ライフサイエンスコーパス: monoaminergic

1 diated by the release of monoamines and that monoaminergic activation of D(1)/D(5) receptors is requi

2 Spatial memory, anxiety and central monoaminergic activities were measured in non-pregnant (

3 Monoaminergic activity (especially dopaminergic and sero

4 = 10.1, P < 0.0001), borderline for striatal monoaminergic activity (F = 1.6, P = 0.13), but not sign

5 Striatal monoaminergic activity correlated positively with odour

6 Changes of monoaminergic activity were not observed in the septum,

7 lcholinesterase activity as well as striatal monoaminergic activity, using odour identification score

8 ceptors modulate extrinsic glutamatergic and monoaminergic afferents and intrinsic GABAergic afferent

9 was administered to assess the influence of monoaminergic agents on performance errors during fMRI d

10 Local perfusion with the monoaminergic agonist quinpirole, 7-OH-DPAT and BHT-920,

11 he effects of dextroamphetamine, an indirect monoaminergic agonist, on cognitively evoked neural acti

12 ults demonstrate that SLC10A4 is a vesicular monoaminergic and cholinergic associated transporter tha

13 articipate in these pathways are actually in monoaminergic and cholinergic cell groups.

14 n and brainstem regions, densely innervating monoaminergic and cholinergic cells.

15 nal Hcrt-r2, Hcrt levels are not affected by monoaminergic and cholinergic drugs, despite the strong

16 usively expressed in presynaptic vesicles of monoaminergic and cholinergic neurons, has a regulatory

17 itory interactions between pontine brainstem monoaminergic and cholinergic neurons.

18 ex and, in animal models, in the subcortical monoaminergic and cholinergic systems, accompanied by wi

19 Moreover, these cytokines can affect monoaminergic and glutamatergic systems, supporting an o

20 ntidepressant therapy involve alterations of monoaminergic and glutamatergic transmission.

21 bances in stress and inflammatory responses, monoaminergic and melatonergic signalling, which point t

22 aq-coupled, TA receptor TYRA-3 on inhibitory monoaminergic and peptidergic neurons.

23 food availability and is translated by both monoaminergic and peptidergic signaling in the fine-tuni

24 wide array of systems-including the immune, monoaminergic, and glutamatergic systems-is implicated i

25 amine induced Fos expression in cholinergic, monoaminergic, and orexinergic arousal systems and compl

26 he atypical antipsychotic medication and pan-monoaminergic antagonist asenapine potently and efficaci

27 erentially altered by i.t. pretreatment with monoaminergic antagonists (100 nmol/rat).

28 GNIFICANCE STATEMENT Treatment resistance to monoaminergic antidepressants is a major problem.

29 ividuals treated with serotonergic and other monoaminergic antidepressants, we found that the express

30 y play a key role in silencing the ascending monoaminergic arousal system during sleep.

31 he TMN and other components of the ascending monoaminergic arousal system.

32 D peptide supported recovery and regrowth of monoaminergic axons in female, but not in male mice.

33 re facilitated by neuromodulatory input from monoaminergic axons originating in the brainstem.

34 antitative responses in both cholinergic and monoaminergic axons to changing ovarian hormone levels.

35 Interestingly, traditional monoaminergic-based antidepressants have been repeatedly

36 Despite the availability of numerous monoaminergic-based antidepressants, most patients requi

37 ta = 0.43, P =0.0001) compared with striatal monoaminergic binding (t = -2.1, beta = 0.22, P = 0.043)

38 = 2.0, beta = 0.22, P = 0.045) and striatal monoaminergic binding (t = -3.5, beta = -0.38, P = 0.000

39 e lateral habenula (LHb), a key regulator of monoaminergic brain regions, is activated by negatively

40 tinct distribution patterns emerged: (1) all monoaminergic brainstem cell groups appeared to contain

41 flow between fronto-limbic brain regions and monoaminergic brainstem nuclei, and is thus anatomically

42 ral preoptic area (VLPO) and the wake-active monoaminergic brainstem populations (MA), as well as cir

43 at there is considerable independence of the monoaminergic bulbospinal pathways.

