ライフサイエンスコーパス: CeA

1 CeA afferents are GABAergic (express Slc32a1/Vgat) and a

2 CeA inactivation also substantially reduced stimulus-evo

3 CeA neurons from abstinent drinkers displayed an elevate

4 CeA rats also emitted consummatory bites toward their la

5 CeA stimulation also elevated the effort cost rats were

6 CeA(GA) neurons also possess basal activity that mostly

7 CeA(GA) neurons have widespread inhibitory projections t

8 CeA->SNL neural responses to appetitive and aversive sti

9 CeA->SNL terminal activation elicited reinforcement when

10 CeA-CRF neurons transition from responding to the uncond

11 CeA-induced maladaptive attractions, even to the painful

12 pyramidal neurons to dopamine receptor 1(+) CeA neurons define a pathway for promoting appetitive be

13 pyramidal neurons to dopamine receptor 2(+) CeA neurons define a pathway for suppressing appetitive

14 Thus, our findings identify a CeA->BST CRF neuropeptide circuit that generates anxiety

15 Acute CeA infusions with the PACAP receptor antagonist PACAP(6

16 tivated by GA in the mouse central amygdala (CeA(GA) neurons).

17 ffering involvement of the central amygdala (CeA) and bed nucleus of the stria terminalis (BNST) in t

18 -expressing neurons in the central amygdala (CeA) antagonize the extinction memory following immediat

19 sing hormone gene (Crh) in central amygdala (CeA) are implicated in threat regulation, yet little is

20 The central amygdala (CeA) has a key role in learning and expression of defens

21 factor (CRF) system in the central amygdala (CeA) has been implicated in the effects of acute ethanol

22 SIGNIFICANCE STATEMENT The central amygdala (CeA) has been implicated in the establishment of defensi

23 The central amygdala (CeA) is critically involved in a range of adaptive behav

24 The central amygdala (CeA) is important for fear responses to discrete cues.

25 in 2 (Tac2) pathway in the central amygdala (CeA) is necessary and sufficient for the modulation of f

26 hat CRF-CRFR1 signaling in central amygdala (CeA) mediates stress-induced hyperalgesia in rats with h

27 f mapping functionality in central amygdala (CeA) neuron populations based on their molecular profile

28 tion of cell bodies in the central amygdala (CeA) or axons in the vBNST, PBN, and NTS produces reward

29 The central amygdala (CeA) orchestrates adaptive responses to emotional events

30 SIGNIFICANCE STATEMENT The central amygdala (CeA) plays a critical role in the development of alcohol

31 rat model showed that the central amygdala (CeA) plays an important role in avoidance of a predator

32 whereas silencing the VTA-central amygdala (CeA) projection had no effect.

33 ogical inactivation of the central amygdala (CeA) severely impaired acquisition and retention of eyeb

34 rons that project from the central amygdala (CeA) to the lateral hypothalamus (LH)] mediates avoidanc

35 it organization within the central amygdala (CeA), a critical regulator of emotional states, includes

36 naptic transmission in the central amygdala (CeA), and circulating cytokine levels were measured.

37 tral tegmental area (VTA), central amygdala (CeA), and nucleus accumbens (NAc) shell had no such effe

38 BLA neurons project to the central amygdala (CeA), which also participates in negative and positive b

39 dysfunction, including the central amygdala (CeA).

40 tatory transmission in the central amygdala (CeA).

41 teral (CeL) nucleus of the central amygdala (CeA).

42 hippocampus (Hippo-DKO) or central amygdala (CeA-DKO) by stereotaxic delivery of AAV-Cre into IR(lox/

43 identified the central nucleus of amygdala (CeA) as a major source of GABAergic inputs to multiple w

44 stimulation of central nucleus of amygdala (CeA) in rats with encountering either sucrose, cocaine,

45 ow that pairing central nucleus of amygdala (CeA) optogenetic stimulation with one option for earning

46 ation in either central nucleus of amygdala (CeA) or basolateral amygdala (BLA) of female rats with o

47 ions in the central nucleus of the amygdala (CeA) and gene expression changes in the medial prefronta

48 ions to the central nucleus of the amygdala (CeA) and nucleus accumbens (NAc).

