ライフサイエンスコーパス: noradrenergic

1 ctions (e.g., serotonergic, cholinergic, and noradrenergic).

2 echolamine innervation of the dLGN is solely noradrenergic.

3 numbers of pontine cholinergic (126,776) and noradrenergic (122,878) neurons are markedly higher than

4 numbers of pontine cholinergic (259,578) and noradrenergic (127,752) neurons, and hypothalamic orexin

5 numbers of pontine cholinergic (274,242) and noradrenergic (203,686) neurons, and hypothalamic orexin

6 e locus ceruleus, which in turn inhibits (by noradrenergic action) the peripheral nociceptive input a

7 The capacity of noradrenergic-activated sacral CPGs to modulate the acti

8 R by APP may have an impact on modulation of noradrenergic activity and sympathetic tone.

9 during the daytime, derepressed sympathetic noradrenergic activity causes predominant BM egress of H

10 astrocytic signaling pathways can integrate noradrenergic activity during vigilance states to mediat

11 These findings provide evidence that BLA noradrenergic activity enables functional interactions b

12 attention have been associated with altered noradrenergic activity in animals.

13 These data also suggest that heightened noradrenergic activity in the BLA underlies stress-induc

14 a suggest that concurrent glucocorticoid and noradrenergic activity prompts an alignment of reward- w

15 or dopamine beta-hydroxylase (DBH; marker of noradrenergic/adrenergic cells) did not affect body grow

16 As the LHb is also targeted by noradrenergic afferents, we examined whether GBR12935 ac

17 cAMP generation with guanfacine, an alpha2A-noradrenergic agonist, normalized the function of SK and

18 ptor affinity, >1000-fold selectivity versus noradrenergic alpha(1), dopamine D(2), serotonin 5-HT(2A

19 acetylcholine (nACh; alpha4 beta2 subtype), noradrenergic alpha1 and alpha2 , serotonergic 5-HT1A an

20 nd nicotinic (nACh) acetylcholine receptors; noradrenergic alpha1 and alpha2 receptors; serotonergic

21 High levels of noradrenergic alpha1-adrenoceptor and dopaminergic D1 re

22 ociated with the differential involvement of noradrenergic alpha2 versus alpha1 receptors.

23 Guanfacine, a noradrenergic alpha2a agonist, reduced tobacco smoking i

24 Conclusions: A combination of noradrenergic and antimuscarinic agents administered ora

25 cent investigations indicate that drugs with noradrenergic and antimuscarinic effects improve geniogl

26 fluctuations in the activity of corticopetal noradrenergic and cholinergic projections.

27 enhanced learning increased the activity of noradrenergic and dopaminergic midbrain neurons.

28 Thus, we also demonstrate that enhancing noradrenergic and dopaminergic systems does not systemat

29 The noradrenergic and p38 mitogen-activated protein kinase (

30 analgesic therapies that exploit descending noradrenergic and serotonergic control pathways.

31 or, might contribute to the dysregulation of noradrenergic and serotonergic neurons implicated in the

32 the brain that originate from predominantly noradrenergic and serotonergic systems.

33 alter pain behaviors by reducing descending noradrenergic and serotoninergic modulation of spinal pa

34 iggered awakening by recruiting cholinergic, noradrenergic, and glutamatergic arousal pathways.

35 ral amygdala (BLA) and that of dopaminergic, noradrenergic, and histaminergic systems in both structu

36 posttraining inactivation of the BLA by the noradrenergic antagonist propranolol abolished the effec

37 esia; this was prevented with beta or alpha1 noradrenergic antagonists.

38 on of presynaptic input and was prevented by noradrenergic antagonists.

39 y reversed the oxytocin effect, a descending noradrenergic antinociception is suggested.

40 and basal ganglia are key components of a LC-noradrenergic arousal circuit.

41 However, in vivo insights into noradrenergic arousal circuitry have been constrained by

42 s suggest that their effects are enhanced by noradrenergic arousal.

43 iods of vigilance were accompanied by robust noradrenergic axonal activity and gradual sustained cAMP

44 ergic axons in the mouse striatum and sparse noradrenergic axons in the mouse cortex in acute brain s

45 e tightly associated with phasic activity in noradrenergic axons, whereas longer-lasting dilations of

46 Finally, systemic blockade of noradrenergic beta receptors led to reduced maternal reg

47 pants received a single dose of 40 mg of the noradrenergic beta-blocker propranolol (n = 15), double-

48 task, participants received a placebo or the noradrenergic beta-receptor blocker propranolol (40 mg).

