbalance and dopamine (DA) dysfunction.

68 rized the specific roles of phasic and tonic dopamine (DA) in action learning and selection, respecti

69 IFICANCE STATEMENT The high vulnerability of dopamine (DA) neurons in the substantia nigra (SN) to ne

70 ed excitatory drive onto reward-specific VTA dopamine (DA) neurons.

71 ed to a corresponding inhibition of midbrain dopamine (DA) neurons.

72 tic strength in ventral tegmental area (VTA) dopamine (DA) neurons.

73 d (GABA) neurons, but not 5-HT2CR expressing dopamine (DA) neurons.

74 and as a hormone, exerting its functions via dopamine (DA) receptors that are present in a broad vari

75 Mesocortical dopamine (DA) regulates a variety of cognitive functions

76 Dopamine (DA) transmission mediates numerous aspects of

77 We report here an atypical dopamine (DA) transporter (DAT) inhibitor, CTDP-32476, t

78 in or non-kin odorants changes the number of dopamine (DA)- or gamma aminobutyric acid (GABA)-express

79 ry and highlights the importance of midbrain dopamine (DA).

80 n the dorsal striatum of dopamine-intact and dopamine-depleted rats during two brain states, respecti

81 s and mice with ventral tegmental area (VTA) dopamine depletion had attenuated delta activity (1-4 Hz

82 issue of Neuron, Chu et al. (2017) show that dopamine depletion using a 6-OHDA model causes a decreas

83 nalysis of mouse brain tissue for monitoring dopamine during electrical stimulation of the striatum r

84 logy from a high-density electrode array and dopamine dynamics from a carbon-fiber microelectrode.

85 linking neonatal hippocampal injury to adult dopamine dysfunction, and provides a potential mechanism

86 behavioral deficits resulting from midbrain dopamine dysfunction.

87 led that both JJ-3-42 and lorcaserin reduced dopamine efflux in the infralimbic cortex, while only JJ

88 Dopamine elevation in A53T mice increased levels of pote

89 Dopamine function and reward processing are highly inter

90 c resonance and molecular imaging studies of dopamine function in bipolar disorder.

91 ippocampal lesions, cause lasting changes in dopamine function in rodents, but it is not known if thi

92 allows the estimation of multiple aspects of dopamine function including dopamine synthesis capacity,

93 ural response that in part reflects striatal dopamine functioning.

94 functions, and the dysfunction of prefrontal dopamine has been associated with cognitive and emotiona

95 noamine neurotransmitters such as serotonin, dopamine, histamine, and noradrenaline have important an

96 d, and evaluated as ligands of 34 serotonin, dopamine, histamine, melatonin, acetylcholine, and adren

97 have revealed that dopamine neurons release dopamine in a synaptic signal mode, and that the neurons

98 le reuptake inhibitors (TRIs), which elevate dopamine in addition to serotonin and norepinephrine, ma

99 Emerging role of dopamine in neovascularization of pheochromocytoma and p

100 Dopamine in prefrontal cortices is implicated in cogniti

101 Dopamine in the PFC is implicated in both these processe

102 changes are alterations of neurons releasing dopamine in the ventral and dorsal territories of the st

103 However, no dopamine increases were observed in the caudate (p = 0.1

104 Dopamine induced phase-advances of the PER2::LUC biolumi

105 site of interaction with dopamine prevented dopamine-induced toxicity.

106 fficacy onto calbindin-negative cells during dopamine inhibition, suggesting that shared inputs are d

107 cacy of excitatory inputs in the presence of dopamine inhibition.SIGNIFICANCE STATEMENT Substantia ni

108 ed unit activities in the dorsal striatum of dopamine-intact and dopamine-depleted rats during two br

109 buting to regional differences in loading of dopamine into synaptic vesicles.

