ライフサイエンスコーパス: synaptosome

1 ed both in cell bodies and at nerve endings (synaptosomes).

2 inephrine (NE) into rat brain nerve endings (synaptosomes).

3 of the active catalytic tetramer within the synaptosome.

4 n EcoRII dimer is the core of the three-site synaptosome.

5 ing protein, were identified in striatum and synaptosome.

6 -gated potassium channel Kv3.1b in brainstem synaptosomes.

7 oteins in the fractions that are enriched in synaptosomes.

8 imilar effects were detected in rat striatal synaptosomes.

9 2a in dendrites, dendritic spines, and brain synaptosomes.

10 e DAT in both DAT-N2A cells and rat striatal synaptosomes.

11 ltage-sensitive sodium channels in rat brain synaptosomes.

12 Ac transferase) were enriched in hippocampal synaptosomes.

13 ells) and with native DAT in murine striatal synaptosomes.

14 not replicate those effects observed in the synaptosomes.

15 MII-sensitive dopamine release from striatal synaptosomes.

16 norepinephrine (NE) exocytosis from cardiac synaptosomes.

17 gmann glia, cerebellar slices and cerebellar synaptosomes.

18 raction compared to forebrain homogenate and synaptosomes.

19 ression system as well as in murine striatal synaptosomes.

20 at modulate [3H]nore-pinephrine release from synaptosomes.

21 proteins in their native state within mouse synaptosomes.

22 oexchange of d-[(3)H]aspartate from cortical synaptosomes.

23 ased after PD169316 or beta-PMA treatment of synaptosomes.

24 nd used as a binding ligand in rat forebrain synaptosomes.

25 apacity (V(max)) after PD169316 treatment of synaptosomes.

26 bition of high-affinity choline transport in synaptosomes.

27 tes its function both in vitro and in intact synaptosomes.

28 PTA-AM also reduced DA release from striatal synaptosomes.

29 E, both under in vitro conditions and in rat synaptosomes.

30 ease in [3H]dopamine (DA) uptake by striatal synaptosomes.

31 functional synapse formation, and engulfing synaptosomes.

32 icotine-elicited rubidium efflux assays from synaptosomes.

33 rts of inhibition of apamin binding to brain synaptosomes.

34 SK-N-MC neuroblastoma cells and hippocampal synaptosomes.

35 ng veratridine-induced influx of sodium into synaptosomes.

36 ally, we analyzed tau phosphoproteome in the synaptosomes.

37 was reduced in the case of nucleus accumbens synaptosomes.

38 amounts from a biological source, rat brain synaptosomes.

39 ted by monitoring the uptake of choline into synaptosomes.

40 were readily detected following oxidation of synaptosomes.

41 cal assays for activity on Na(+) channels in synaptosomes.

42 modulating Abeta(1-42)-induced oxidation to synaptosomes.

43 is of endogenous norepinephrine from cardiac synaptosomes.

44 cium-dependent phosphorylation of NSF in rat synaptosomes.

45 biquitin-conjugating enzyme UBE2N (Ubc13) in synaptosomes.

46 in e4 synaptosomes as compared to e2 and e3 synaptosomes.

47 ty was not eliminated by repeated washing of synaptosomes.

48 nce of glutamate uptake into crude forebrain synaptosomes.

49 to decrease 5-HT uptake by SERT in midbrain synaptosomes.

50 that GPR30 protein can be found in rat brain synaptosomes.

51 e used FASS-LTP for drug evaluation in human synaptosomes.

52 tyrosine kinase form protein associations in synaptosomes.

53 mmunoprecipitates with DAT in mouse striatal synaptosomes.

54 ates and neuroligins increase selectively in synaptosomes.

55 on with that of the residual nondopaminergic synaptosomes.

56 r snapin in neuroblastoma cells and in brain synaptosomes.

57 In rat striatal synaptosomes, 6c was almost fivefold more potent at inhi

58 ncreased surface GluR1 levels in hippocampal synaptosomes, a key index of spine plasticity.