49 aptive performance staircasing revealed that noradrenergic blockade (40 mg propranolol) significantly

50 The noradrenergic brain nucleus locus coeruleus (LC) modulat

51 ption through activation of serotonergic and noradrenergic bulbospinal circuits.

52 inal cortex and dentate gyrus, with no frank noradrenergic cell body loss.

53 the brainstem, at a location consistent with noradrenergic cell group 5 (A5), which appeared to be de

54 ups of cladistians are dopaminergic, whereas noradrenergic cells are located within the rhombencephal

55 Thus, CB1 receptors on adrenergic and noradrenergic cells provide previously unrecognized cros

56 ssure, supernumerary pontine cholinergic and noradrenergic cells, and an enlarged peripheral division

57 ere the NAT gene is selectively expressed in noradrenergic cells.

58 ing model, we characterise the influences of noradrenergic, cholinergic, and dopaminergic receptor an

59 enal medulla revealed decreased LDCV size in noradrenergic chromaffin cells, increased adrenal norepi

60 Activation of noradrenergic circuitry in the basolateral amygdala is t

61 fear conditioning test, and deregulation of noradrenergic circuits, consistent with downregulation o

62 Altogether, these data suggest that the noradrenergic component in tapentadol has the potential

63 Noradrenergic compounds have shown promise in altering t

64 pupillary responses to action, hinting at a noradrenergic contribution to impaired action-learning u

65 -amplifies a proximal enhancer driven by the noradrenergic core regulatory circuit (CRC).

66 In contrast, noradrenergic cortical stimulation activates the cortex

67 ucture vis-a-vis the involvement of the beta-noradrenergic, D1/D5-dopaminergic, and H2-histaminergic

68 is suitable for quantitative neuroimaging of noradrenergic deficits in human brain in vivo.

69 Based on preclinical models we proposed that noradrenergic denervation contributes to the impairment

70 his was the first specific quantification of noradrenergic denervation in PD patients in vivo.

71 In the lamina propria, noradrenergic-dependent increases in gut permeability in

72 al OX) to determine how chronically elevated noradrenergic-derived galanin, alone, alters anxiogenic-

73 Here we identify cholecystokinin (CCK) and noradrenergic, dopamine beta-hydroxylase (DBH)-expressin

74 mechanism underlying the connection between noradrenergic dysfunction and AD.

75 tau accumulation in the locus coeruleus and noradrenergic dysfunction may be a critical early step i

76 pathology affects LC neurons and how central noradrenergic dysfunction may contribute to early PD pat

77 Noradrenergic dysfunction may play a significant role in

78 se and support the hypothesis that targeting noradrenergic dysfunction may represent a new parallel a

79 Profound noradrenergic dysfunction occurs consistently in patient

80 y patients into clinical trials according to noradrenergic dysfunction.

81 The glutamate amplifies noradrenergic effects (GANE) model emphasizes the role o

82 r the predictions of the glutamate amplifies noradrenergic effects (GANE) model.

83 The "glutamate amplifies noradrenergic effects" (GANE) model proposed by Mather a

84 In our "glutamate amplifies noradrenergic effects" (GANE) model, high glutamate at t

85 ion models such as GANE (glutamate amplifies noradrenergic effects) may be able to explain these find

86 I argue that the GANE (glutamate amplifies noradrenergic effects) model basically explains an arous

87 els complement the GANE (glutamate amplifies noradrenergic effects) model by describing a mechanism t

88 I extend the GANE (glutamate amplifies noradrenergic effects) model by examining its success in

89 The GANE (glutamate amplifies noradrenergic effects) model described by Mather et al.

90 ith respect to the GANE (glutamate amplifies noradrenergic effects) model described by Mather et al.

91 The GANE (glutamate amplifies noradrenergic effects) model proposed by Mather et al. a

92 The GANE (glutamate amplifies noradrenergic effects) model proposes that local glutama

93 s described by the GANE (glutamate amplifies noradrenergic effects) model seem to modulate the precis

94 n extension of the GANE (glutamate amplifies noradrenergic effects) model to conditions with minimal

95 ccordance with the GANE (glutamate amplifies noradrenergic effects) model's sustaining the double rol

96 n the light of the GANE (glutamate amplifies noradrenergic effects) model, we suggest how to interpre

97 The GANE (glutamate amplifies noradrenergic effects) theory posits a mechanism for amp

98 The GANE (glutamate amplifies noradrenergic effects) theory proposes a complete accoun

99 xecutive syndrome, yet the direct effects of noradrenergic enhancement have not to date been addresse

100 function with XPro1595 correlates with less noradrenergic fiber sprouting and normalized norepinephr

101 Two recent studies have identified the noradrenergic fibres originating in the locus coeruleus

102 Altered adrenergic and noradrenergic function has been long believed to have a

103 , to unravel its effects on dopaminergic and noradrenergic functional circuits in the healthy brain a

104 However, research linking noradrenergic functioning to attention in aging humans i

105 ngs support a role for chronically increased noradrenergic galanin in mediating resilience to stress.

