ライフサイエンスコーパス: SERT

1 SERT binding increases correlated with treatment-induced

2 SERT has garnered significant clinical attention partly

3 SERT is a target for antidepressant and psychostimulant

4 SERT is encoded by the same gene expressed in trophoblas

5 SERT knockdown in the MRN increased cocaine intake selec

6 SERT knockdown in the MRN or DRN produced anxiety-like b

7 SERT mediates the reuptake of serotonin into the presyna

8 SERT mediates the reuptake of serotonin through an alter

9 SERT nondisplaceable binding potential was quantified in

10 SERT(+) fibers were shown to distributed moderately to d

11 SERT-mediated substrate uptake was neither affected by i

12 (4) SERT-K(610)Y, which harbors a mutation converting it int

13 Here we utilize the C57BL/6J SERT Met172 model to evaluate SERT dependence for the ac

14 -MEC displays unusual 'hybrid' activity as a SERT substrate (ie, 5-HT releaser) and DAT blocker, wher

15 Consistent with its activity as a SERT substrate, 4-MEC evoked inward current in SERT-expr

16 ade (citalopram dosing) or genetic ablation (SERT(-/-)) of SERT function in vivo led to reduced serot

17 on scales down the population size of active SERT molecules and, as a consequence, lowers the effecti

18 In addition, SERT is a major molecular target for psychostimulants su

19 In addition, SERT Met172 mice are insensitive to chronic fluoxetine a

20 DRD2, DRD3, DAT1, COMT, DDC, GRIN2B, ADRA2C, SERT, TPH2, HTR2A, OPRK1 and OPRM1 genes.

21 ing a protective effect of estradiol against SERT loss.

22 Here, we show that not only DAT, but also SERT, is regulated by alphaCaMKII.

23 Although SERT(-/-) platelets displayed no difference in P-selecti

24 ed chimeric proteins to test whether DAT and SERT N and C termini contribute to transporter substrate

25 merous studies have investigated the DAT and SERT structural elements contributing to inhibitor and s

26 methylphenidate and desipramine for DAT and SERT, respectively, can be accounted for by their rate o

27 4-MePPP into the binding pockets for DAT and SERT.

28 In contrast, SERT-R607A/I608A and SERT-P601A/G602A were only rendered susceptible to inhib

29 ith the stalled mutants SERT-R607A/I608A and SERT-P601A/G602A.

30 esulting mutants SERT-F604Q, SERT-I608Q, and SERT-I612Q were retained in the endoplasmic reticulum, b

31 MA analogs inhibited uptake at DAT, NET, and SERT, but lengthening the amine substituent from methyl

32 norepinephrine, and serotonin (DAT, NET, and SERT, respectively).

33 gth of 4-MA on interactions at DAT, NET, and SERT.

34 T - SERT," where GoRT is the go trial RT and SERT is the stop error RT.

35 17-item Hamilton Depression Rating Scale and SERT binding as imaged by [(11)C]DASB positron emission

36 rforming reuptake of released serotonin, and SERT is the primary target for antidepressants.

37 ERT-DeltaN32 than that of wild type SERT and SERT-DeltaN22.

38 ell surface expression of wild type SERT and SERT-F604Q.

39 thermore, SSRIs protected both wild-type and SERT knockout mice from behavioral despair induced by ch

40 slices reveal that alphavbeta3 receptors and SERTs are enriched in presynaptic membranes from several

41 All analogs acted as SERT substrates, though N-butyl 4-MA had very weak effec

42 t male mice expressing the autism-associated SERT Ala56 variant have altered central serotonin (5-HT)

43 aCaMKII modulation for amphetamine action at SERT in vivo as well.

44 nity interactions of many antidepressants at SERT have been ablated via knock-in substitution (SERT M

45 differential effects of 4-MEC and 4-MePPP at SERT.

46 The interaction between SERT and alphaCaMKII was verified using biochemical assa

47 s were rescued in DAT chimeras encoding both SERT N and C termini.

48 In contrast, in Li(+) -containing buffer, SERT showed only low force interactions.

49 However, amphetamine-induced efflux by SERT-DeltaN32 or SERT-DeltaN42 (but not by SERT-DeltaN22

50 ver to support amphetamine-induced efflux by SERT.

51 y SERT-DeltaN32 or SERT-DeltaN42 (but not by SERT-DeltaN22) was markedly diminished.