59 Using spinal cord synaptosomes, a significant reduction (43%) in the maxim

60 r protein abundance in striatal and cortical synaptosomes after amphetamine administration.

61 uced SERT proteins in the plasma membrane of synaptosomes after p38 MAPK inhibition and PKC activatio

62 Its enrichment in synaptosomes also indicated a synaptic localization in t

63 te the efflux of (86)Rb(+) from rat cortical synaptosomes, an indication of agonist activity.

64 ive oxygen species (ROS) production, whereas synaptosome analysis revealed decreased complex I activi

65 an increased localization of mGluR5 to both synaptosome and postsynaptic density-enriched fractions

66 decreased spare respirator capacity of brain synaptosomes and caused abnormal mitochondrial morpholog

67 Fz5 is present in synaptosomes and colocalizes with the pre- and postsynap

68 was only observed in intact but not in lysed synaptosomes and could not be inhibited by general kinas

69 and carrier-mediated NE release from cardiac synaptosomes and cultured neuroblastoma cells; this was

70 [(14)C]guanidinium ion flux in rat forebrain synaptosomes and displaced binding of the sodium channel

71 de also released norepinephrine from cardiac synaptosomes and dopamine from nerve growth factor-diffe

72 tated the InsP3R1-PP1 complex from rat brain synaptosomes and from the neostriatal lysate.

73 ng of p42 and p44 MAPK in untreated striatal synaptosomes and HEK 293 cells, consistent with constitu

74 The presence of phospho-p38 MAPK in synaptosomes and human embryonic kidney 293 (HEK-293) ce

75 ansporter assays were performed in rat brain synaptosomes and in cells expressing human transporters,

76 Both in synaptosomes and in nonneuronal cells, this decrease was

77 biologically validated using mouse cortical synaptosomes and liver mitochondria attached to XF24 V7

78 ndexed by the levels of protein carbonyls in synaptosomes and neuronal cells.

79 rborizations, the biochemical composition of synaptosomes and postsynaptic densities, and brain-deriv

80 However, pretreatment of synaptosomes and primary neuronal cell culture with X-34

81 In both, synaptosomes and slices, the effect of KA was antagonize

82 ular fractionation, CSP-beta was enriched in synaptosomes and synaptic vesicle fractions.

83 We used striatal synaptosomes and telencephalic mitochondria to further i

84 Collectively, the enrichment of CSP-beta in synaptosomes and the association of CSP-beta with synapt

85 and GluR2 copurified in the fractionation of synaptosomes and the postsynaptic density, two fractions

86 In striatal synaptosomes and transfected cells, DAT was in cholester

87 (3)H]WIN35428 binding to DAT in rat striatal synaptosomes and transfected cells.

88 to measure efflux of [(3)H]5-HT in rat brain synaptosomes and transporter-mediated ionic currents in

89 t hippocampus using isolated nerve terminal (synaptosome) and slice preparations.

90 nals isolated from guinea pig heart (cardiac synaptosomes) and in a model human neuronal cell line (S

91 d hearts, sympathetic nerve endings (cardiac synaptosomes), and PC12 cells bearing a sympathetic neur

92 ossibility, we found ASIC in hippocampus, in synaptosomes, and in dendrites localized at synapses.

93 PMCA2a was enriched in forebrain synaptosomes, and in hippocampal CA3 it colocalized with

94 MPH and METH in model cells and rat striatal synaptosomes, and in striatum of rats given subcutaneous

95 inal mutant htt fragments in the nucleus and synaptosomes, and this accumulation was most pronounced

96 ed in soluble preparations of human cortical synaptosomes; apoE/Abeta levels were lower in AD patient

97 Mitochondria isolated from synaptosomes are more sensitive to Ca2+ overload and the

98 d lipid oxidation were always greatest in e4 synaptosomes as compared to e2 and e3 synaptosomes.