110 Dopamine is a catecholamine that acts both as a neurotra

111 a reversibly cross-linked network formed by dopamine-Laponite interfacial interactions to a covalent

112 n, although consistent increases in cortical dopamine levels (from 88 to 180%) were reported in the l

113 To address this, we manipulated both dopamine levels and alpha-synuclein expression.

114 We also observed increased subcortical dopamine levels in fatigued mice: a marker of individual

115 The lack of EFhd2 reduced extracellular dopamine levels in the brain, but enhanced responses to

116 of clozapine rapidly increased extracellular dopamine levels in the mPFC and improved alternation T-m

117 The correlation between disease severity and dopamine loss appears linear, but the majority of longit

118 negative exponential progression pattern of dopamine loss in PD.

119 out a systematic review and meta-analysis of dopamine measures in the rodent, human and primate brain

120 vel and familiar stimuli as a consequence of dopamine-mediated plasticity at the Kenyon cell-MBONalph

121 ey only exhibit mild motor phenotypes, minor dopamine metabolism abnormalities, and no signs of dopam

122 We tested whether dopamine might act more broadly to support learning of a

123 During oestrus, ventral tegmental area (VTA) dopamine neuron activity is enhanced and drives post tra

124 d cotransmission convey discrete patterns of dopamine neuron activity to striatal neurons.

125 ons not only in dopamine release but also in dopamine neuron connectivity, cotransmission, modulation

126 tors to improve their derivation and predict dopamine neuron content after engraftment.

127 plicated in psychiatric disorders, including dopamine neuron differentiation and innate immune respon

128 Midbrain dopamine neuron dysfunction contributes to various psych

129 athologically characterized by nigrostriatal dopamine neuron loss and the postmortem presence of Lewy

130 Regional differences in dopamine neuron signaling are likely to be differentiall

131 not only in a signaling role at a subset of dopamine neuron synapses, but also in mediating vesicula

132 Dopamine neuron synaptic actions vary across the striatu

133 gical alpha-syn conformers in human midbrain dopamine neurons and tested their contribution to the ag

134 Substantia nigra pars compacta (SNc) dopamine neurons and their targets are involved in addic

135 ed that substantia nigra pars compacta (SNc) dopamine neurons are a key node in the circuitry that dr

136 Midbrain dopamine neurons are crucial for many behavioral and cog

137 ve strategy for Parkinson's disease in which dopamine neurons are generated by direct conversion of a

138 Dopamine neurons are thought to encode novelty in additi

139 Although all dopamine neurons fire action potentials in a pacemaker p

140 nstitution experiments that Kenyon cells and dopamine neurons from axoaxonic reciprocal synapses.

141 This suggests that dopamine neurons have access to a wider variety of infor

142 Genetic deletion of GABAB receptors from dopamine neurons in adult mice did not affect general or

143 adaptive coding has been linked to midbrain dopamine neurons in nonhuman primates, and evidence in s

144 Dopamine neurons in the substantia nigra pars compacta a

145 toms accompanied by the preferential loss of dopamine neurons in the substantia nigra pars compacta.

146 Here, we show that, in contrast to dopamine neurons in the substantia nigra, vagal motoneur

147 Dopamine neurons in the ventral tegmental area (VTA) are

148 ient direct lineage reprogramming to induced dopamine neurons in vitro and in vivo.

149 ved by distinct subtypes of mesodiencephalic dopamine neurons located in the substantia nigra pars co

150 decades of research, it remains unclear how dopamine neurons make this calculation.

151 ne-induced inhibitory synaptic plasticity in dopamine neurons of the ventral tegmental area (VTA).

152 ontaneous tonic discharge activity of nigral dopamine neurons plays a fundamental role in dopaminergi

153 Optogenetic studies have revealed that dopamine neurons release dopamine in a synaptic signal m

154 behavior; most critically, it indicates that dopamine neurons selectively modulate signal reception p

155 Midbrain dopamine neurons signal reward prediction error (RPE), o

156 We identified dopamine neurons that uniquely coexpress the Onecut3 and

157 se data indicate that the features that make dopamine neurons unique are highly concordant and not a

158 sive alpha-synucleinopathies earlier than SN dopamine neurons while exhibiting milder cell loss in PD

159 cleus sends glutamatergic projections to VTA dopamine neurons, and that stimulation of this circuit p

160 ibitory postsynaptic currents (IPSCs) in VTA dopamine neurons, and these effects were mediated by a p

161 In dopamine neurons, both variants can act as autoreceptors

162 erized the cell-specific connectivity of VTA dopamine neurons, their mRNA translational profile, and

163 nce between excitation and inhibition in VTA dopamine neurons, while PDE4 inhibition reestablishes th

164 DAT-mediated increases in firing activity of dopamine neurons.

165 ibitory pauses in subpopulations of midbrain dopamine neurons.