49 ject to the central nucleus of the amygdala (CeA) and that the CeA is involved in mediating the defen

50 tion on the central nucleus of the amygdala (CeA) and the hypothalamic paraventricular nucleus (PVN)

51 ling in the central nucleus of the amygdala (CeA) and these neuroadaptive responses differentiate alc

52 licated the central nucleus of the amygdala (CeA) as an important site for mediating the somatic symp

53 c area, and central nucleus of the amygdala (CeA) contain the densest concentrations of NTS-projectin

54 NI into the central nucleus of the amygdala (CeA) decreased alcohol intake.

55 mble in the central nucleus of the amygdala (CeA) during alcohol withdrawal has been hypothesized to

56 ways to the central nucleus of the amygdala (CeA) in brainstem slices by recording from retrogradely

57 a (PFC) and central nucleus of the amygdala (CeA) in monkeys.

58 rons in the central nucleus of the amygdala (CeA) in nondependent rats that binge drink alcohol and i

59 role of the central nucleus of the amygdala (CeA) in the expression of such behaviors [3-5], and the

60 The central nucleus of the amygdala (CeA) is a key player in alcohol-dependence associated be

61 within the central nucleus of the amygdala (CeA) promotes cataplexy.

62 rons of the central nucleus of the amygdala (CeA) target brainstem regions known to regulate muscle t

63 rons in the central nucleus of the amygdala (CeA) that produce the neuropeptide corticotropin-releasi

64 ye from the central nucleus of the amygdala (CeA) to identify CeA-projecting nucleus of the solitary

65 rons in the central nucleus of the amygdala (CeA) triggered cataplexy of sleep disorder narcolepsy.

66 ling in the central nucleus of the amygdala (CeA) underlies key behaviors associated with alcohol dep

67 ings in the central nucleus of the amygdala (CeA), we found that rats with high addiction-like behavi

68 sion in the central nucleus of the amygdala (CeA).

69 MP-9 in the central nucleus of the amygdala (CeA).

70 rons in the central nucleus of the amygdala (CeA).

71 lPBN to the central nucleus of the amygdala (CeA).

72 rons in the central nucleus of the amygdala (CeA).

73 ala (in the central nucleus of the amygdala [CeA]) PACAP immunoreactivity, extracellular signal-regul

74 cortex, the core and shell of NAc, BLA, and CeA, on cue- and drug-induced cocaine-seeking in the rat

75 bstantia nigra, infralimbic cortex, BLA, and CeA.

76 changes in the medial prefrontal cortex and CeA from the same animals used for behavioral studies.

77 c) genes in the medial prefrontal cortex and CeA.

78 Consequently, both Hippo-DKO and CeA-DKO mice have decreased levels of the GluA1 subunit

79 the previously described functions of IC and CeA through direct projections to the LH.

80 hat PKCepsilon signaling in both the NAc and CeA is a major contributor to binge alcohol drinking and

81 e p(Ser729)-PKCepsilon levels in the NAc and CeA.

82 preferentially target SNL GABA neurons, and CeA->SNL and SNL dopamine neurons respond similarly to s

83 we measured Nr3c2 mRNA levels in the PFC and CeA of dependent and nondependent rats and the correlate

84 y tract (ST) always (93%) triggered EPSCs at CeA projecting NTS neurons.

