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

19 ntidepressant therapy involve alterations of monoaminergic and glutamatergic transmission.

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

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

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

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

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

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

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

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

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

29 Interestingly, traditional monoaminergic-based antidepressants have been repeatedly

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

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

32 = 2.0, beta = 0.22, P = 0.045) and striatal monoaminergic binding (t = -3.5, beta = -0.38, P = 0.000

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

49 ironmental) influences on the development of monoaminergic circuitry.

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

51 y be modulated by systemic administration of monoaminergic compounds.

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

53 yperaltruistic disposition is susceptible to monoaminergic control.

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

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

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

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

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

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

60 Monoaminergic drugs have been shown to improve attention

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

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

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

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

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

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

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

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

69 Appositions between monoaminergic fibres and the labelled somata and dendrit

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

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

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

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

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

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

76 tigation of preoptic area efferents to these monoaminergic groups.

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

78 The monoaminergic innervation of cerebral cortex has long be

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

80 Monoaminergic innervation of the spinal cord has importa

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

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

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

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

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

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

87 , as expected from elimination of descending monoaminergic input.

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

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

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

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

92 Immunohistochemistry for monoaminergic markers showed dense innervation of the VL

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

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

95 Hyperphenylalanemia also adversely affects monoaminergic metabolism in the brain.

96 these mutants suggests, may reflect impaired monoaminergic modulation.

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

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

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

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

101 roarray expression profiling of this unitary monoaminergic neuron type.

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

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

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

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

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

107 Monoaminergic neurons are critical functional components

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

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

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

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

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

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

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

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

116 Monoaminergic neurons include the physiologically import

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

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

119 The number of monoaminergic neurons remained unchanged in the transgen

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

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

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

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

124 function that are associated with damage to monoaminergic neurons.

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

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

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

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

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

130 efine the terminally differentiated state of monoaminergic neurons.

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

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

133 the effects of stress and glucocorticoids on monoaminergic neurotransmission.

134 effects of acute stress or corticosterone on monoaminergic neurotransmission.

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

136 To optimally ameliorate brain monoaminergic neurotransmitter concentrations, LNAA supp

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

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

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

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

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

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

143 Brainstem monoaminergic nuclei express glucocorticoid receptors (G

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

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

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

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

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

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

150 rebrain areas and innervating major midbrain monoaminergic nuclei.

151 uromodulatory afferents from cholinergic and monoaminergic nuclei.

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

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

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

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

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

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

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

159 Descending monoaminergic pathways are thought to depress sensory in

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

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

162 frontostriatal and frontolimbic circuits and monoaminergic pathways.

163 nd regulates neurogenesis and development of monoaminergic pathways.

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

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

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

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

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

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

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

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

172 bases of disorders associated with abnormal monoaminergic profiles.

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

174 In addition, monoaminergic projections show anterior-posterior guidan

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

176 milar thresholds of inhibition to spinopetal monoaminergic projections.

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

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

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

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

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

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

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

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

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

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

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

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

189 Monoaminergic stimulation has the opposite effects.

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

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

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

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

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

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

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

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

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

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

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

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

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

203 Descending monoaminergic systems modulate spinal cord function, yet

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

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

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

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

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

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

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

211 mation during development, including central monoaminergic systems.

212 the diffuse PIC facilitation from descending monoaminergic systems.

213 changes in frontal cortical and subcortical monoaminergic systems.

214 o not constitute a generalized activation of monoaminergic systems.

215 use that causes deleterious effects to brain monoaminergic systems.

216 fects are attributed to its interaction with monoaminergic systems.

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

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

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

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

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

222 tion with limited therapeutic options beyond monoaminergic therapies.

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

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

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

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

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

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

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

230 d control the secretion of neuropeptides and monoaminergic transmitters.

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

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

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

234 ession and are associated with resistance to monoaminergic treatment.

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

236 Monoaminergic varicosities in apposition to dendrites gr