52 The 5-HT deficits produced by SERT substrates are dependent upon transporter proteins,

53 ons is sufficient to decrease 5-HT uptake by SERT in midbrain synaptosomes.

54 substrate efflux in both cells coexpressing SERT and alphaCaMKII and brain tissue preparations.

55 Expression of the most common SERT variant (Ala56) in mice increases 5-HT clearance an

56 Consistent SERT pathology in raphe nuclei, striatum, thalamus, and

57 pared the results with those of constitutive SERT knockout.

58 To provide molecular insight, we constructed SERT homology models based on the Drosophila melanogaste

59 In contrast, SERT knockdown in the DRN increased cocaine intake selec

60 In contrast, SERT-R607A/I608A and SERT-P601A/G602A were only rendered

61 olecular and cellular mechanisms controlling SERT levels in the membrane remain poorly understood.

62 es that resulted from increased or decreased SERT activity support the idea that 5-HT signaling regul

63 ation constant (K(D)) of chemically distinct SERT and DAT inhibitors, with high temporal precision an

64 In order to distinguish SERT-dependent and -independent effects of SSRIs, we dev

65 ted RNA interference to locally downregulate SERT expression and compared the results with those of c

66 ifferent combinations of maternal and embryo SERT Ala56 genotypes to examine effects on blood, placen

67 inding of only one radioligand was enhanced; SERT radioligand binding was minimally affected.

68 f defective insulin signaling, which entraps SERT with ERp44 and impairs its glycosylation.

69 e the C57BL/6J SERT Met172 model to evaluate SERT dependence for the actions of two widely prescribed

70 GI perturbations, suggesting that excessive SERT activity leads to inadequate 5-HT4-mediated neuroge

71 distribution of both endogenously expressed SERT and heterologously expressed variants of human SERT

72 Both endogenous and heterologously expressed SERT were delivered to the extensive axonal arborization

73 Using membranes from HeLa cells expressing SERT and intact rat basophilic leukemia cells, we show t

74 he bulk of the resulting mutants SERT-F604Q, SERT-I608Q, and SERT-I612Q were retained in the endoplas

75 For SERT analysis, patients on selective serotonin reuptake

76 t new information on the molecular basis for SERT/NET selectivity of antidepressants, and provide the

77 state, currents was significantly lower for SERT-DeltaN32 than that of wild type SERT and SERT-Delta

78 ent test-retest reliability was observed for SERT binding in the striatum.

79 adiol levels as a novel treatment option for SERT deficiency associated obesity and metabolic abnorma

80 Time-activity curves were derived from SERT-rich structures and fit to 2 models: a simplified r

81 aling hampers the dissociation of ERp44 from SERT.

82 nserin revealed that platelets isolated from SERT(-/-) or citalopram-treated mice have reduced activa

83 ssants that are not recapitulated by genetic SERT insufficiency.

84 beta3 and significantly contribute to global SERT function at 5-HT synapses in the midbrain.

85 between go and stop error trials or "GoRT - SERT," where GoRT is the go trial RT and SERT is the sto

86 t SFG also correlated negatively with GoRT - SERT.

87 By using TacSERT and HA-SERT in antibody-based internalization assays, we show t

88 tag in the extracellular loop 2 of SERT (HA-SERT).

89 of the 5-HT signalling system (5-HT, 5-HIAA, SERT) and TNF-alpha expression were examined in the dist

90 However, how SERT deficiency promotes obesity is unknown.

91 -MEC and 4-MePPP with transporters for 5-HT (SERT) and dopamine (DAT) using molecular, cellular, and

92 try to study conformational changes in human SERT (hSERT) during 5-HT transport and inhibitor binding

93 Mutations in human SERT are associated with psychiatric disorders and autis

94 t X-ray crystallographic structures of human SERT at 3.15 A resolution bound to the antidepressants (

95 d heterologously expressed variants of human SERT in dissociated rat dorsal raphe neurons to examine

96 ) in the extracellular loop 4 (EL4) of human SERT, which induced a remarkable gain-of-potency (up to

97 ling the conformational equilibrium of human SERT.

98 ard-facing conformational state of the human SERT induced by serotonin.

99 the dynamic changes that occur in the human SERT upon binding of ions, the translocation of substrat

100 ne the mechanism of antidepressant action in SERT, and provide blueprints for future drug design.