85 on from basolateral to central amygdala (BLA-CeA) develops rapidly during the first 10 postnatal days

86 A release was attenuated, suggesting blunted CeA 5-HT sensitivity, which partially recovered in protr

87 ssociation between the roles of the central (CeA) and basolateral amygdala (BLA) in regulating social

88 Consequently, CeA rats quickly came to pursue their CeA ChR2-paired co

89 Conversely, CeA inhibition by muscimol/baclofen microinjections prev

90 Our findings identify a CRF(CeA)->CRF(dlBST) circuit for generating anxiety-like beh

91 These results suggest that the CRF(CeA-BNST) pathway could be targeted for the treatment of

92 inalis (BNST) and that inhibition of the CRF(CeA-BNST) pathway is mediated by inhibition of the CRF-C

93 ol exposure on inhibitory signaling in CRF1+ CeA neurons, we used CRF1:GFP mice subjected to chronic

94 we show that the inhibitory control of CRF1+ CeA neurons is lost with chronic ethanol exposure, likel

95 lcium sensor GCaMP6 into genetically defined CeA GABAergic neurons.

96 These results demonstrate CeA-CRF neurons are an important substrate for the persi

97 w that chemogenetic activation of the entire CeA produces a marked increase in cataplexy attacks.

98 ctivation and inactivation of NTS-expressing CeA neurons promoted and suppressed non-REM (NREM) sleep

99 ive behaviors have been studied extensively, CeA circuits for appetitive behaviors and their relation

100 Finally, CeA ChR2 valence can be switched to neutral by pairing w

101 negative behaviors, and the causal role for CeA circuits underlying appetitive behaviors is poorly u

102 that most of its GABAergic inputs arise from CeA.

103 ne nucleus at the confluence of outputs from CeA that may support amygdala modulation of CS input to

104 Ex vivo electrophysiological recordings from CeA neurons indicated that oxytocin decreases evoked GAB

105 e found that chemogenetic inhibition of GABA CeA cells does not prevent cataplexy, suggesting these c

106 e found that chemogenetic activation of GABA CeA cells triggered a 253% increase in the number of cat

107 ate that virtually all NTS-->lPBN and lPBN-->CeA CGRP projections coexpress vesicular glutamate trans

108 Inhibition of lPBN-->CeA neurons attenuated cisplatin-induced anorexia and bo

109 To test whether lPBN-->CeA projection neurons are required for cisplatin-induce

110 PVT->CeA activity associates morphine reward to the environme

111 However, CeA ChR2 laser on its own lacked any reinforcement value

112 al nucleus of the amygdala (CeA) to identify CeA-projecting nucleus of the solitary tract (NTS) neuro

113 expression in DYN+ neurons was confirmed in CeA of Pdyn-IRES-Cre mice and functionality of an inhibi

114 preprodynorphin (PDYN) and KOR expression in CeA neurons, we performed region-specific conditional kn

115 luA1-Ser831 phosphorylation was increased in CeA and lateral amygdala of mice that lever-pressed for

116 iders exhibited higher CRF peptide levels in CeA that did not appear to be locally synthesized.

117 olves MMP-9-dependent synaptic plasticity in CeA.

118 5-HT2CR in the BLA plays a critical role in CeA plasticity and neuropathic pain behaviors in the rat

119 to assess the role of CRF-CRFR1 signaling in CeA in stress-induced hyperalgesia.

120 a that is mediated by CRF-CRFR1 signaling in CeA.

121 lly inhibiting or activating LC terminals in CeA is sufficient to achieve this bidirectional modulati

122 an existing models, and identifies increased CeA GABAergic signaling and a distinct pro-hematopoietic

123 postsynaptic measures, suggesting increased CeA GABA release in naive rats.

124 , indicative of hyperarousal, with increased CeA GABAergic transmission in NOV females.

125 Alcohol increases CeA activity (neuronal firing rates and GABA release) in

126 Here we report that acute alcohol increases CeA neuronal activity in naive rats by engaging L-type c

127 ed kinase signaling attenuated PACAP-induced CeA neuronal activation and nociceptive responses.

128 Intra-CeA infusions of N/OFQ (1 mug per site) reversed the esc

129 Intra-CeA levels of N/OFQ were lower in HA rats than in LA rat

130 reinstatement of cocaine-seeking after intra-CeA SB-334867 (10 nmol) administration.