44 ar signaling processes (e.g., glutamatergic, monoaminergic, calcium, cyclic adenosine monophosphate [

45 d NE) and their metabolites were measured in monoaminergic cell body, cortical and limbic brain regio

46 osite to that demonstrated by wake-promoting monoaminergic cell groups and was previously found in ce

47 raoptic, and arcuate), major cholinergic and monoaminergic cell groups, and specific sensory relay an

48 pression of the genes that define individual monoaminergic cell types may be brought about by transcr

49 tionality and release properties of cultured monoaminergic cell types that later can be transplanted

50 stics, distinguishing it from those of other monoaminergic cells in periphery and brain.

51 particularly dense excitatory projections to monoaminergic centers such as the noradrenergic locus co

52 explants were innervated by a source of non-monoaminergic (cholinergic) axons from the E18 basal for

53 or and superior colliculi and the autonomic, monoaminergic, cholinergic, and classical reticular nucl

54 We identified multiple monoaminergic, cholinergic, and peptidergic cell types l

55 ironmental) influences on the development of monoaminergic circuitry.

56 Dysfunction of monoaminergic circuits has been implicated in various ne

57 ere associated with the vesicular (including monoaminergic) compartment.

58 y be modulated by systemic administration of monoaminergic compounds.

59 duration) in one recording versus (b) lower monoaminergic concentrations accompanied reduced seizure

60 itary prolactin secretion is primarily under monoaminergic control, via tuberoinfundibular dopamine (

61 yperaltruistic disposition is susceptible to monoaminergic control.

62 izing AD classification, not solely based on monoaminergic conventional drug mechanism of action, but

63 gent manner: placental mammals have lost the monoaminergic CSF-c cells, while teleosts have increased

64 apability of (18)F-DTBZ PET in detecting the monoaminergic degeneration in early Parkinson disease (P

65 serve as an in vivo biomarker to detect the monoaminergic degeneration in the premotor phase of PD.

66 These findings indicate that monoaminergic degeneration predates the onset of memory

67 rom the nucleus, a large compartment free of monoaminergic degradation pathways that has not been imp

68 inhibited in REM sleep by the combination of monoaminergic disfacilitation and cholinergic inhibition

69 At high monoaminergic drive levels, the PIC dominates synaptic i

70 ntributions of synaptic vesicular actions of monoaminergic drugs and neurotoxins and suggest that int

71 Monoaminergic drugs have been shown to improve attention

72 t study, we have investigated the effects of monoaminergic drugs on cataplexy in narcoleptic canines

73 bserve many critical roles in the brain, and monoaminergic drugs such as amphetamine have a long hist

74 Other monoaminergic drugs tested in these two brain areas; pra

75 sorders might serve as biomarkers of central monoaminergic dysfunction, thus promoting ERG measuremen

76 Pb exposure during development alters normal monoaminergic expression in the auditory brainstem.

77 The data suggest that cortically projecting monoaminergic fibers play an important role in normal co

78 e (Mus musculus) after neonatal depletion of monoaminergic fibers projecting to the neocortex and hip

79 could potentially apply to all degenerating monoaminergic fibre types, throughout the brains of pati

80 Appositions between monoaminergic fibres and the labelled somata and dendrit

81 wever, be of use in probing other aspects of monoaminergic function and dysfunction in the brain, the

82 ive developmental periods can modulate adult monoaminergic function and thereby alter risk for aggres

83 th deficits in anxiety responses and altered monoaminergic function in adulthood.

84 noamine metabolites and examined the role of monoaminergic function in the intergenerational transmis

85 It has been hypothesized that anomalies in monoaminergic function underlie some of the manifestatio

86 that control the expression of what we term monoaminergic gene batteries (enzymes and transporters f

87 tigation of preoptic area efferents to these monoaminergic groups.

88 Past work has highlighted monoaminergic influences on aggression, but a mechanisti

89 The monoaminergic innervation of cerebral cortex has long be

90 investigation was to search for evidence of monoaminergic innervation of gamma-motoneurones.

91 Monoaminergic innervation of the spinal cord has importa

92 nate stress responses and receive convergent monoaminergic innervation suggested that substance P ant

93 s accumbens shell (NAcSh) receives extensive monoaminergic input from multiple midbrain structures.

94 e) in order to elucidate the effect of Pb on monoaminergic input into the SOC.

95 A problem with this gain control is that monoaminergic input to the cord is very diffuse, affecti

96 In a decerebrate preparation with tonic monoaminergic input to the cord, the MRRFs tended to be

97 toneurone dendrites, which is facilitated by monoaminergic input, amplified the MRRF about 2-fold, co

98 n thus displays maladaptation to the loss of monoaminergic input, effects that may augment the functi

99 , as expected from elimination of descending monoaminergic input.