99 Accordingly, the cAMP formation in synaptosomes as well as the hypolocomotion induced by a

100 rtly related to those of the oxidant-treated synaptosomes as well as the ischemia-elicited oxidative

101 he C-terminal nine amino acids of the 25 kDa synaptosome-associated protein (SNAP-25) by BoNT A preve

102 requires the carboxyl terminus of the 25-kDa synaptosome-associated protein (SNAP25) and is downstrea

103 serves as a protein kinase to phosphorylate synaptosome-associated protein 23 (SNAP-23), which in tu

104 nhibits endogenous interactions of Stx4 with synaptosome-associated protein 23 (SNAP23) and vesicle-a

105 at vesicle-associated membrane protein-2 and synaptosome-associated protein 23 kDa coimmunoprecipitat

106 gi and to palmitoylate the neuronal proteins synaptosome-associated protein 25 (SNAP-25), PSD-95 (pos

107 r, VAMP 8-positive granules also contain the synaptosome-associated protein 29, whereas VAMP 2-expres

108 ltured astrocytes from visual cortex express synaptosome-associated protein of 23 kDa (SNAP23), but n

109 regulated by two cognate t-SNAREs, SNAP-23 (synaptosome-associated protein of 23 kDa) and syntaxin 1

110 ex, including synaptobrevin 2, syntaxin, and synaptosome-associated protein of 23 kDa.

111 Syntaxin, synaptosome-associated protein of 25 kD (SNAP25), and ve

112 pid (<1 s) and was attenuated by cleavage of synaptosome-associated protein of 25 kD (SNAP25).

113 ansmission after proteolytic cleavage of the synaptosome-associated protein of 25 kDa (SNAP-25) by bo

114 The synaptosome-associated protein of 25 kDa (SNAP-25) inter

115 Synaptosome-associated protein of 25 kDa (SNAP-25) is a

116 The plasma membrane protein synaptosome-associated protein of 25 kDa (SNAP-25) is th

117 n substrate proteins, synaptobrevin (Syb) or synaptosome-associated protein of 25 kDa (SNAP-25), were

118 binding and proteolysis of natural substrate synaptosome-associated protein of 25 kDa (SNAP-25).

119 of a C-terminal deletion mutant (Delta9) of synaptosome-associated protein of 25 kDa (SNAP-25).

120 Synaptosome-associated protein of 25 kDa (SNAP25) is a p

121 In neuroendocrine cells, synaptosome-associated protein of 25 kDa (SNAP25) is loc

122 SNAREs) complex, comprised of syntaxin (Sx), synaptosome-associated protein of 25 kDa (SNAP25), and s

123 d inhibit exocytosis through cleavage of the synaptosome-associated protein of 25 kDa (SNAP25).

124 s consisting of syntaxin, synaptobrevin, and synaptosome-associated protein of 25 kDa on deposited li

125 x, composed of synaptobrevin 2, syntaxin and synaptosome-associated protein of 25 kDa or 23 kDa (SNAP

126 synaptic vesicle and syntaxin 1 and SNAP-25 (synaptosome-associated protein of 25 kDa) at the presyna

127 fluorescent protein (GFP) flanking SNAP-25 (synaptosome-associated protein of 25 kDa) residues 134-2

128 naptobrevin as well as those of syntaxin and synaptosome-associated protein of 25 kDa.

129 , we found that snapin, which binds SNAP-25 (synaptosome-associated protein of 25,000 Da) and enhance

130 inhibited the cleavage of substrate SNAP25 (synaptosome-associated protein of 25,000 Da) by BoNT/A L

131 ties linked via residues 134-206 of SNAP-25 (synaptosome-associated protein of 25kDa), the protein su

132 athway is phosphorylation of SNAP-25 (25 kDa synaptosome-associated protein) at Ser187 by PKC.

133 NARE proteins syntaxin-1 and SNAP-25 (25 kDa synaptosome-associated protein).

134 hat resistance in barley requires a SNAP-25 (synaptosome-associated protein, molecular mass 25 kDa) h

135 sequence and the N-terminal SNARE domain of synaptosome-associated protein-23 (SNAP-23).