131 ) in naive rats by engaging LTCCs, and intra-CeA LTCC blockade reduces alcohol intake in nondependent

132 Systemic and intra-CeA microinfusions of the HCRT-receptor 1 antagonist, SB

133 gesia that was reversed by systemic or intra-CeA injection of a CRFR1 antagonist.

134 type calcium channels (LTCCs) and that intra-CeA LTCC blockade reduces alcohol intake in nondependent

135 ant training, rats were implanted with intra-CeA guide cannula and exposed to long-term intermittent

136 by subpopulations of neurons in the lateral CeA and the dorsolateral bed nucleus of the stria termin

137 ogenetic strategies to target and manipulate CeA activity selectively in narcoleptic (orexin(-/-)) mi

138 Consistent with a disinhibitory mechanism, CeA inputs preferentially target SNL GABA neurons, and C

139 (GABAergic) neurotransmission in the medial CeA and the sensitivity of GABAergic synapses to modulat

140 ABAergic neurotransmission within the medial CeA in LgA rats, which was blocked with SB-334867 (10 mu

141 t) and are distributed largely in the medial CeA subdivision.

142 Here, we report that a previously neglected CeA-to-globus pallidus external segment (GPe) circuit pl

143 Activation of the BLA but not CeA suppressed social behavior.

144 receptor subtype 5-HT2CR in the BLA, but not CeA, has been implicated anxiogenic behaviors and anxiet

145 NTS-CeA neurons received greater numbers of ST-related input

146 ded neuron pairs: one dye positive (i.e. NTS-CeA) and a second unlabelled neighbour.

147 tary tract (ST) afferents converged onto NTS-CeA second-order sensory neurons in greater numbers, as

148 The remaining NTS-CeA neurons received viscerosensory input only via polys

149 spite multifibre convergence, all single NTS-CeA neurons received inputs derived from only unmyelinat

150 Half of the NTS-CeA neurons received at least one primary afferent input

151 and polysynaptic ST afferent pathways to NTS-CeA neurons were organized exclusively as either transie

152 Within the amygdala, the central nucleus (CeA) is critical in acute alcohol's reinforcing actions,

153 The central nucleus (CeA) serves major amygdala output functions and can gene

154 Optogenetic activation of CeA(GA) potently suppressed both pain-elicited reflexive

155 corticolimbic circuitry under the control of CeA activation.

156 ms and reduce neuronal inhibitory control of CeA glutamatergic synapses.

157 not alter either 5-HT1A-mediated decrease of CeA GABA release or Htr1a expression but disrupted 5-HT2

158 erent GA drugs activate a shared ensemble of CeA(GA) neurons.

159 plasticity by driving synaptic excitation of CeA neurons.

160 ehaviors is observed after the inhibition of CeA CRF projections to the bed nucleus of the stria term

161 Conversely, inhibition of CeA(GA) activity exacerbated pain, produced strong avers

162 Inhibition of CeA-CRF neurons during immediate extinction training is

163 oider rats), that chemogenetic inhibition of CeA-LH projections attenuates avoidance in male Avoider

164 rovides detailed insights into modulation of CeA activity by the 5-HT system and unravels the vulnera

165 Here, we examined neuroadaptations of CeA 5-HT signaling in adult, male Sprague Dawley rats us

166 several genetically distinct populations of CeA neurons that mediate appetitive behaviors and dissec

167 Extracellular single-unit recordings of CeA neurons in anesthetized rats showed that 5-HT2CR kno

168 Here we investigated the specific role of CeA LTCCs in the effects of acute alcohol at the molecul

169 neurons, in vivo optogenetic stimulation of CeA Tac2-expressing neurons during fear acquisition enha

170 e and female mice, we found that a subset of CeA neurons send projections to the GPe, and the majorit