101 The coordinated conformational changes in SERT associated with substrate translocation are not ful

102 ed to determine whether there are changes in SERT availability in the early symptomatic state and if

103 Conformational changes in SERT occur upon binding of ions and substrate and are cr

104 RT substrate, 4-MEC evoked inward current in SERT-expressing Xenopus oocytes, whereas 4-MePPP was ina

105 in the midbrain, accompanied by decreases in SERT activity and reduced localization of SERTs to integ

106 e-to-female transsexuals led to decreases in SERT binding in insula, anterior, and mid-cingulate cort

107 tolerance, supporting a role for estrogen in SERT deficiency-associated obesity and glucose intoleran

108 and citalopram fail to reduce immobility in SERT Met172 mice.

109 namic across pregnancy and were increased in SERT Ala56 dams at E14.5.

110 ort that estrogen suppression is involved in SERT deficiency-induced obesity and glucose intolerance,

111 bbeta3 activation by ADP and 5-HT is lost in SERT(-/-) platelets.

112 inding site and orientation of paroxetine in SERT remain controversial.

113 cular basis for high-affinity recognition in SERT and selectivity over NET for the prototypical antid

114 iated alphaIIbbeta3 activation is reduced in SERT(-/-) platelets.

115 terations arising from genetic reductions in SERT.

116 17beta-estradiol replacement in SERT (-/-) mice reversed the obesity and glucose intoler

117 in the dualistic conformational response in SERT induced by serotonin.

118 duces a dualistic conformational response in SERT.

119 tine, specifically its fluorophenyl ring, in SERT's substrate binding site directly depends on this p

120 An opposite phenotype was seen in SERT-deficient mice and in progeny of WT dams given the

121 ce for the existence of two binding sites in SERT when accessed in a physiological context.

122 ficant mammalian membrane proteins including SERT and DAT, neither of which tolerates complete remova

123 ent in female-to-male transsexuals increased SERT binding in amygdala, caudate, putamen, and median r

124 vels, suggesting that testosterone increases SERT expression on the cell surface.

125 ) such as fluoxetine or escitalopram inhibit SERT and are currently the principal treatment for depre

126 central nervous system, and drugs inhibiting SERT are widely used for the treatment of a variety of c

127 nfocal images of constitutively internalized SERT demonstrated that SERT primarily co-localized with

128 Furthermore, internalized SERT co-localized with the lysosomal marker LysoTracker

129 ility of the SERT Met172 model for isolating SERT/5-HT contributions of drug actions in vivo.

130 Antidepressants lock SERT in an outward-open conformation by lodging in the c

131 Maternal SERT Ala56 genotype effects on forebrain 5-HT levels wer

132 Maternal SERT Ala56 genotype was associated with decreased placen

133 4.5 indicated substantial impact of maternal SERT Ala56 genotype, with alterations in immune and meta

134 ively, these findings indicate that maternal SERT function impacts offspring placental 5-HT levels, f

135 , before trafficking to the plasma membrane, SERT must be dissociated from ERp44; and this process is

136 d TNF-alpha expression and decreased mucosal SERT expression and 5-HIAA.

137 ort activity to the folding-deficient mutant SERT-(601)PG(602)-AA.

138 Conversely, the vestibular mutant SERT-G402H merely displayed the high force population.

139 ding and flux assays on wild-type and mutant SERTs.

140 The bulk of the resulting mutants SERT-F604Q, SERT-I608Q, and SERT-I612Q were retained in

141 -immunoprecipitated with the stalled mutants SERT-R607A/I608A and SERT-P601A/G602A.

142 ere associated with increases in neocortical SERT binding in the GnRHa group relative to placebo (p =

143 SSRIs revealed that functional 5-HT2ARs, not SERTs, are necessary for the synergistic activation of a

144 glutinin) tag in the extracellular loop 2 of SERT (HA-SERT).

145 n both in the presence and in the absence of SERT.

146 D2R, antagonists of 5-HT6R, and blockers of SERT.

147 favor a more outward-facing conformation of SERT can explain the reduced turnover rate and increased

148 of H(+) to the inward-facing conformation of SERT in (i) cancelling out the electrogenic nature of in

149 detect a more outward-facing conformation of SERT.