136 e-associated membrane protein-2, syntaxin-4, synaptosome-associated proteins 23 kDa and 25 kDa, and t

137 ab3a, vesicle-associated membrane protein-2, synaptosome-associated proteins of 23 kDa and 25 kDa, an

138 ducts were detected in nonoxidized rat brain synaptosomes at a level of 0.09 ng/mg of protein, which

139 s) or alpha 7nAChR antagonists (in cells and synaptosomes) attenuated A beta-induced tau phosphorylat

140 test this hypothesis, we separated isolated synaptosomes bearing dopamine transporters using immunom

141 , were not detected in nonoxidized rat brain synaptosomes but were readily detected following oxidati

142 uoxetine-sensitive efflux of [(3)H]5-HT from synaptosomes, but d-fenfluramine and its bioactive metab

143 y to measure HACU and ChAT simultaneously in synaptosomes, but the same for cultured cells is lacking

144 mulated dopamine release from mouse striatal synaptosomes by alpha-CtxMII occurs within minutes; reco

145 This result was confirmed in in vitro synaptosomes by using total internal reflection fluoresc

146 complete prevention of lipid peroxidation in synaptosomes caused by OH radicals (TBARS), and signific

147 ther direct application of this stimulant to synaptosomes causes changes in DAT similar to those obse

148 In studies with rat hippocampal synaptosomes, chemically evoked aspartate release differ

149 ,7-dichlorofluorescein (DCF) fluorescence in synaptosomes; complete prevention of lipid peroxidation

150 r the interaction with lambdaexo to form the synaptosome complex.

151 ther component of the Red system, to form a "synaptosome" complex that somehow integrates the end res

152 hibition of glutamate uptake in rat cortical synaptosomes, consistent with the predominant contributi

153 Furthermore, synaptosomes contain NPRAP-GRIP complexes, and NPRAP loc

154 change by assembling an elaborate interwound synaptosome containing catalytic and regulatory Sin tetr

155 e available, binding affinity in depolarized synaptosomes correlated well with apparent affinity for

156 oprecipitation studies from cross-linked rat synaptosomes demonstrate that an endogenous syntaphilin-

157 ha complexes were also observed in rat brain synaptosomes, demonstrating that this interaction is not

158 The studies reported here used synaptosomes derived from the cortex, hippocampus, stria

159 tosis, because neurotransmitter release from synaptosomes did not require a Ca2+-dependent KHC dephos

160 ice was due to the selective loss of damaged synaptosomes during sample preparation.

161 ity also rescued PI(4,5)P(2) deficiency in a synaptosome-enriched fraction from the brain of Tg2576 m

162 late blood pressure; (iii) is present within synaptosome-enriched fractions of brain where its releas

163 Depolarization of synaptosomes evokes a Ca2+-dependent botulinum neurotoxi

164 igation/reperfusion, blood analysis, cardiac synaptosome exocytosis, microarray and pathway analysis,

165 K1R interaction were studied using rat brain synaptosomes expressing native NET and NK1R as well as h

166 D-associated Mn accumulation on NE uptake in synaptosomes, extracellular NE concentrations, and expre

167 detecting surface AMPA receptors in isolated synaptosomes: fluorescence analysis of single-synapse lo

168 when tested in vitro on rat cerebral cortex synaptosomes for inhibition of [(3)H]histamine release.

169 Using synaptosome fractionation, immunostaining, and coimmunop

170 Synaptosome fractions from cortex and striatum of HD(140

171 rrelate with a reduction in RacGTP levels in synaptosome fractions from the p75(-/-) cerebellum, but

172 ining NMDA receptors in frontal cortex crude synaptosome from 3, 12, and 26-month-old C57BL/6 mice.

173 inding to striatal membranes and function in synaptosomes from (alpha4-/-)(beta3+/+) and (alpha4-/-)(

174 from the three models; only APP/PS cortical synaptosomes from 14-month-old mice showed an increase i

175 respectively) as potent enhancers of LTP in synaptosomes from AD cases.