171 The superfusion of CeA slices with nociceptin/orphanin FQ peptide (N/OFQ; 5

172 e abnormal activation and synchronization of CeA GABAergic neurons may trigger emotion-induced catapl

173 ranslationally profiled the transcriptome of CeA Crh-expressing cells (Crh neurons) after fear condit

174 r study further expands our understanding of CeA cellular mechanisms involved in the pathophysiology

175 ceptors (CRF1s) mediate alcohol's effects on CeA activity and drive the escalated alcohol intake of a

176 ceptors (CRF1s) mediate alcohol's effects on CeA activity and drive the escalated alcohol intake of a

177 may result from altered oxytocin effects on CeA GABA transmission in alcohol dependence.

178 owever, there is still no direct evidence on CeA GABAergic neurons' real-time dynamic during cataplex

179 chioamygdaloid projections have an impact on CeA stress- and nociception-associated maladaptive respo

180 ated NTS knockdown in either the thalamic or CeA neurons greatly reduced their sleep-promoting effect

181 Yet the motivational effects of paired CeA stimulation can be reversed to negative valence in a

182 Pnoc(CeA) neurons project to the ventral bed nucleus of the s

183 pressing cells in the central amygdala (Pnoc(CeA)) that are activated by palatable food consumption.

184 Additionally, ablation of Pnoc(CeA) cells reduces high-fat-diet-driven increases in bod

185 These data suggest that the Pnoc(CeA) network is necessary for promoting the reinforcing

186 Pe, and the majority of these GPe-projecting CeA neurons express the neuropeptide somatostatin.

187 gest that a major function of GPe-projecting CeA neurons is to represent and convey US-related inform

188 otably, chronic inhibition of GPe-projecting CeA neurons with the tetanus toxin light chain (TeLC) co

189 d with intrinsic properties of LH-projecting CeA cells.

190 of the anatomy of the underlying long-range CeA network remains fragmentary.

191 Notably, the role of 5-HT regulating rat CeA activity in alcohol dependence is poorly investigate

192 Alcohol dependence reduces CeA LTCC membrane abundance and disrupts this LTCC-based

193 l alcohol research aims to identify relevant CeA neuroadaptions that promote the transition to depend

194 We conclude that CeA ChR2 excitation paired with a cocaine option specifi

195 test of incentive motivation confirmed that CeA ChR2 amplified rats' motivation, raising their break

196 Furthermore, we found that CeA GABAergic neurons became highly synchronized during

197 n suppressed cocaine intake, indicating that CeA circuitry is needed for ordinary cocaine motivation.

198 We demonstrated previously that CeA glutamate receptor signaling mediates cisplatin-indu

199 However, we also show that CeA laser had no reinforcing properties at all when give

200 Here we show that CeA neurons that release the stress neuropeptide cortico

201 Here, we show that CeA projections to the lateral hypothalamus (LH) are pre

202 Collectively, these data show that CeA-LH projections are important for persistent avoidanc

203 Further tracing showed that CeA GABAergic NTS neurons are innervated by glutamatergi

204 The CeA is reciprocally connected with the dorsal raphe nucl

205 The CeA receives dense innervation from the dorsal raphe nuc

206 The CeA receives excitatory and inhibitory inputs from the b

207 at viscerosensory information arrives at the CeA conveyed via a pathway involving as few as two synap

208 ation may impinge on action selection by the CeA.SIGNIFICANCE STATEMENT Our current knowledge of the

209 sults build upon prior work to establish the CeA as a crucial element in the neural mechanisms of cat

210 ther, these results highlight a role for the CeA in the gating of CS-related input to the cerebellum

211 lateral parabrachial (LPB) neurons from the CeA in animals of either sex.

212 ior was mediated by CRF projections from the CeA to the dlBST and depended on activation of CRF1 rece

213 ol, and the output of these neurons from the CeA.

