ライフサイエンスコーパス: noradrenergic

1 echolamine innervation of the dLGN is solely noradrenergic.

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

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

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

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

6 and pharmacological treatments that augment noradrenergic activity (atomoxetine; norepinephrine reup

7 This shift is mediated by an interaction of noradrenergic activity and glucocorticoid stress hormone

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

9 s suggest that concurrent glucocorticoid and noradrenergic activity disrupts the neural bases of goal

10 resentations or pharmacologically increasing noradrenergic activity during extinction training result

11 n regulating rapid glucocorticoid effects on noradrenergic activity in impairing memory retrieval of

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

13 Because high noradrenergic activity in the BSTv can also increase anx

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

15 d on rapid interactions with arousal-induced noradrenergic activity, the exact mechanism underlying t

16 inhibitory control of central nervous system noradrenergic activity.

17 ion responses as an indirect index of phasic noradrenergic activity.

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

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

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

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

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

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

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

25 scent protein behind a promoter selective to noradrenergic and adrenergic neurons.

26 tasks paired with local bulbar infusions of noradrenergic and cholinergic drugs, we then show that r

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

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

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

30 The noradrenergic and p38 mitogen-activated protein kinase (

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

32 offer protection to all of the dopaminergic, noradrenergic and serotonergic fibre types degenerating

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

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

35 of catecholaminergic neurons (dopaminergic, noradrenergic, and adrenergic) in the songbird brain.

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

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

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

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

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

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

42 This work highlights the key role of noradrenergic autoreceptor signaling in the persistent m

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

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

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

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

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

48 The noradrenergic brain nucleus locus coeruleus (LC) modulat

49 ption through activation of serotonergic and noradrenergic bulbospinal circuits.

50 esions of nigrostriatal axons nor the dorsal noradrenergic bundle decreased the number of PF neurons

51 c drugs, we then show that rats engage their noradrenergic, but not their cholinergic system, to bett

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

53 Thus, the pontine noradrenergic cell groups project in a roughly topograph

54 The pontine noradrenergic cell groups, A5, A6 (locus coeruleus), and

55 They also innervate pontine noradrenergic cell groups, including the locus coeruleus

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

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

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

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

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

61 Activation of noradrenergic circuitry in the basolateral amygdala is t

62 be the result of a functional impairment in noradrenergic circuits associated with locus coeruleus (

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

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

65 Noradrenergic compounds have shown promise in altering t

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

67 In contrast, noradrenergic cortical stimulation activates the cortex

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

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

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

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

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

73 mpared a serotonin reuptake inhibitor with a noradrenergic/dopaminergic antidepressant in major depre

74 mechanism underlying the connection between noradrenergic dysfunction and AD.

75 ss disorder (PTSD), which has been linked to noradrenergic dysfunction in humans.

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

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 havioral changes coincided with irruption of noradrenergic dysfunction, evident as: an increase in LC

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

90 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 cts of CUS, and that repeated elicitation of noradrenergic facilitatory activity is one mechanism by

101 Previous studies suggest that the density of noradrenergic fibers in rat is relatively uniform across

102 These findings suggest noradrenergic fibers may be the primary source of DA rel

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

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

105 targeting disturbances of the serotonergic, noradrenergic, glutamatergic, GABAergic, and cholinergic

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

107 ice, and (3) L-DOPS treatment may ameliorate noradrenergic hypofunction in Menkes disease.

108 ice, and (3) L-DOPS treatment may ameliorate noradrenergic hypofunction in Menkes disease.

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

110 ibition of nociception in C. elegans and the noradrenergic inhibition of nociception in mammals that

111 milarities of this modulatory network to the noradrenergic inhibition of nociception in mammals, wher

112 The effect of the noradrenergic inhibitor propranolol on (14)C-FBnTP respo

113 Our data indicate that noradrenergic inhibitory feedback is impaired for at lea

114 The vBNST receives dense noradrenergic innervation and expresses beta adrenergic

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

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

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

118 (locus coeruleus), and A7, provide the only noradrenergic innervation of the spinal cord, but the in

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

120 erotonergic input from the raphe nuclei, and noradrenergic input from the nucleus locus coeruleus.

121 tial distribution during immobility, whereas noradrenergic input was necessary for the tonic depolari

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

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

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

125 Galanin and GalR3 mRNA were found in many noradrenergic LC neurons, and GalR3 overlapped with sero

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

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

128 ure involve differential dopaminergic versus noradrenergic lesions.

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

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

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

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

133 The noradrenergic locus coeruleus (LC) regulates arousal, me

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

135 orexin acts upstream of the amygdala via the noradrenergic locus coeruleus to enable threat (fear) le

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

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

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

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

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

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

142 eases in vasoconstriction were mediated by a noradrenergic mechanism.

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

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

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

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

147 Together, these noradrenergic mechanisms promote selective attention and

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

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

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

151 t for odor decorrelation and discrimination, noradrenergic modulation is important for signal-to-nois

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

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

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

155 neuromodulatory systems that originate from noradrenergic (NA) and serotonergic (5-HT) neurons.

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

157 Noradrenergic (NA) receptor systems have also been impli

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

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

160 Using a model of 6-hydroxydopamine-mediated noradrenergic nerve ablation, we show that elimination o

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

162 ongoing synchronized cortical activity, and noradrenergic neuromodulation.

163 is discussed in relation to dopaminergic and noradrenergic neuromodulation.