100 nd are directly proportional to the level of monoaminergic input.

101 The NAc integrates diverse monoaminergic inputs to coordinate motivated behavior.

102 the PFC network is profundedly influenced by monoaminergic inputs via the activation of dopamine, adr

103 t are independent of norepinephrine or other monoaminergic inputs, identifying a potential mechanism

104 , like many brain regions, receives multiple monoaminergic inputs.

105 e transcriptomic effects of dopaminergic and monoaminergic ligands.

106 In this study, because monoaminergic (MAergic) neurons show degenerative change

107 To that effect we compared both behavior and monoaminergic markers in wild type (WT) and PrP(C)-null

108 Immunohistochemistry for monoaminergic markers showed dense innervation of the VL

109 pe values, accompanied by smaller changes in monoaminergic markers, heart rate, and blood pressure.

110 ossible that antidepressants may have common monoaminergic mechanism(s) that reduce the risk of devel

111 as justified the use of antidepressants with monoaminergic mechanisms of action for patients with PTS

112 timethod, multisystem approaches to studying monoaminergic mechanisms of resilience to AD pathology.

113 Hyperphenylalanemia also adversely affects monoaminergic metabolism in the brain.

114 volutionary origin of the genes required for monoaminergic modulation is uncertain.

115 ory system (DPMS) shapes pain perception via monoaminergic modulation of sensory information in the s

116 these mutants suggests, may reflect impaired monoaminergic modulation.

117 aled the presence of non-cholinergic and non-monoaminergic mutually inhibitory REM-off and REM-on are

118 vestigated by measuring striatal presynaptic monoaminergic nerve density with PET and (11)C-dihydrote

119 ts, therefore, that Parkinson's disease is a monoaminergic neurodegenerative disorder.

120 n associated with changes in the function of monoaminergic neuromodulatory systems.

121 roarray expression profiling of this unitary monoaminergic neuron type.

122 fferentiation and an increased production of monoaminergic neuronal subtypes in WT.

123 lly associated not only with cholinergic and monoaminergic neurons (which include dopaminergic neuron

124 Monoaminergic neurons [serotonergic (5-HT) and dopaminer

125 vern aggression has proven difficult because monoaminergic neurons also regulate other behaviors.

126 velopment in zebrafish, displays deficits of monoaminergic neurons and cranial sensory ganglia, where

127 Also, brainstem nuclei containing monoaminergic neurons and neurons in the thalamic motor

128 Monoaminergic neurons are critical functional components

129 sm1 is expressed in hindbrain progenitors of monoaminergic neurons as they exit the cell cycle, in a

130 distribution and density of cholinergic and monoaminergic neurons between tau-transgenic and wild ty

131 ceptors, exerts a positive trophic effect on monoaminergic neurons during embryogenesis.

132 , for its effects on the firing frequency of monoaminergic neurons ex vivo, and for its properties in

133 f the various groups of pontine or medullary monoaminergic neurons express DNPI/VGLUT2 mRNA and, thus

134 e Purkinje cell layer in cerebellum, and the monoaminergic neurons in the mouse midbrain.

135 VLPO produced modest numbers of CTB-labeled monoaminergic neurons in the tuberomammillary nucleus, r

136 y component in regulating the development of monoaminergic neurons in the vertebrate brain.

137 Monoaminergic neurons include the physiologically import

138 differentiated state of individual types of monoaminergic neurons is defined by the coordinated expr

139 far suggesting significant expression within monoaminergic neurons of both human and monkey brain.

140 The number of monoaminergic neurons remained unchanged in the transgen

141 a and serotonergic neurons of the raphe, all monoaminergic neurons that do not express DBH, survived

142 nin (5-HT) and dopamine (DA) from subsets of monoaminergic neurons to modulate locomotory behaviors t

143 Monoamine compartmentalization in monoaminergic neurons uses serial action of the plasma m

144 ns as well as the pattern of cholinergic and monoaminergic neurons were investigated.

145 yogenesis interferes with the development of monoaminergic neurons, we used mice in which the number

146 efine the terminally differentiated state of monoaminergic neurons.

147 function that are associated with damage to monoaminergic neurons.

148 in neocortical GABAergic, glutamatergic, and monoaminergic neurons.