166 and reinstated by optogenetically activating dopamine neurons.

167 PA receptor (AMPAR)/NMDAR ratios in midbrain dopamine neurons.

168 X6 to be required for development of gastric dopamine neurons.

169 ced reduction of GABAergic inhibition in VTA dopamine neurons.

170 ptic regulation that control the activity of dopamine neurons.

171 et both cortical and striatal dysfunction in dopamine neurotransmission and hence have the potential

172 a novel mechanism for sigma1R regulation of dopamine neurotransmission in response to methamphetamin

173 to which variants in the AKT1 gene influence dopamine neurotransmission is not well understood.

174 The role of the protein kinase Akt1 in dopamine neurotransmission is well recognized and has be

175 to the mate's song, although their striatal dopamine neurotransmission was only slightly elevated.

176 s model of tauopathy, while loss of no other dopamine or serotonin synthesis genes tested had this ef

177 GABA-mediated tonic current was enhanced by dopamine or the D1 agonist SKF81297 but not quinpirole,

178 AT) blockers also differentially affects the dopamine output in striosomes and matrix.

179 administration reduced both AMPH-stimulated dopamine overflow and AMPH-induced locomotor effects.

180 The dopamine partial agonist aripiprazole is increasingly us

181 neuropeptides (beta-endorphin, oxytocin, and dopamine) play particularly important roles, with each b

182 oradrenaline, midodrine plus octreotide, and dopamine plus furosemide over placebo to reduce mortalit

183 lein mutated at the site of interaction with dopamine prevented dopamine-induced toxicity.

184 This presents implications for understanding dopamine processing of motivated behavior; most critical

185 This dopamine profile is specific to behavioral choice, scala

186 In this study, poly(dopamine-quinone chromium (III))-microspheres (PDQCM) we

187 beta2-adrenergic receptor (beta2-AR) and D1 dopamine receptor (D1-R).

188 receptor (mGluRI) activation, facilitates D1 dopamine receptor (D1R) expression, and ensures long-ter

189 n the striatum and, by doing so, promotes D1 dopamine receptor (D1R) expression.

190 D offspring was associated with up-regulated dopamine receptor (DRD)-1 and -2 in the nucleus accumben

191 emale, deletion animals overexpress mRNA for dopamine receptor 2 and adenosine receptor 2a in the str

192 ion and depression-like symptoms, than other dopamine receptor antagonists.

193 is a persistent movement disorder induced by dopamine receptor blockers, including antipsychotics.

194 clear whether any of these genes, other than dopamine receptor D2, are immediately relevant to antips

195 nnel in dopaminergic neurons and the D2-like dopamine receptor DOP-3.

196 , we determined crystal structures of the D4 dopamine receptor in its inactive state bound to the ant

197 Here, we combine dopamine receptor reporter lines, anatomical tracing tec

198 To illuminate dopamine receptor structure, function, and ligand recogn

199 investigated activities at two off-targets: dopamine receptor subtype D2 and endocannabinoid recepto

200 human fatty acid amide hydrolase (FAAH) and dopamine receptor subtype D3 (D3R).

201 en gray-matter thickness and BPnd for either dopamine receptor subtype in the control group.

202 previous studies neither isolated a role of dopamine receptor subtype nor identified the site of its

203 ed higher affinity for D4, relative to other dopamine receptor subtypes, and that this activity might

204 arious types of mPFC neurons express several dopamine receptor subtypes, previous studies neither iso

205 s and alpha2A-adrenergic receptor, GABAB, or dopamine receptor type 2 receptors did not reveal any in

206 The D3 dopamine receptor, a member of the Gi-coupled D2 family

207 ceptors in PFC.SIGNIFICANCE STATEMENT The D3 dopamine receptor, a member of the Gi-coupled D2 family

208 lume signals in striatal target regions in a dopamine receptor-dependent manner.