176 .2 level is reduced in brain and spinal cord synaptosomes from alpha2delta-1(-/-) mice, and alpha2del

177 lutamate clearance at disease end stage with synaptosomes from cortex, hippocampus, striatum, cerebel

178 However, so did dopaminergic synaptosomes from cortex, indicating a lack of the predi

179 ine uptake into caudate or nucleus accumbens synaptosomes from DAT knock-out mice.

180 s of mitochondrial and glucose metabolism in synaptosomes from four brain regions in basal and stress

181 itor, cocaine, on uptake of 3H-dopamine into synaptosomes from frontal cortex, caudate nucleus, and n

182 e lack of functional bioenergetic defects in synaptosomes from J20 mice was due to the selective loss

183 Thalamic cultures and synaptosomes from L9'A mice were hypersensitive to nicot

184 dopaminergic and nondopaminergic presynaptic synaptosomes from mice do not differ.

185 he readily releasable pool was suppressed in synaptosomes from mice expressing dominant inhibitory Ra

186 each inhibited dopamine uptake into caudate synaptosomes from NET knock-out mice, but cocaine effect

187 to block dopamine uptake into frontal cortex synaptosomes from NET knock-out mice.

188 Flow sorting of synaptosomes from patients with Alzheimer's disease demo

189 llel, we found that epsilonPKC activation in synaptosomes from preconditioned animals resulted in alt

190 at IPC increases the levels of epsilonPKC in synaptosomes from rat hippocampus, resulting in improved

191 Biochemical fractionation of synaptosomes from rTg4510 brain demonstrates a significa

192 matic with conventional methods, we prepared synaptosomes from samples of cryopreserved human associa

193 ocaine, prevented by ZM241385, and absent in synaptosomes from stA2ARKO.

194 levels of synaptobrevin and synaptophysin in synaptosomes from stg cerebellum.

195 As predicted, dopaminergic synaptosomes from striatum had lower respiratory rates.

196 calcium handling, and membrane potentials of synaptosomes from symptomatic J20 mice under calcium-imp

197 Furthermore, synaptosomes from the dentate gyrus of FX mice displayed

198 IL15 decreased the uptake of (3)H-GABA in synaptosomes from the forebrain of wild-type mice.

199 t bioenergetic deficiencies were detected in synaptosomes from the three models; only APP/PS cortical

200 d agonist-evoked P2X7 receptor currents, and synaptosomes from these animals showed increased P2X7 re

201 , synapsin, and SNAP-25, were all reduced in synaptosomes from these transgenic mice.

202 take by 20% in caudate and nucleus accumbens synaptosomes from wild-type and DAT knock-out mice but h

203 tine, but not by GBR12909, in frontal cortex synaptosomes from wild-type or DAT knock-out mice.

204 and hippocampal presynaptic nerve terminals (synaptosomes) from commonly used mouse models with AD-li

205 eta-potentials of entities such as cells and synaptosomes have been determined, but zeta of brain tis

206 Recent studies in synaptosomes have confirmed this view, with calcineurin-

207 the release of [(3)H]dopamine from striatal synaptosomes; however, only 17c was effective at stimula

208 au was elevated in individual Abeta-positive synaptosomes in early AD.

209 ze the bioenergetic competence of individual synaptosomes in the two fractions.

210 constitutive, but the elevation of Ca(2+) in synaptosomes increased CAPS Ser-5 and -6 dephosphorylati

211 tro cocaine (30-50 muM) treatment of rat PFC synaptosomes increased native NET function, surface expr

212 Thus, the S-S synaptosome is formed as a result of the self-organizing

213 of astrocytic GLT-1 to glutamate uptake into synaptosomes is less than expected, and the contribution

214 surement of specific markers of oxidation in synaptosomes isolated from mice that express one of the

215 mass spectrometry to identify proteins from synaptosomes isolated from Mongolian gerbils.

216 We found that Abeta oligomer binding to CNS synaptosomes isolated from wild type (wt) mice treated w

217 Compared with wild-type controls, striatal synaptosomes isolated from young mutant mice exhibited s

218 o bind synaptic vesicle protein complexes in synaptosome lysates.