106 ngs support a role for chronically increased noradrenergic galanin in mediating resilience to stress.

107 The involvement of dopaminergic as well as noradrenergic, glutamatergic, serotonergic and adenosine

108 h brains to determine which dopaminergic and noradrenergic groups may use GABA or glutamate as a seco

109 l analyses, we show that activation of Hoxb1-noradrenergic (Hoxb1-NE) neurons decreases anxiety-like

110 rtex are modulated by atypically high phasic noradrenergic influences originating in the locus coerul

111 The vBNST receives dense noradrenergic innervation and expresses beta adrenergic

112 cus coeruleus was negatively correlated with noradrenergic innervation in the medial entorhinal corte

113 ike therapy were associated with a decreased noradrenergic innervation of lymphoid organs and counter

114 g the vasculature were GFRalpha3-IR, but the noradrenergic innervation of the detrusor was GFRalpha3-

115 Increased BM noradrenergic innervation promotes beta(2)-adrenergic-re

116 tainty about environmental rules, changes in noradrenergic input alter ACC output and prevent erroneo

117 hannels in nociceptive neurons by descending noradrenergic inputs may constitute a mechanism for nora

118 ed by partial lesion of the dopaminergic and noradrenergic inputs to striatum and hippocampus.

119 specificity of the memory, is enhanced when noradrenergic inputs to the olfactory bulb are unaltered

120 cedes other AD-related neuronal loss, and LC noradrenergic integrity is important for executive funct

121 contribute to the growing evidence that the noradrenergic LC is essential for behavioral adaptation

122 Arousal responses linked to locus coeruleus noradrenergic (LC-NA) activity affect cognition.

123 Increased tonic activity of locus coeruleus noradrenergic (LC-NE) neurons induces anxiety-like and a

124 The locus coeruleus noradrenergic (LC-NE) system is one of the first systems

125 but is unable to do so at tonically elevated noradrenergic levels associated with acute stress.

126 We propose that the noradrenergic-like system defines an ancient regulatory

127 The noradrenergic-linked behaviors of sociability and arousa

128 uromodulatory input from regions such as the noradrenergic locus ceruleus (LC) in the brainstem.

129 Loss of noradrenergic locus coeruleus (LC) neurons is a prominen

130 GAL and GALR3 mRNA levels, especially in the noradrenergic locus coeruleus and the dorsal raphe nucle

131 ncluding neuromodulatory systems such as the noradrenergic locus coeruleus, providing information abo

132 rol of cortical arousal state, including the noradrenergic locus coeruleus.

133 Consistent with a noradrenergic mechanism of action of methylphenidate, in

134 DHD), suppress social play in rats through a noradrenergic mechanism of action.

135 affect infant brain activity, in part via a noradrenergic mechanism, suggesting a powerful influence

136 e to a rapidly engaged descending inhibitory noradrenergic mechanism, which affected withdrawal respo

137 eases in vasoconstriction were mediated by a noradrenergic mechanism.

138 attern dependency in Wistar rats is due to a noradrenergic mechanism.

139 action boosts episodic memory encoding via a noradrenergic mechanism.

140 that consolidation of emotional memories by noradrenergic mechanisms alters systems consolidation dy

141 (LC) neurons have long suggested a role for noradrenergic mechanisms in mediating arousal.

142 Emotional enhancement of memory by noradrenergic mechanisms is well-described, but the long

143 Together, these noradrenergic mechanisms promote selective attention and

144 This work suggests that MPH, acting via noradrenergic mechanisms, can substantially affect early

145 ransmission and activating descending spinal noradrenergic mechanisms.

146 Most prescriptions are for noradrenergic medications, despite their approval only f

147 ual signals from retina to cortex, receiving noradrenergic modulation from the LC.

148 Thus, the temporal structure of noradrenergic modulation may selectively and dynamically

149 s (LC) neurons has long suggested a role for noradrenergic modulation of arousal.