164 UT2(flox/flox) mice, into the caudal VLM (A1 noradrenergic neuron-rich region) of DbetaH(Cre/0) mice

165 ethynyl] pyridine, reduces dopaminergic and noradrenergic neuronal loss in monkeys rendered parkinso

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

167 mined the effect of C1 activation on pontine noradrenergic neurons (LC and A5) using a more selective

168 stimulation of C1 neurons activates pontine noradrenergic neurons and sympathetic nerve discharge, p

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

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

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

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

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

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

175 Noradrenergic neurons have been identified to be a speci

176 nerve ablation, we show that elimination of noradrenergic neurons improves survival during Klebsiell

177 App) gene to degeneration of cholinergic and noradrenergic neurons in DS mouse models.

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 ectivity between Hcrt neurons and downstream noradrenergic neurons in the locus coeruleus (LC) during

181 the dopaminergic nigrostriatal system and of noradrenergic neurons in the locus coeruleus are importa

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

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

184 previously, anti-DBH-SAP selectively killed noradrenergic neurons in the NTS while SAP conjugated to

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

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

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

188 Brainstem noradrenergic neurons innervate the mesocorticolimbic re

189 Degeneration of noradrenergic neurons may underlie the disabling nonmoto

190 ate the locus coeruleus as well as A1 and A2 noradrenergic neurons monosynaptically by releasing glut

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

192 s, including midbrain dopamine (DA) neurons, noradrenergic neurons of the locus ceruleus, and retinal

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

194 These results suggest that noradrenergic neurons regulate the immune response throu

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

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

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

198 Activity of locus coeruleus (LC) noradrenergic neurons was determined in anaesthetized ra

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

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

201 However, the influence of peripheral noradrenergic neurons, which are primarily sympathetic n

202 sed norepinephrine in central and peripheral noradrenergic neurons.

203 instem GABAergic interneurons that innervate noradrenergic neurons.

204 se the firing of both peripheral and central noradrenergic neurons.

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

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

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

208 c receptor (alpha(2A)AR), a key regulator of noradrenergic neurotransmission with altered expression

209 lack of radioligands that are selective for noradrenergic neurotransmission.

210 emotional autobiographical memories enhances noradrenergic neurotransmission.

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

212 ation of the locus coeruleus (LC), the major noradrenergic nucleus in the brain, occurs early and is

213 The noradrenergic nucleus locus ceruleus (LC) is associated

214 dopamine-beta-hydroxylase and were therefore noradrenergic or adrenergic.

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

216 transmission deficits are not seen at either noradrenergic or serotoninergic terminals.

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

218 To better understand the noradrenergic/peptidergic modulation of nociception, we

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

220 CAmy GABAergic neurons may directly inhibit noradrenergic principal neurons.

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

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

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

224 s by showing that adult-born neurons receive noradrenergic projections and are responsive to noradren

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

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

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

228 etic mechanisms are recruited by hippocampal noradrenergic receptor activation.

229 i of the amygdala administration of the beta-noradrenergic receptor antagonist, propranolol, reversed

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

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

232 phrine in the amygdala and the activation of noradrenergic receptors are essential for stress hormone

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

234 Thus, we conclude that blockade of noradrenergic receptors in mPFC protected against the de

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

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

237 nse to NA, indicating a common mechanism for noradrenergic regulation of GCMC inhibition throughout t

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

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

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

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

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

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

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

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

246 An aversive stimulus, quinine, activated noradrenergic signaling but inhibited dopaminergic signa

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

248 Genetic variants involved in noradrenergic signaling contribute to individual differe

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

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

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

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

253 Noradrenergic signaling is known to maintain glutamaterg

254 Noradrenergic signaling may contribute to extinction imp

255 cular interactions between glutamatergic and noradrenergic signaling pathways for long-lasting synapt

256 Noradrenergic signaling strengthens synaptic plasticity

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

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

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

260 idence that NPY promotes sleep by inhibiting noradrenergic signaling.

261 Pain modulation is complex, but noradrenergic signalling promotes anti-nociception, with

262 evoked currents could both be attributed to noradrenergic silencing of spontaneous spiking in glycin

263 holinergic agonists activate the sympathetic noradrenergic splenic nerve to control systemic inflamma

264 ibit systemic inflammation by activating the noradrenergic splenic nerve via the alpha7nAChR nicotini

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

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

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

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

269 Many noradrenergic sympathetic axons innervating the vasculat

270 gy to eliminate Bmpr1a and Smad4 in immature noradrenergic sympathetic neurons we now show that dendr

271 used pharmacological means to manipulate the noradrenergic system and neurogenesis and to assess thei

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

273 hanges are consistent with the impairment of noradrenergic system described in depressive disorders.

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

275 nt of affective disorders, and highlight the noradrenergic system in the vBNST as a common substrate

276 We propose that activity of the noradrenergic system is a critical mediator providing a

277 The noradrenergic system is intimately related to the autono

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

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

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

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

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

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

284 n, rapidly activates a descending inhibitory noradrenergic system.

285 so capable of broadly activating the brain's noradrenergic system.

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

287 consequent release of norepinephrine (NE) in noradrenergic terminal fields.

288 Noradrenergic terminals are found in the glomerular laye

289 ocampal inputs, particularly cholinergic and noradrenergic terminals, leads to de-afferentation of th

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

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

292 We have shown that enhancing noradrenergic tone acutely in the rat mPFC facilitated e

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

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

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

296 Based upon these data we argue that noradrenergic transmission is a key mechanism selecting

297 with our hypotheses, direct manipulation of noradrenergic transmission significantly effect on adult

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

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

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