209 ic afferents to the striatum; and one of two dopamine-receptor-expressing efferent pathways of the st

210 us work indicated that activation of D1-like dopamine receptors (D1DRs) in the nucleus accumbens shel

211 We found previously that loss of D2-family dopamine receptors ameliorated tauopathy in multiple mod

212 To better understand how loss of D2-family dopamine receptors can ameliorate tau toxicity, we scree

213 Song reinforcement diminished when dopamine receptors were blocked.

214 tor, a member of the Gi-coupled D2 family of dopamine receptors, are expressed throughout limbic circ

215 tor, a member of the Gi-coupled D2 family of dopamine receptors, is expressed throughout limbic circu

216 dative stress and altered mRNA expression of dopamine receptors, tyrosine hydroxylase, and dopamine t

217 nteract with the orthosteric binding site of dopamine receptors, was actually a negative allosteric m

218 ium spiny neurons (MSNs) expressing D1 or D2 dopamine receptors.

219 as associated with the relative somatostatin/dopamine-receptors levels, especially sst5 and sst5TMD4.

220 n METH dysregulation of dopamine release and dopamine-related behaviors.

221 ened a collection of C. elegans mutations in dopamine-related genes (n = 45) for changes in tau trans

222 try, we show that METH-enhancement of evoked dopamine release and basal efflux is dependent on sigma

223 ptor has a key role in METH dysregulation of dopamine release and dopamine-related behaviors.

224 y of VTA neurons but significantly decreased dopamine release and reuptake in the nucleus accumbens (

225 ation of D1R-SPNs reduces stimulation-evoked dopamine release and that bath application of a KOR anta

226 e striatum, involving variations not only in dopamine release but also in dopamine neuron connectivit

227 Conversely, ACC dopamine release by progressive ratio responding to rewa

228 ovides full rescue of both LTP induction and dopamine release during optogenetic activation of D1R-SP

229 out the brain, not typically associated with dopamine release events.

230 have reported increased amphetamine-induced dopamine release in subjects with schizophrenia (SCH) re

231 Lower dopamine release in the associative striatum correlated

232 ereas psychosis is associated with excessive dopamine release in the striatum.

233 We found neither dopamine release or uptake tracked individual difference

234 al dopamine synthesis capacity and increased dopamine release to stress.

235 ith little benefit, through a deficit of ACC dopamine release triggered by high-effort cost behavior,

236 the dorsolateral striatum (DLS), where less dopamine release was measured compared to the adjacent m

237 Dopamine release was quantified as the difference in spe

238 ction including dopamine synthesis capacity, dopamine release, and D2/3 receptor binding.

239 eptors to regulate neuronal excitability and dopamine release, but the roles of each variant are inco

240 muscarinic receptors had no effect on evoked dopamine release, suggesting that feedback inhibition of

241 mal models has been shown to reduce cortical dopamine release, which is critically involved in the re

242 nergic afferents and can negatively regulate dopamine release.

243 ternal behavior is associated with increased dopamine responses to the mother's infant and stronger i

244 PET scanner to simultaneously probe mothers' dopamine responses to their infants and the connectivity

245 nd without methylphenidate, a norepinephrine-dopamine reuptake inhibitor.

246 dysregulates both dopamine transmission and dopamine reuptake, the specific mechanism of action rema

247 t results with previously published data for dopamine revealed a unique pattern of innervation for hu

248 Dopamine, serotonin, the neuropeptide receptor NPR-1, an

249 flexibility, and suggest a revised model of dopamine-serotonin opponency with potential clinical imp

250 These behaviors were accompanied by striatal dopamine/serotonin abnormalities and cortical excitation

251 ng, aversive, and neutral stimuli whereas VS dopamine showed excitation only to reward or reward-pred

252 Additionally, TS dopamine showed excitation to several types of stimuli i

253 NP is mediated by a motivational dopamine signal that increases in response to novel stim

254 cocaine-exacerbated D1-cAMP/protein kinase A dopamine signaling in pyramidal neurons that in turn pat

255 e subtypes of dorsal horn neurons engaged by dopamine signaling in the hyperalgesic priming model, we

256 pattern selectivity requires touch-dependent dopamine signaling, including the mechanosensory TRP-4 c

257 Hence, dopamine signalling mediates an energy switch in the mus

258 imals with cocaine-associated alterations in dopamine signals for reward magnitude failed to subseque

259 populations resulting in distinct downstream dopamine signals.