214 However, the CeA has primarily been studied as the site for negative

215 gy, inhibitory GABAergic transmission in the CeA and excitatory glutamatergic transmission in the PVN

216 symptoms in relation to KOR signaling in the CeA and help clarify the nature of the stimulus that dri

217 alamus (LH) with a monosynaptic relay in the CeA and shed new light on the previously described funct

218 tural alterations of dendritic spines in the CeA and, moreover, whole-cell patch clamp analysis of th

219 CRF-producing neurons and CRF in the CeA are required for discriminative fear, but both are d

220 receptor 1-expressing (CRF1+) neurons in the CeA are under tonic inhibitory control and are different

221 ts demonstrate that DYN/KOR signaling in the CeA contributes to excessive alcohol consumption in a bi

222 he recruitment of a neuronal ensemble in the CeA during abstinence is required for excessive alcohol

223 ndicates that neuronal signals arrive in the CeA eliciting both aversive and appetitive behaviors, ou

224 recruitment of this neuronal ensemble in the CeA is causally related to excessive alcohol drinking or

225 anced by CRF and that CRFR1 signaling in the CeA is critical for discriminative fear.

226 solated CRF-receptive (CRFR1) neurons in the CeA is potently enhanced by CRF and that CRFR1 signaling

227 at the downregulation of N/OFQ levels in the CeA may be responsible for hyper-GABAergic tone in the C

228 ects of acute alcohol on GABA release in the CeA of dependent but not nondependent rats.

229 synaptic transmission in PDYN neurons in the CeA of either sex, but excitability of PDYN neurons was

230 nt and reduced c-Fos immunoreactivity in the CeA of IP3K-A KO mice suggest that IP3K-A has a profound

231 e assessed the effects of NE activity in the CeA on behavioral expression using receptor-specific pha

232 indicate that PDYN and KOR signaling in the CeA plays an important role in regulating excessive alco

233 dependence-induced neuronal ensemble in the CeA reversed excessive alcohol drinking and somatic sign

234 Neurons in the CeA send long-range projections to a number of extra-amy

235 responsible for hyper-GABAergic tone in the CeA that is observed in individuals who develop addictio

236 -releasing hormone-expressing neurons in the CeA that project to the parabrachial nucleus.

237 targeted "silencing" of DYN+ neurons in the CeA was accomplished using a chemogenetic strategy.

238 NR3C2 expression in the CeA was negatively correlated to average ethanol intake

239 Low Nr3c2 expression levels in the CeA were significantly associated with increased anxiety

240 xts, increased GABAergic transmission in the CeA, and a profile of increased G-CSF, GM-CSF, IL-13, IL

241 d baseline glutamatergic transmission in the CeA, and dysregulated CRF-FAAH facilitates stress-induce

242 ceptor-mediated synaptic transmission in the CeA, supporting the hypothesis that microglia regulate d

243 glitazone (0, 2.5, 5, and 10 mug/mul) in the CeA, VTA, and RMTg but not in the NAc shell.

244 found that a subpopulation of neurons in the CeA, which are mainly those that express the neuropeptid

245 ate N-arachidonoylethanolamine levels in the CeA.

246 nimals that were injected with Daun02 in the CeA.

247 withdrawal dysregulate 5-HT signaling in the CeA.

248 er cataplexy by activating GABA cells in the CeA.SIGNIFICANCE STATEMENT Although cataplexy has been c

249 pendent DREADDs or a control vector into the CeA of orexin knock-out mice crossed with vGAT-Cre mice,

250 of SB-334867 (20 nmol) bilaterally into the CeA significantly reduced cocaine intake in LgA rats.

251 M(+)) neurons in the lateral division of the CeA (CeL) are essential for the acquisition and recall o

252 gion of the lateral and capsular part of the CeA (CeL/C), and four principal output streams of this n

253 system and unravels the vulnerability of the CeA 5-HT system to chronic alcohol and protracted withdr

254 1+ and CRF1- neurons that project out of the CeA and into the bed nucleus of the stria terminalis.