150 that stabilize outward-open conformations of SERT decreased phosphorylation and agents that stabilize

151 lyzed their impact on the transport cycle of SERT by biochemical approaches and by electrophysiologic

152 diction was verified by tryptic digestion of SERT-expressing membranes: in the absence of Na(+), the

153 BPND agreed with the distribution of SERT in the rat brain.

154 The conformational dynamics of SERT transport function and inhibition is currently poor

155 n important role in the uptake efficiency of SERT.

156 a-helix to Lys reduced surface expression of SERT-E615K.

157 llular loop 1 restored surface expression of SERT-R152E/E615K to wild type levels.

158 ormational search associated with folding of SERT.

159 (603)-Thr(613)) was important for folding of SERT.

160 uited to the C terminus to assist folding of SERT.

161 humans yet they vary in their time frames of SERT disruption.

162 our results demonstrate that an increase of SERT activity is sufficient to cause the apneas in Necdi

163 igomerization was found to be independent of SERT surface density, and oligomers remained stable over

164 -type Ca(2+) channels and was independent of SERT.

165 nnels and synaptic plasticity independent of SERT.

166 Here, we examine how sustained inhibition of SERT activity alters serotonergic signaling and influenc

167 ice with paroxetine, a chemical inhibitor of SERT, also resulted in Cyp19a1 suppression, decreased ci

168 ) to various conformational intermediates of SERT during the transport cycle.

169 determine the IR activity, surface level of SERT, and their 5-HT uptake rates.Interestingly, no sign

170 bition of HSP90 also increased the levels of SERT, indicating that endogenously expressed transporter

171 In mice, constitutive loss of SERT causes life-long increases in anxiety-related behav

172 e results are consistent with a mechanism of SERT regulation that is activated by the transport of 5-

173 substituted cysteine accessibility method of SERT.

174 Thus, the exchange mode of SERT-DeltaN32 was selectively impaired.

175 a meta-analysis to identify the patterns of SERT pathology and the relevance to symptoms.

176 The phenotype of SERT knockout rats was a summation of the phenotypes gen

177 n-of-potency (up to >40-fold) for a range of SERT inhibitors.

178 of these mutations affect the regulation of SERT activity by cGMP-dependent phosphorylation.

179 the factors mediating the down-regulation of SERT in GDM trophoblast.

180 Rp44, binds to Cys200 and Cys209 residues of SERT to build a disulfide bond.

181 definitive support for an essential role of SERT antagonism in the acute and chronic actions of two

182 Here, we review the role of SERT in the development of motor and nonmotor complicati

183 m dosing) or genetic ablation (SERT(-/-)) of SERT function in vivo led to reduced serotonin (5-hydrox

184 indicate the existence of a subpopulation of SERT responding differently to serotonin binding than hi

185 havbeta3 colocalizes with a subpopulation of SERT-containing synapses in raphe nuclei.

186 sterol plays a role in this subpopulation of SERT.

187 C-dependent ER export in axonal targeting of SERT.

188 substituting the DAT C terminus with that of SERT affected neither substrate nor inhibitor affinities

189 Replacing the DAT N terminus with that of SERT had no effect on DA transport Vmax but significantl

190 t the concept that the folding trajectory of SERT is sampled by a cytoplasmic chaperone relay.

191 The folding trajectory of SERT is thought to proceed through the inward facing con

192 d, due to impairment in the translocation of SERT molecules to the cell surface.

193 in SERT activity and reduced localization of SERTs to integrin adhesion complexes in synapses of KI m

194 to wild-type levels, suggesting that loss of SERTs causes a deficiency in platelet activation.

195 ent with the existence of a subpopulation of SERTs that are tightly modulated by integrin alphavbeta3

196 d DAT internalization, but had no effects on SERT endocytosis.

197 mouse integrin beta3 subunit gene (Itgb3) on SERT function and selective 5-hydroxytryptamine (5-HT) r

198 HT, which increases the level of inward-open SERT and may lead to unwinding of the TM5 helix to allow

199 phetamine-induced efflux by SERT-DeltaN32 or SERT-DeltaN42 (but not by SERT-DeltaN22) was markedly di

200 diabetes mellitus (GDM)-associated placenta, SERT is found entrapped in the cytoplasm of the GDM-trop

201 sults indicate kinetic trapping of preformed SERT oligomers at the plasma membrane.

202 Conversely, pregnant SERT (-/-) mice displayed normalized estrogen levels, ma

203 in rats, (11)C-DASB can be used to quantify SERT density with good reproducibility.