150 The locus coeruleus (LC), the origin of noradrenergic modulation of cognitive and behavioral fun

151 Noradrenergic modulation of mPFC firing represents a mec

152 ic receptors are mediators of adrenergic and noradrenergic modulation throughout the brain.

153 ts) theory posits a mechanism for amplifying noradrenergic modulatory actions and enhancing the proce

154 Serotonergic (5-HT) and noradrenergic (NA) input to spinal motoneurons is essent

155 he pre-registered hypothesis that putatively noradrenergic (NA)-dependent functions would be more str

156 The vSub receives dense noradrenergic (NE) inputs from the locus coeruleus (LC),

157 sensitization of basolateral amygdala (BLA) noradrenergic (NE) receptors (alpha1) via a corticotropi

158 characterization of mouse celiac ganglia and noradrenergic nerves in two target tissues, spleen and s

159 Likewise, TH and NPY were colocalized in noradrenergic nerves throughout the spleen and in stomac

160 itor cells but, is observed in proliferating noradrenergic neuroblasts.

161 s indicate that the locus coeruleus (LC) and noradrenergic neuromodulation may also play an important

162 ioral tagging) is caused by dopaminergic and noradrenergic neuromodulation of hippocampal plasticity

163 ongoing synchronized cortical activity, and noradrenergic neuromodulation.

164 is discussed in relation to dopaminergic and noradrenergic neuromodulation.

165 pain-related behaviours mediated by distinct noradrenergic neuronal populations provides evidence for

166 transgenic mice that overexpress galanin in noradrenergic neurons (Gal OX) to determine how chronica

167 rsectional genetic strategy to ablate NPY(+) noradrenergic neurons and/or adrenal chromaffin cells.

168 Locus ceruleus (LC) noradrenergic neurons are critical in generating alertne

169 om recording studies in animals reveals that noradrenergic neurons are excited mainly by any change i

170 Quantification of the loss of noradrenergic neurons by means of neuroimaging has been

171 A decrease in DBH expression in noradrenergic neurons can elevate dopamine levels, which

172 ow that genetic overexpression of galanin in noradrenergic neurons causes resilience to a stressor an

173 hese experiments demonstrate that loss of LC noradrenergic neurons exacerbates multiple phenotypes ca

174 pses between mitral and granule cells (GCs), noradrenergic neurons extending from the brainstem provi

175 from the substantia nigra pars compacta and noradrenergic neurons from the locus coeruleus in monkey

176 Noradrenergic neurons have been identified to be a speci

177 We identify cholinergic neurons and noradrenergic neurons in an intrinsic cardiac ganglion a

178 tudy, we test directly whether activation of noradrenergic neurons in the LC influences brainstem par

179 the laterodorsal tegmental nucleus; lateral noradrenergic neurons in the LC; medial GABAergic neuron

180 amine, recent studies have demonstrated that noradrenergic neurons in the locus coeruleus (LC) corele

181 substantia nigra pars compacta (SNpc) and of noradrenergic neurons in the locus coeruleus is accompan

182 Pharmacogenetic activation of noradrenergic neurons in the locus coeruleus mimics this

183 ject to, synapse on, and positively regulate noradrenergic neurons in the locus coeruleus, a brain ce

184 Conversely, the firing of noradrenergic neurons increased with both pupil dilation

185 re and supernumerary pontine cholinergic and noradrenergic neurons indicate that the control of unihe

186 This study demonstrates LC noradrenergic neurons inhibit the brainstem CVNs that ge

187 Degeneration of noradrenergic neurons may underlie the disabling nonmoto

188 e of dopamine in the dorsal hippocampus from noradrenergic neurons of the LC.

189 results suggest that DR serotonergic and LC noradrenergic neurons play differential roles in orexin

190 ic or chemogenetic activation, we found that noradrenergic neurons progressively activated brainstem

191 ed wakefulness correlated with the number of noradrenergic neurons restored in the LC.

192 Whole-brain calcium imaging revealed noradrenergic neurons that responded specifically to fai

193 particular vulnerability of dopaminergic and noradrenergic neurons to neurodegeneration in PARK7-rela

194 el previously inaccessible subpopulations of noradrenergic neurons to reveal details of their three-d

195 y ES at the abdomen activates NPY(+) splenic noradrenergic neurons via the spinal-sympathetic axis; t

196 ere phenocopied by galanin overexpression in noradrenergic neurons, and Gal OX mice were resistant to

197 neurons contact locus coeruleus, A1, and A2 noradrenergic neurons, and ultrastructural evidence that

198 Here we identify a subpopulation of noradrenergic neurons, defined by developmental expressi

199 brain stem nucleus containing cell bodies of noradrenergic neurons, dynamically tracks the level of u

200 ate the trafficking itinerary of NET in live noradrenergic neurons.