255 between long-range inputs and outputs of the CeA and pave the way to a better understanding of how in

256 ts demonstrate that GABAergic neurons of the CeA are sufficient and necessary for the production of c

257 se results demonstrate the importance of the CeA in regulating responses to rewarding stimuli, sheddi

258 es to and reflects the prominent role of the CeA in the negative emotional state that drives excessiv

259 is switch reflects the important role of the CeA in the pathophysiology of alcohol dependence and rep

260 neurons comprise a specific component of the CeA microcircuitry that is selectively engaged by acute

261 Further characterization of the CeA-LH circuit may improve our understanding of the neur

262 r rats, that chemogenetic stimulation of the CeA-LH circuit produces conditioned place avoidance (CPA

263 ological and autonomic output centers of the CeA.

264 ecent findings also implicate neurons of the CeA.

265 ory hM4 receptor in GABAergic neurons of the CeA.

266 convergent viscerosensory signals reach the CeA.

267 rmation followed separate lines to reach the CeA.

268 Recent findings indicate that the CeA also contributes to states of sustained apprehension

269 t human and primate data suggesting that the CeA and BST act together to generate states of anxiety.S

270 l nucleus of the amygdala (CeA) and that the CeA is involved in mediating the defensive behavior.

271 In the present study we describe that the CeA neuronal ensemble that is activated by withdrawal fr

272 Our results indicate that the CeA promotes cataplexy onset and that emotionally reward

273 Here, we demonstrate that the CeA sends robust inhibitory projections to the lateral s

274 These findings demonstrate that the CeA-LPB pathway is critically involved in pain regulatio

275 ormation is appraised and routed through the CeA to the different output channels.

276 nd convey US-related information through the CeA-GPe circuit, thereby regulating learning in fear con

277 ters the molecular mechanisms underlying the CeA's response to alcohol (from LTCC- to CRF1-driven).

278 Then, we show that GABA cells within the CeA are responsible for mediating this effect.

279 ggest that HCRT neurotransmission within the CeA is implicated in compulsive-like cocaine-seeking.

280 to dynorphin or KOR arising from within the CeA itself or other input brain regions.

281 dogenous opioids, acting via MOR, within the CeA promote this form of appetitive behavior.

282 ently, CeA rats quickly came to pursue their CeA ChR2-paired cocaine option intensely and exclusively

283 Therefore, CeA laser pairing makes its associated cocaine option an

284 These CeA GABA neurons express dynorphin, somatostatin, and/or

285 revealed NTS as a prominent marker for these CeA neurons.

286 d that the optogenetic inactivation of these CeA CRF+ neurons prevents recruitment of the neuronal en

287 us pallidus external segment (GPe), and this CeA-GPe circuit conveys unconditioned stimulus (US)-rela

288 We find that the efficacy of this CeA-LPB pathway is suppressed in chronic pain.

289 atch clamp analysis of the basal amygdala to CeA projections showed that alcohol consumption and with

290 rease in excitatory transmission from BLA to CeA recorded in brain slices from SNL rats using whole-c

291 turbed development of glutamatergic input to CeA, identifying KARs as a physiological mechanism regul

292 Our study points to CeA(GA) as a potential powerful therapeutic target for a

293 upport the hypothesis that LC projections to CeA are critical for the expression of defensive respons

294 t sorting provides viscerosensory signals to CeA about visceral conditions with respect to being eith

295 appetitive behaviors and dissect the BLA-to-CeA circuit for appetitive behaviors.

296 n a Pavlovian fear learning situation, where CeA ChR2 pairing increases defensive reactions.

297 abnormal spatial learning and memory whereas CeA-DKO mice have impaired cold-induced thermogenesis.

298 administration and laser preference, whereas CeA inhibition by optogenetic halorhodopsin suppressed c

299 While CeA substrates for defensive behaviors have been studied

300 These findings suggest that CREB, within CeA Crh neurons, may function as a molecular switch that