260 at-expressing transgenic mice, we found that dopamine subtype 2 (D2) receptor-expressing medium spiny

261 Dopamine synthesis capacity (Kicer) and clinical measure

262 f schizophrenia have found elevated striatal dopamine synthesis capacity and increased dopamine relea

263 Moreover, dopamine synthesis capacity in the dorsal putamen and ca

264 t patients treated with clozapine show lower dopamine synthesis capacity than patients who have respo

265 tiple aspects of dopamine function including dopamine synthesis capacity, dopamine release, and D2/3

266 Dopamine synthesis was 16% higher in the caudate body, 1

267 hydroxylase phosphorylation and, thereby, of dopamine synthesis, supporting a major presynaptic role

268 These results suggest that when the dopamine system is challenged, D2L signaling is required

269 The ventral tegmental area (VTA) dopamine system is important for reward, motivation, emo

270 and environmental factors may sensitize the dopamine system so that it is vulnerable to acute stress

271 ral tegmental area and substantia nigra; the dopamine systems themselves; glutamatergic afferents to

272 To examine the effect of ketamine on the dopamine systems, we carried out a systematic review and

273 Here, we aimed to directly relate dopamine to learning about variable rewards, and the neu

274 se brain slices, nAChR-dependent spontaneous dopamine transients and the mechanisms underlying the or

275 errors and that, contrary to existing canon, dopamine transients are both sufficient and necessary to

276 Thus, although spontaneous dopamine transients are reliant on nAChRs, the frequency

277 Morphine increased dopamine transients in the NAc, but did not elicit norep

278 This result suggests that dopamine transients play a general role in error signali

279 (5)]enkephalin (1 mum) decreased spontaneous dopamine transients.

280 ough it is known that METH dysregulates both dopamine transmission and dopamine reuptake, the specifi

281 syndrome is characterized by an increase in dopamine transmission and structural as well as function

282 strated that somatosensory stimuli influence dopamine transmission in the mesolimbic reward system an

283 The dopamine transporter (DAT) belongs to the neurotransmitt

284 related human alpha-synuclein A53T mutant or dopamine transporter (DAT) blockers also differentially

285 To determine the usefulness of dopamine transporter (DAT) imaging to identify idiopathi

286 As the dopamine transporter (DAT) plays a prominent role in the

287 ives post translational modifications at the dopamine transporter (DAT) to increase the ability of co

288 we link tolerance to cocaine effects at the dopamine transporter (DAT) with aberrant cocaine-taking

289 ed significant group differences in striatal dopamine transporter binding (all age ranges in caudate

290 Striatal dopamine transporter binding, VMAT2 binding, (18)F-FDOPA

291 n which Cre- recombinase expression is under dopamine transporter gene (DAT) promoter control to abla

292 opamine receptors, tyrosine hydroxylase, and dopamine transporter genes in the zebrafish brain.

293 ar depression imaging studies show increased dopamine transporter levels, but changes in other aspect

294 molecular dynamics trajectories of the human dopamine transporter, in which multiple spontaneous Na(+

295 o cholesterol/CHS in Drosophila melanogaster dopamine transporter.

296 important role in regulating the function of dopamine transporters in the striatum.SIGNIFICANCE STATE

297 ng mutant mice exhibited significantly lower dopamine uptake after rotenone toxicity, due to reduced

298 The implication of dopamine was assessed by comparing performance ON and OF

299 Moreover, no release of dopamine was observed, ruling out amphetamine-like effec

300 Neurons co-storing glutamate and dopamine were found to project from the primal SNc to th