219 Our studies on IPn synaptosomes obtained from +/+ and alpha2, alpha4, alpha

220 urther rise at 6 and 12 months compared with synaptosomes of age-matched wild-type (WT) mice.

221 ked reduction in synaptophysin expression in synaptosomes of aged compared with young rats.

222 icant increase of hyperphosphorylated tau in synaptosomes of demented dogs compared with nondemented

223 K(+)-evoked fractional dopamine release from synaptosomes of MPTP-lesioned animals, suggesting that n

224 Furthermore, mitochondria from brain synaptosomes of presymptomatic HD model mice and from mu

225 synaptic output of dopamine from slices and synaptosomes of rat corpus striatum.

226 ssessment of amino acid uptake into cortical synaptosomes of v7-3 knockouts identified 15% and 40% re

227 Treatment of synaptosomes or cells with 2BP using higher doses or lon

228 Incubation of striatal synaptosomes or epitope-tagged human DAT (hDAT) human em

229 o and metabolized by astrocytes, rather than synaptosomes or neurons, and labeled acetate is used as

230 Treatment of rat brain synaptosomes or syntaphilin-transfected HEK 293 cells wi

231 n vesicular glutamate release from rat brain synaptosomes or the cystine/glutamate exchange in astroc

232 By profiling hundreds of synaptosomes, our data provide the first direct evidence

233 pared to controls, and the fraction of large synaptosome particles did not change, although a strikin

234 We now use chemical cross-linking in synaptosomes, pinched-off nerve terminals that are capab

235 In synaptosomes, PKC activation but not p38 MAPK inhibition

236 olute need for glucose in vivo, we find that synaptosomes prefer to respire on non-glycolytic substra

237 However, addition of ATP during synaptosome preparation resulted in partial recovery of

238 The recovery of marker proteins during synaptosome preparation was the same, ruling out the pos

239 Use of synaptosome preparations also allowed detection of neuro

240 The expression of Par-4 in synaptosome preparations and PSDs are developmentally an

241 Flow cytometric analysis of synaptosome preparations was used to quantify Abeta and

242 MDAR) activities are severely compromised in synaptosomes prepared from AD and Abeta(1-42) (Abeta42)-

243 erminals, flow cytometry was used to analyze synaptosomes prepared from cryopreserved Alzheimer's dis

244 In synaptosomes prepared from striatal slices, we found tha

245 e-stimulated (86)Rb(+) efflux was studied in synaptosomes prepared from the frontal cortex, hippocamp

246 -stimulated (86)Rb(+) efflux was measured in synaptosomes prepared from the frontal cortex, hippocamp

247 nsitive elevation in intraterminal Ca(2+) in synaptosomes prepared from the rat VTA.

248 ne transporter (DAT), as assessed ex vivo in synaptosomes prepared from treated rats.

249 erotonin clearance rates in brain liposomes (synaptosomes) prepared from mice with 50% (SERT(+/)(-))

250 been shown to release glutamate in cortical synaptosomes, presumably by inhibiting a subthreshold-ac

251 at depolarization-dependent Ca2+ influx into synaptosomes produces a global, rapid (range of seconds)

252 n of 10(-7) to 10(-5) m nicotine to striatal synaptosomes promoted a sustained efflux of [3H]dopamine

253 ichiometry and arrangement of DNA within the synaptosome, remains poorly understood.

254 nicotine-stimulated DA release from striatal synaptosomes requires alpha4 subunits, implicating alpha

255 cocaine treatment of mouse prefrontal cortex synaptosomes resulted in enhanced NET function, surface

256 inetic studies with each of the compounds in synaptosomes revealed a competitive mechanism of inhibit

257 Phosphorylation studies using synaptosomes revealed decreased SERT phosphorylation by

258 In vitro release assays using rat brain synaptosomes revealed that mephedrone and methylone are

259 ed [3H]dopamine release from monkey striatal synaptosomes revealed that release was calcium-dependent

260 (86)Rb efflux experiments on brain synaptosomes showed an increased fraction of function at

261 Fractionation of ADDLs bound to forebrain synaptosomes showed association with postsynaptic densit

262 Cleavage of rat-brain synaptosome SNAP-25 by BoNTs was used to assay endopepti

263 ing BoNT serotype A (BoNT/A) and mouse brain synaptosomes (SNPs) and protective antibodies against to

264 es by 13-fold for the cleavage of SNAP-25 in synaptosomes, suggesting a possible functional role of H

265 release of [(3)H]acetylcholine from cortical synaptosomes, suggesting differential selectivity.