149 n activity on the development or function of monoaminergic neurons.

150 ression of distinct TRP-like channels on the monoaminergic neurons.

151 c cotransmission may be the rule for central monoaminergic neurons.

152 subtypes, respectively, within each class of monoaminergic neurons.

153 roup of nuclei that regulate the activity of monoaminergic neurons.

154 n protein, and is accompanied by the loss of monoaminergic neurons.

155 an function as a bona fide co-transmitter in monoaminergic neurons.

156 eptor 1 (hTAAR1, hTA1) is a key regulator of monoaminergic neurotransmission and the actions of psych

157 Monoaminergic neurotransmission has long been recognized

158 heumatoid arthritis, have various effects on monoaminergic neurotransmission, neurotrophic factors an

159 tive effects of proinflammatory cytokines on monoaminergic neurotransmission, neurotrophic factors, a

160 h tricyclic antidepressants rapidly activate monoaminergic neurotransmission, these drugs must be adm

161 gs support the hypothesis that alteration of monoaminergic neurotransmission, which can be reversed b

162 the effects of stress and glucocorticoids on monoaminergic neurotransmission.

163 effects of acute stress or corticosterone on monoaminergic neurotransmission.

164 ain and plasma amino acid profiles and brain monoaminergic neurotransmitter concentrations were measu

165 To optimally ameliorate brain monoaminergic neurotransmitter concentrations, LNAA supp

166 the regulation of locomotor activity by the monoaminergic neurotransmitter dopamine.

167 nts with primary mechanisms of action on the monoaminergic neurotransmitter system to augmentation ag

168 Disruption of key monoaminergic neurotransmitter systems, such as the dopa

169 otransmitters, and identifies novel sites of monoaminergic neurotransmitter uptake.

170 s, Insm1 regulates the synthesis of distinct monoaminergic neurotransmitters by acting combinatoriall

171 The monoaminergic neurotransmitters dopamine, noradrenaline,

172 has evolved from a focus on an imbalance of monoaminergic neurotransmitters to a multifactorial pict

173 s, an essential cofactor in the synthesis of monoaminergic neurotransmitters.

174 B play important roles in the homeostasis of monoaminergic neurotransmitters.

175 t selective lesions of either cholinergic or monoaminergic (noradrenergic, serotoninergic or dopamine

176 Cell-based seeding experiments revealed monoaminergic NTs as inhibitors of tau.

177 Among those identified were monoaminergic NTs.

178 The monoaminergic nuclei are thought to be some of the earli

179 Brainstem monoaminergic nuclei express glucocorticoid receptors (G

180 ined unchanged in the transgenic mice, while monoaminergic nuclei in Alzheimer brainstem showed a dis

181 tem regions express this transcript, notably monoaminergic nuclei including the locus coeruleus and d

182 rget several forebrain regions and brainstem monoaminergic nuclei involved in regulating core motivat

183 ngs, these results suggest that the VLPO and monoaminergic nuclei may be reciprocally connected.

184 and human post-mortem studies indicates that monoaminergic nuclei undergo degeneration at the pre-sym

185 ificity of [3H]nisoxetine binding to NETs in monoaminergic nuclei was assessed by measuring the inhib

186 ment, we hypothesised that the MRI signal of monoaminergic nuclei would be a statistically significan

187 om the LHb and projects strongly to midbrain monoaminergic nuclei, is believed to underlie the transi

188 rebrain areas and innervating major midbrain monoaminergic nuclei.

189 uromodulatory afferents from cholinergic and monoaminergic nuclei.

190 also affected the galaninergic system in the monoaminergic nuclei: Electroconvulsive shock elevated g

191 ajority of LHb projection neurons target one monoaminergic nucleus only, and 3) very few, heterogeneo

192 parate and interconnected circuits with each monoaminergic nucleus, permitting the LHb to modulate it

193 rons project to only one or to more than one monoaminergic nucleus.

194 other neurotransmitter systems, such as the monoaminergic ones.

195 ttle colocalization (< or =15%) with VGLUT1, monoaminergic or inhibitory terminals.

196 However, the neural mechanisms of monoaminergic orchestration of behavior are poorly under

197 n by sleep deficiency, including the opioid, monoaminergic, orexinergic, immune, melatonin, and endoc

198 ith other TAARs, as well as with its closest monoaminergic orthologue, the serotonin receptor 5-HT4R.