201 sed norepinephrine in central and peripheral noradrenergic neurons.

202 enhancement points to a regulatory role for noradrenergic neurotransmission in perceptual metacognit

203 Alternatively, different key proteins of noradrenergic neurotransmission might be affected.

204 Here, we tested the effects of attenuating noradrenergic neurotransmission on learning under uncert

205 lack of radioligands that are selective for noradrenergic neurotransmission.

206 emotional autobiographical memories enhances noradrenergic neurotransmission.

207 the brainstem that provides the far-reaching noradrenergic neurotransmitter system of the brain.

208 Quantitative analysis of the cholinergic and noradrenergic nuclei of the pontine region revealed that

209 vement of selected brainstem cholinergic and noradrenergic nuclei.

210 The noradrenergic nucleus locus ceruleus (LC) is associated

211 en by the neuropeptide galanin from the main noradrenergic nucleus, the locus coeruleus (LC).

212 the previously reported photostimulation of noradrenergic or hypocretin neurons that induces wake tr

213 reatening infections, thought to result from noradrenergic overactivation and excess glucocorticoid r

214 t majority of mouse celiac neurons express a noradrenergic phenotype, which includes tyrosine hydroxy

215 it is unclear whether noradrenergic plasticity also affects the input to the M

216 genotyping studies for examining effects of noradrenergic processes on stimulus prioritization in hu

217 the RTPJ and the locus ceruleus, suggesting noradrenergic processes underlying the response-facilita

218 b levels resulted in opposite behavioral and noradrenergic profile with higher freezing time and incr

219 nations in vitro, we discovered a decline of noradrenergic projections in vivo in brain of PD patient

220 theories of brain function due to its broad noradrenergic projections throughout the CNS.

221 glucagon-like peptide-1 (GLP-1) neurons and noradrenergic prolactin-releasing peptide (PrRP) neurons

222 t cognitive flexibility through the alpha 2A noradrenergic receptor (a2A-NAR) acting in prefrontal co

223 etic mechanisms are recruited by hippocampal noradrenergic receptor activation.

224 of the olfactory bulb with a broad-spectrum noradrenergic receptor antagonist.

225 tion of propranolol (10 mg/kg, i.p.), a beta-noradrenergic receptor antagonist.

226 To account for developmental changes in noradrenergic receptor expression, we measured expressio

227 over, it is demonstrated that the sensitized noradrenergic receptors colocalize with CRF1 receptors o

228 Hence, this stress-induced sensitization of noradrenergic receptors on basolateral nucleus efferents

229 were blocked, as well as during blockade of noradrenergic receptors, suggesting a non-neuronal origi

230 imentally observed phenomena associated with noradrenergic regulation of sensory signal transfer.

231 IL-1beta acts via a noradrenergic relay from the nucleus tractus solitarii (

232 lts showed compromised attention and reduced noradrenergic responsiveness as indicated by interrelate

233 in the ASD group, thus suggesting heightened noradrenergic responsivity in line with compromised neur

234 under chronic treatment with atomoxetine, a noradrenergic reuptake inhibitor used to treat attention

235 estinal pain and painful FGIDs and serotonin noradrenergic reuptake inhibitors can also be recommende

236 ative similarity relates to the cholinergic, noradrenergic, serotonergic and orexinergic systems, and

237 ative similarity relates to the cholinergic, noradrenergic, serotonergic, and orexinergic systems and

238 ear organization relates to the cholinergic, noradrenergic, serotonergic, and orexinergic systems and

239 e discuss how T. gondii infection suppresses noradrenergic signaling and how the restoration of this

240 s ceruleus (LC) neurons and dysregulation of noradrenergic signaling are ubiquitous features of Parki

241 rying stress susceptibilities have different noradrenergic signaling changes in response to stress.

242 refore next determined whether inhibition of noradrenergic signaling during memory reactivation would

243 linical trials indicating that disruption of noradrenergic signaling during reconsolidation may aboli

244 rders are comorbid with substance abuse, and noradrenergic signaling in the bed nucleus of the stria

245 this, investigations have now revealed that noradrenergic signaling is a critical mechanism for reco

246 Noradrenergic signaling is known to maintain glutamaterg

247 Noradrenergic signaling may contribute to extinction imp

248 Noradrenergic signaling plays a well-established role in

249 Noradrenergic signaling strengthens synaptic plasticity

250 stent with the hypothesis that TEN modulates noradrenergic signaling to suppress sympathetic activity

251 s linked to dopaminergic, serotoninergic and noradrenergic signaling, metabolism (DBH, TPH1, TPH2, DD

252 usal, which has been associated with optimal noradrenergic signaling, the salience network is optimal

253 idence that NPY promotes sleep by inhibiting noradrenergic signaling.