204 he alphavbeta3-mediated mechanism of reduced SERT function indicate that decreased integrin beta3 sub

205 elated negatively with decreases in regional SERT binding, indicating a protective effect of estradio

206 els were correlated with changes in regional SERT nondisplaceable binding potential.

207 as well as a mechanism whereby the reported SERT stoichiometry can be obtained despite the presence

208 ition of focal adhesion kinase (FAK) rescued SERT function in synapses of KI mice, demonstrating that

209 To study trafficking of the surface resident SERT, two functional epitope-tagged variants were genera

210 ymporters for the biogenic amines serotonin (SERT), dopamine (DAT), and norepinephrine (NET) are targ

211 he presynaptic dopamine (DAT) and serotonin (SERT) transporters, respectively.

212 e transporters for the monoamines serotonin (SERT) and dopamine (DAT) are prominent targets of variou

213 6A2, NET) and serotonin transporter (SLC6A4, SERT) genes and remission in depressed older adults trea

214 henotypes generated by MRN- and DRN-specific SERT knockdown.

215 In both acute and chronic studies, SERT Met172 mice maintained sensitivity to paroxetine, a

216 have been ablated via knock-in substitution (SERT Met172) without disrupting 5-HT recognition or upta

217 Upon rapid application of a substrate, SERT and DAT display an inwardly directed current compri

218 e Pro32Pro33 integrin alphavbeta3 suppresses SERT activity.

219 ether, these data demonstrate that sustained SERT loss of function reduces 5-HT2AR surface expression

220 The consequences of therapies targeting SERT during pregnancy warrant further evaluation.

221 Here, we demonstrated that SERT (-/-) mice display abnormal fat accumulation in bot

222 tutively internalized SERT demonstrated that SERT primarily co-localized with the late endosomal/lyso

223 Finally, we found that SERT internalized in response to stimulation with 12-myr

224 y-based internalization assays, we show that SERT undergoes constitutive internalization in a dynamin

225 These results suggest that SERT inhibition by FLX may hinder survival in hypoxia.

226 This suggests that SERT and VMAT2 reach the presynaptic specialization by i

227 5-HT uptake rates of GDM-trophoblast and the SERT expression on their surface were severalfold lower

228 riatum (caudate nucleus and putamen) and the SERT-rich extrastriatal brain regions (thalamus, hypotha

229 ent mice and in progeny of WT dams given the SERT antagonist fluoxetine.

230 occupies Cys200/Cys209 residues, one of the SERT glycosylation sites, Asp208 located between the two

231 Given the central role of the SERT in the treatment of depression and anxiety disorder

232 hese tests, and reinforce the utility of the SERT Met172 model for isolating SERT/5-HT contributions

233 y to obtain the oligomerization state of the SERT via brightness analysis of single diffraction-limit

234 was specific for DAT, because replacing the SERT N and/or C termini affected neither substrate nor i

235 one-transmembrane segment protein Tac to the SERT N terminus generated a transporter with an extracel

236 After fecal microbiota transplantation, the SERT expression in the colonic tissue was significantly

237 her, intestinal dysbiosis may upregulate the SERT expression and contribute to the development of chr

238 impact on clearance into enterocytes through SERT.

239 methylphenidate, and desipramine binding to SERT and DAT.

240 AT and hypothalamic (123)I-FP-CIT binding to SERT are significantly lower in MSA-P and PSP than in PD

241 AT and hypothalamic (123)I-FP-CIT binding to SERT are significantly lower in MSA-P and PSP than in PD

242 extrastriatal (123)I-FP-CIT SPECT binding to SERT between MSA, PSP, and PD.

243 ion, our data suggest that Cl(-) is bound to SERT during the entire catalytic cycle.

244 cteristic binding strengths of citalopram to SERT were revealed in Na(+)-containing buffer.

245 Transfusion of wild-type platelets to SERT(-/-) mice normalized bleeding times to wild-type le

246 ose of ESC and, although somewhat similar to SERT deficiency, were not associated with changes in hip

247 the low-capacity, high-affinity transporter SERT.

248 there is much support for 5-HT transporter (SERT) antagonism as a basis of antidepressant efficacy,

249 tamine), into cells by the 5-HT transporter (SERT).

250 via its modulation of the 5-HT transporter (SERT).