199 via overlapping neural circuits that include monoaminergic pathways and the parabrachial nucleus netw

200 Descending monoaminergic pathways are thought to depress sensory in

201 reveals how pharmacological manipulation of monoaminergic pathways can affect this phenotype.

202 We found that two distinct monoaminergic pathways mediate learned food aversions in

203 noamines' synthesis and structural damage to monoaminergic pathways within the brain.

204 frontostriatal and frontolimbic circuits and monoaminergic pathways.

205 nd regulates neurogenesis and development of monoaminergic pathways.

206 in Caenorhabditis elegans through a complex monoaminergic/peptidergic cascade, and suggest that this

207 id signaling functions as part of a complex, monoaminergic/peptidergic signaling cascade and appears

208 tion, confer protection not only of cultured monoaminergic perikarya, but also of monoamine neurotran

209 with, or independently of, Ascl1 in specific monoaminergic populations.

210 mote NREM sleep, and they innervate multiple monoaminergic populations.

211 cholinesterase and caudate nucleus [11C]DTBZ monoaminergic positron-emission tomography imaging based

212 nazine ([+]-[(11)C]DTBZ) to examine striatal monoaminergic presynaptic terminal density in 20 patient

213 sitron emission tomography to study striatal monoaminergic presynaptic terminals in 4 patients with m

214 sitron emission tomography to study striatal monoaminergic presynaptic terminals in 7 male severe chr

215 bases of disorders associated with abnormal monoaminergic profiles.

216 s serotonin and norepinephrine; however, the monoaminergic projection to the cord is diffusely organi

217 In addition, monoaminergic projections show anterior-posterior guidan

218 ll bodies, including regions receiving dense monoaminergic projections, suggests an important role fo

219 milar thresholds of inhibition to spinopetal monoaminergic projections.

220 is large-scale screen, we identify TyrRII, a monoaminergic receptor required in astrocytes for sleep

221 actuator drugs with affinity for endogenous monoaminergic receptor systems.

222 nsformation into lasting changes by specific monoaminergic receptors anchored to postsynaptic protein

223 s involved in cell-cell signaling, including monoaminergic receptors and transporters.

224 w-acting antidepressants, in which targeting monoaminergic receptors identified several efficacious d

225 now report that, in contrast to these other monoaminergic "REM-off" cell groups, histamine neurons a

226 ppocampal volume, cortical connectivity, and monoaminergic responses.

227 Results are discussed in terms of possible monoaminergic sensitization induced by TNFalpha and the

228 To begin to elucidate monoaminergic signal transduction in pyloric neurons, we

229 potential role of cannabinoids in modulating monoaminergic signaling and the advantages of studying c

230 Neuropeptides that modulate the central monoaminergic signaling are promising targets for develo

231 in Caenorhabditis elegans and also modulate monoaminergic signaling at multiple levels.

232 suggest that inhibition of sleep centers via monoaminergic signaling is an evolutionarily conserved m

233 data are consistent with the scaffolding of monoaminergic signaling modules by PrP(C), and may help

234 ulate locomotory behaviors through a complex monoaminergic signaling pathway involving multiple serot

235 ates the cannabinoid-dependent activation of monoaminergic signaling, and highlights the advantages o

236 he role of TRP channels in the modulation of monoaminergic signaling, and the cannabinoid-dependent m

237 ogs that could involve modulatory effects on monoaminergic signaling, inflammatory and oxidative stat

238 aling system in C. elegans and also modulate monoaminergic signaling, potentially affecting an array

239 tor (CRF) and an interaction between CRF and monoaminergic signaling.

240 e disturbances in neuronal-glial plasticity, monoaminergic signalling, inflammatory homoeostasis, cel

241 nsduction mechanisms that link the different monoaminergic signals to specific intracellular response

242 Monoaminergic stimulation has the opposite effects.

243 elated abnormalities in the concentration of monoaminergic synaptic terminals may be present in patie

244 pression and, by extension, concentration of monoaminergic synaptic terminals, may represent a trait-

245 o observed unusual co-expression patterns of monoaminergic synthesis pathway genes, suggesting the ex

246 cial stress can lead to dysregulation of the monoaminergic system and increase the vulnerability of d

247 h comorbidity, suggesting alterations in the monoaminergic system as a common origin of this disease.