254 pupillary dilatation as a measure of central noradrenergic signalling, we tested the hypothesis that

255 Autonomic sympathetic noradrenergic signals have been shown to regulate HSPC a

256 volatility and has previously been linked to noradrenergic signals that originate in the locus coerul

257 ng human wild-type asyn under control of the noradrenergic-specific dopamine beta-hydroxylase promote

258 We found that selective cholinergic and noradrenergic stimulation of the barrel cortex produces

259 -adrenergic antagonist yohimbine (increasing noradrenergic stimulation), hydrocortisone, both substan

260 ramming their firing rate, responsiveness to noradrenergic stimulation, intrinsic electrical properti

261 asting sensitization of basolateral amygdala noradrenergic substrates [via a corticotropin-releasing

262 Many noradrenergic sympathetic axons innervating the vasculat

263 bgenual prefrontal cortex, the amygdala, the noradrenergic system and the CRH/HPA axis participate in

264 the stress response, demonstrating that the noradrenergic system contains multiple functionally dist

265 we provide evidence of an involvement of the noradrenergic system during an attentional task.

266 n aging and underscore the importance of the noradrenergic system in late-life cognition.

267 The noradrenergic system is intimately related to the autono

268 reover, as the functional sensitivity of the noradrenergic system is likely to change with disease pr

269 icate that a common genetic variation of the noradrenergic system modulates the impact of stress on t

270 udied whether age-related differences in the noradrenergic system predict differences in attention.

271 by using selective lesions of the LC and the noradrenergic system to demonstrate an exacerbation of c

272 In the study described here, the noradrenergic system was found to be suppressed with dec

273 ially, in both age groups, a more responsive noradrenergic system was strongly associated with attent

274 uli to experimentally activate participants' noradrenergic system while recording pupillometry and EE

275 here that a common genetic variation of the noradrenergic system, a known risk factor for post-traum

276 tionally aversive stimuli, which recruit the noradrenergic system, modulate the mnemonic advantage co

277 Galanin is highly expressed in the noradrenergic system, particularly the locus coeruleus (

278 cending neuromodulatory systems, such as the noradrenergic system, via changes in neural gain (in ter

279 ase has been made for the involvement of the noradrenergic system, which modulates cognitive processe

280 a proof-of-principle analysis of the central noradrenergic system.

281 alpha(2A)AR is a key component of the brain noradrenergic system.

282 n, rapidly activates a descending inhibitory noradrenergic system.

283 al systems, such as the CRH/HPA axis and the noradrenergic systems, are at their maxima.

284 Noradrenergic terminals are found in the glomerular laye

285 ces vigilance-dependent Ca(2+) transients in noradrenergic terminals, but has little effect on astrog

286 This regimen anticipates that noradrenergic therapies for behavioural symptoms would b

287 stratification in future clinical trials of noradrenergic therapies for Parkinson's disease.

288 hetic cholinergic signals dampen sympathetic noradrenergic tone and decrease BM egress of HSPCs and l

289 asticity in the mouse brain are modulated by noradrenergic tone fluctuations between arousal states a

290 e that under basal physiological conditions, noradrenergic tone in awake mice suppresses microglial p

291 rs and suggest a reduction of the inhibitory noradrenergic tone in lymphoid organs as one of the poss

292 size-a peripheral index of arousal linked to noradrenergic tone-associated with reduced distractor in

293 pression affects the function of the central noradrenergic transmission and associated behaviors.

294 e results support an arousal circuit whereby noradrenergic transmission at astrocytic alpha1ARs activ

295 The degeneration of the LC and loss of noradrenergic transmission have been recognized as ubiqu

296 s associated with decreased 5-HT2A-dependent noradrenergic transmission.

297 However, the noradrenergic transmitter system may be affected on a di

298 To confirm that the noradrenergic transmitter system was responsible for the

299 betaARs) is required for PF-PC LTP, although noradrenergic varicosities are apposed in PF-PC contacts

300 ttenuated with ageing, as was the decline in noradrenergic vasoconstriction; genetic deletion of IL-1