251 expression and activity of 5-HT Transporter (SERT/Slc6a4) in 5-HT neurons leading to an increase of 5

252 Serotonin (5-HT) transporter (SERT) regulates the level of 5-HT in placenta.

253 Serotonin (5-HT) transporter (SERT) substrates like fenfluramine and 3,4-methylenediox

254 ariants of the serotonin (5-HT) transporter (SERT, encoded by SLC6A4) have been identified in ASD.

255 estradiol on serotonin reuptake transporter (SERT) binding in female-to-male and male-to-female trans

256 The serotonin transporter (SERT) and other monoamine transporters operate in either

257 serotonergic markers: serotonin transporter (SERT) and serotonin 1A (5-HT1A) receptor.

258 on forces between the serotonin transporter (SERT) and the S- and R-enantiomers of citalopram on the

259 Inhibitors of the serotonin transporter (SERT) are widely used antidepressant agents, but the str

260 th change in cerebral serotonin transporter (SERT) binding following intervention.

261 for quantification of serotonin transporter (SERT) density and affinity in vivo in rats and mice.

262 C-HOMADAM) imaging of serotonin transporter (SERT) density in healthy control subjects.

263 the C terminus of the serotonin transporter (SERT) disrupt folding and export from the endoplasmic re

264 -binding to the human serotonin transporter (SERT) expressed in HEK-293 cells.

265 tributed to a reduced serotonin transporter (SERT) function.

266 timization of DAT and serotonin transporter (SERT) functional assays, as well as cell surface express

267 eractions between the serotonin transporter (SERT) gene and ITGB3, which encodes the beta3 subunit th

268 T studies imaging the serotonin transporter (SERT) have been used and provided evidence for the key r

269 indings implicate the serotonin transporter (SERT) in autism spectrum disorder (ASD).

270 Serotonin transporter (SERT) is a transmembrane transport protein which re-upta

271 The serotonin transporter (SERT) is an integral membrane protein that exploits pree

272 Serotonin transporter (SERT) is responsible for reuptake and recycling of 5-hyd

273 om wild-type rats and serotonin transporter (SERT) knockout mice.

274 ot potentiated by the serotonin transporter (SERT) or the noradrenaline transporter (NET) inhibitors

275 ced expression of the serotonin transporter (SERT) promotes anxiety and cocaine intake in both humans

276 The serotonin transporter (SERT) regulates neurotransmission by the biogenic monoam

277 The serotonin transporter (SERT) terminates serotonergic neurotransmission by perfo

278 The serotonin transporter (SERT) terminates serotonergic signalling through the sod

279 only observed at the serotonin transporter (SERT), dopamine D2-like, and sigma1 receptors.

280 t the plasma membrane serotonin transporter (SERT), modulate hemostasis.

281 dest affinity for the serotonin transporter (SERT), predominantly represented in extrastriatal bindin

282 Rodents exposed to serotonin transporter (SERT)-inhibiting antidepressants during development show

283 by the high-affinity serotonin transporter (SERT).

284 the membrane-embedded serotonin transporter (SERT).

285 mpairment/loss in the serotonin transporter (SERT).

286 The serotonin transporter (SERT/SLC6A4) has a rich pharmacology including inhibitor

287 orting folding of the serotonin transporter (SERT; SLC6A4).

288 anslocation of serotonin (5-HT) transporter, SERT to the plasma membrane of the trophoblast in placen

289 mmunostaining for the serotonin transporter, SERT, we describe the complete pattern of distribution o

290 t uptake by serotonin reuptake transporters (SERTs) prevented the pooling of serotonin from prolongin

291 second site suppressor mutations, which trap SERT in the inward facing state, or (ii) by the pharmaco

292 ects were not observed in paroxetine-treated SERT (-/-) mice.

293 ity markedly decreased amphetamine-triggered SERT-mediated substrate efflux in both cells coexpressin

294 wer for SERT-DeltaN32 than that of wild type SERT and SERT-DeltaN22.

295 sed the cell surface expression of wild type SERT and SERT-F604Q.

296 patients with constipation also upregulated SERT in Caco-2 cells.

297 Fluoxetine persistently upregulated SERT, but not 5-HT1A receptors, in both the neocortex an

298 administered to juvenile monkeys upregulates SERT into young adulthood.

299 ments that govern drug selectivity at DAT vs SERT.

300 voltage-independent rate-limiting step where SERT may return to the outward-facing state in a KCl- or