248 om this discovery, scientists pinpointed the monoaminergic system as the primary target associated wi

249 e behaviors has been largely ascribed to the monoaminergic system in limbic regions, the contribution

250 Experimental models show that the brain monoaminergic system is susceptible to uraemic neurotoxi

251 pressants have been engineered to act on the monoaminergic system more selectively, primarily on sero

252 n the anterior-posterior organization of the monoaminergic system.

253 sleep.SIGNIFICANCE STATEMENT The function of monoaminergic systems and circuits that regulate sleep a

254 function as regulators that are activated by monoaminergic systems and neuropeptides in response to a

255 Alterations in both monoaminergic systems associated with age and strain wer

256 eractions of the prion protein (PrP(C)) with monoaminergic systems due to: the role of PrP(C) in both

257 early life adversity (ELA) on primate brain monoaminergic systems during adolescence is scarce and i

258 strating that ammonia leads to dysfunctional monoaminergic systems in brain which may underlie neurol

259 study investigated the effects of ammonia on monoaminergic systems in brains of fathead minnows (Pime

260 gested more pronounced degeneration of other monoaminergic systems in multiple-system atrophy (MSA) a

261 f stress-induced metabolic activation of the monoaminergic systems in the m-PFC, as well as amygdalar

262 of abuse that has long been known to damage monoaminergic systems in the mammalian brain.

263 merging evidence supports a dysregulation of monoaminergic systems in the pathogenesis of MS, seconda

264 ontrol of the stress activation of the m-PFC monoaminergic systems is at present unknown.

265 Descending monoaminergic systems modulate spinal cord function, yet

266 Various hormonal and monoaminergic systems play determinant roles in the regu

267 t attributable to alterations in subcortical monoaminergic systems, because transgenic animals respon

268 nal antidepressant medications, which act on monoaminergic systems, display significant limitations,

269 currents (PICs) in motoneurons by brainstem monoaminergic systems, generates both amplification and

270 ant drug responses and in diseases linked to monoaminergic systems, including substance abuse and Par

271 hese differences in the development of brain monoaminergic systems, it remains difficult to declare t

272 This microstructure regulates monoaminergic systems, notably dopamine and serotonin, a

273 urone excitability is mediated by descending monoaminergic systems, which have diffuse effects on mul

274 s such as sleep regulation and modulation of monoaminergic systems.

275 mation during development, including central monoaminergic systems.

276 the diffuse PIC facilitation from descending monoaminergic systems.

277 changes in frontal cortical and subcortical monoaminergic systems.

278 o not constitute a generalized activation of monoaminergic systems.

279 use that causes deleterious effects to brain monoaminergic systems.

280 fects are attributed to its interaction with monoaminergic systems.

281 to potential identification of the first non-monoaminergic target with comparable efficacy as convent

282 coholic patients suggests that nigrostriatal monoaminergic terminals are reduced, with or without los

283 Ns were strongly targeted by cholinergic and monoaminergic terminals, suggesting significant subcorti

284 examined the density of striatal presynaptic monoaminergic terminals, using a ligand for the type 2 v

285 tion with limited therapeutic options beyond monoaminergic therapies.

286 unctional impact of the highlighted genes on monoaminergic transmission and neuropsychiatric phenotyp

287 pic-mediated transmission in general, and on monoaminergic transmission in particular, is less well u

288 cted=0.014), a gene previously implicated in monoaminergic transmission, major depressive disorder an

289 difference was observed in the expression of monoaminergic transmission-related genes in either model

290 rapy, and its action includes alterations in monoaminergic transmission.

291 These include, but are not limited to, monoaminergic transmitter systems, the hypothalamic-pitu

292 epression is associated with deficiencies in monoaminergic transmitters and possibly neurotrophins.

293 d control the secretion of neuropeptides and monoaminergic transmitters.

294 way genes, suggesting the existence of novel monoaminergic transmitters.

295 derwent (11)C-dihydrotetrabenazine vesicular monoaminergic transporter type 2 and (11)C-methylpiperid

296 grity were obtained, i.e. striatal vesicular monoaminergic transporter type 2 binding (distribution v

297 he ability to inhibit transport by all three monoaminergic transporters may exhibit "partial" cocaine

298 ession and are associated with resistance to monoaminergic treatment.

299 Furthermore, changes in monoaminergic turnover were coincident with altered aggr

300 Monoaminergic varicosities in apposition to dendrites gr