266 lized to the number of respiration-competent synaptosomes, suggesting that differences reflected the

267 ions of SERT with Hic-5 are evident in brain synaptosomes, suggesting the existence of parallel mecha

268 ous expression system and in murine striatal synaptosomes that AMPH causes a time-dependent decrease

269 ampal slices and in purified rat hippocampal synaptosomes, the cellular and molecular mechanisms wher

270 mate content in the nerve ending preparation synaptosome; this decrease was reflected in reduction of

271 ed rat retinas, cortical cultures, and brain synaptosomes to compare the effectiveness of flunarizine

272 capacity of dopaminergic and nondopaminergic synaptosomes to maintain plasma membrane and mitochondri

273 lated protein-2 as significantly oxidized in synaptosomes treated with Abeta(1-42).

274 We show that in synaptosomes treated with three stimuli that induce exoc

275 xonal transport vesicles from mouse cortical synaptosomes using electron microscopy, biochemical, and

276 brane potentials in whole unseparated single synaptosomes using fluorescent imaging, and then identif

277 d Nox ROS production was assayed in isolated synaptosomes using spin trapping electron paramagnetic r

278 independent immunoprecipitation analyses of synaptosomes validated protein interactions.

279 loyed uptake and release assays in rat brain synaptosomes, voltage-clamp current measurements in cell

280 Inhibition of [3H]DA uptake in synaptosomes was also evaluated.

281 -stimulated [(3)H]GABA release from thalamic synaptosomes was not significantly affected by alpha5 ge

282 isolation of purified dopaminergic striatal synaptosomes was used to study the impact of dopaminergi

283 s using established radiochemical methods in synaptosomes, we determined 60% reductions in serotonin

284 Using synaptosomes, we found that 5-HT treatment causes RII pr

285 reporters and biochemical assays of isolated synaptosomes, we found that mutant htt decreases synapti

286 lease was examined using hippocampal slices, synaptosomes were chosen to characterize the uptake proc

287 In the current study, synaptosomes were prepared from apoE KO mice to determin

288 in the presence of oxygen and abolished when synaptosomes were stirred.

289 inephrine (NE) into rat brain nerve endings (synaptosomes) were evaluated.

290 Treatment of rat striatal synaptosomes with 2BP using lower doses or shorter times

291 creased NE uptake by prefrontal cortex (PFC) synaptosomes with a parallel increase in the surface exp

292 Furthermore, coincubation of isolated synaptosomes with alpha(2)AR and DOP agonists resulted i

293 pathological event in AD, and incubation of synaptosomes with amyloid beta peptide 1-42 (Abeta 1-42)

294 n different cell lines, primary neurons, and synaptosomes with C3-RGD mutants.

295 Treatment of mouse brain synaptosomes with H2O2, diamide, and sodium nitroprussid

296 Rapid treatment (1 min) of rat striatal synaptosomes with low-dose amphetamine increases surface

297 o the ex vivo effect, incubation of striatal synaptosomes with METH decreased DAT activity, but not W

298 Treatment of rat midbrain synaptosomes with p38 MAPK-specific inhibitors, PD169316

299 In vitro treatment of synaptosomes with TAT-NET-Thr(30) (wild-type peptide) co

300 Incubation of rat dorsal striatal (dSTR) synaptosomes with the Cdk5 inhibitors roscovitine, olomo

301 unoreactivity of phospho-p38 MAPK in the PFC synaptosomes without affecting the total p38 MAPK.