ライフサイエンスコーパス: CeA

1 CeA gene expressions of AMPA and NMDA glutamate receptor

2 CeA inactivation also substantially reduced stimulus-evo

3 CeA LV-PKCtheta injected rats increased food intake, bod

4 CeA rats also emitted consummatory bites toward their la

5 CeA stimulation also elevated the effort cost rats were

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

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

8 els compared to control rats that received a CeA-LV-GFP construct.

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

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

11 xazole receptor (AMPAR) in central amygdala (CeA) and phosphorylation of AMPAR GluA1 subunit at a CaM

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

13 factor (CRF) system in the central amygdala (CeA) has been implicated in the effects of acute and chr

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

15 The central amygdala (CeA) is a key structure at the limbic-motor interface re

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

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

18 The central amygdala (CeA) nucleus, a subcortical structure composed of mostly

19 The central amygdala (CeA) plays a central role in physiologic and behavioral

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

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

22 Prolonged exposure of the central amygdala (CeA) to elevated corticosteroids (CORT) facilitates long

23 CeM), a subdivision of the central amygdala (CeA), is believed to be the main output station of the a

24 The central amygdala (CeA), once viewed as a passive relay between the amygdal

25 ere we studied the role of central amygdala (CeA), ventral medial prefrontal cortex (vmPFC), and orbi

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

27 cortex (ilPFC) to inhibit central amygdala (CeA)-mediated Pavlovian reactions.

28 tatory transmission in the central amygdala (CeA).

29 ial nucleus (LPB), and the central amygdala (CeA).

30 dysfunction, including the central amygdala (CeA).

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

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

33 In the central nucleus of amygdala (CeA), a limbic structure critically involved in the affe

34 n of neurons in central nucleus of amygdala (CeA), paired with earning a particular sucrose reward in

35 The central nucleus of the amygdala (CeA) and its connections with the nigral dopamine system

36 within the central nucleus of the amygdala (CeA) and the bed nucleus of the stria terminalis (BNST),

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

38 ns from the central nucleus of the amygdala (CeA) and ventral tegmental area (VTA).

39 (lPBN), and central nucleus of the amygdala (CeA) as potential sites of action in mediating the side

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

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

42 ease in the central nucleus of the amygdala (CeA) in Nf1 heterozygous null mice (Nf1(+/-)).

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

44 ns into the central nucleus of the amygdala (CeA) in these animals.

45 yme) in the central nucleus of the amygdala (CeA) is crucial for appetitive, but not for aversive, le

46 The central nucleus of the amygdala (CeA) mediates several addiction-related processes and no

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

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

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

50 PSPs in the central nucleus of the amygdala (CeA) to explore functional interactions between CRF and

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

52 tein in the central nucleus of the amygdala (CeA) were also investigated.

53 uses on the central nucleus of the amygdala (CeA), a brain region that has been implicated in negativ

54 ACAP in the central nucleus of the amygdala (CeA), a limbic structure implicated in the emotional com

55 In the central nucleus of the amygdala (CeA), a rostrocaudal gradient characterized the normal q

56 rons of the central nucleus of the amygdala (CeA), an important brain region for emotional processing

57 ide) in the central nucleus of the amygdala (CeA), the basolateral nucleus of the amygdala (BlA), or

58 ched in the central nucleus of the amygdala (CeA), which plays a pivotal role in the processing and e

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

60 NAc and the central nucleus of the amygdala (CeA).

61 in the rat central nucleus of the amygdala (CeA).

62 within the central nucleus of the amygdala (CeA).

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

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

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

66 (LHA, 25%), central nucleus of the amygdala (CeA, 77%), sublenticular extended amygdala (SLEA, 86%),

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

68 strated atypical intra- and extra-amygdaloid CeA-dominant paths with compensatory modulation of emoti

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

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

71 rsely, detected increased anxiety levels and CeA/LA activity in LAB mice that experienced chronic mil

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

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

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

75 evaluated by the elevated plus-maze test and CeA/LA activity.

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

77 on and a complex interaction with ethanol at CeA glutamatergic synapses.

78 ortantly, in stress-restraint rats, baseline CeA GABAergic responses were elevated and N/OFQ exerted

79 It is likely that BNST-CeA interactions are involved in modulating responses to

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

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

82 Conversely, CeA inhibition by muscimol/baclofen microinjections prev

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

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

85 Nor did CeA stimulation by itself induce any aversive state that

86 nded to the conditioned stimulus (CS) during CeA inactivation.

87 example, 4-5 g kg(-1) per 2 h(-1)) elevated CeA levels of mGluR1, GluN2B, Homer2a/b and phospholipas

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

89 d tonic inhibitory activity of NOP on evoked CeA glutamatergic transmission only in ethanol-dependent

90 Finally, CeA microinfusion of norBNI blocked cocaine-induced loco

91 Finally, CeA stimulation also failed to enhance 'liking' reaction

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

93 diated by GABAA receptors were isolated from CeA neurons under whole-cell voltage clamp, and their re

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

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

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

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

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

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

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

101 However, CeA stimulation by itself failed to support behavioral s

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

103 In CeA neurons, we found that CeA GluA1 expression was sign

104 an increased number of CRF-positive cells in CeA--but not in BlA or BNST--of Chow/Palatable rats, dur

105 uld serve as a target for ethanol effects in CeA.

106 ceptin-induced inhibition of evoked EPSPs in CeA neurons of naive rats.

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

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

109 tly, silencing of Tac2-expressing neurons in CeA with DREADDs impairs fear consolidation.

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

111 erized by increased baseline GABA release in CeA.

112 5-HT2CR in the BLA plays a critical role in CeA plasticity and neuropathic pain behaviors in the rat

113 subunit at a CaMKII locus (GluA1-Ser831) in CeA and lateral amygdala.

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

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

116 enoviral overexpression of GluA1 subunits in CeA accelerated associative learning, as shown by reduce

117 CPP inhibited GABA synaptic transmission in CeA neurons.

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

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

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

121 AMPA receptors in adenoviral GluA1-infected CeA neurons.

122 Muscimol+baclofen injections into CeA but not BLA decreased cue-induced methamphetamine se

123 Intra-CeA (but not intra-basolateral amygdala) PACAP dose-depe

124 Intra-CeA CRF infusion mimicked stress-induced hyperalgesia.

125 Intra-CeA injections of N/OFQ significantly and selectively re

126 Intra-CeA PACAP-induced anorexia was blocked by coinfusion of

127 Intra-CeA R121919 blocked both excessive palatable food intake

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

129 An intra-CeA infusion of mGluR1, mGluR5 and PLC inhibitors all do

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

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

132 Finally, intra-CeA infusion of tetrodotoxin produced thermal hyperalges

133 e present study examined the impact of intra-CeA KOR antagonism on escalated operant alcohol self-adm

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

135 Animals received intra-CeA infusions of the KOR antagonist nor-binaltorphimine

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

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

138 ced PTSD-like model, or following lentiviral CeA overexpression, are sufficient to enhance fear conso

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

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

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

142 This calculation yielded the metric "CeA/LA activity." Our data clearly demonstrate a positiv

143 a separate measure of incentive motivation, CeA stimulation also increased the progressive ratio bre

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

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

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

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

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

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

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

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

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

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

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

155 being basolateral (BLA) and central nucleus (CeA).

156 Pharmacological activation of CeA GABAA receptors reduced the pain and inhibited CPP i

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

158 Adenoviral shRNA-mediated downregulation of CeA GluA1 produced opposite effects, inhibiting the proc

159 We then determined the functional effects of CeA KOR blockade in cocaine-related behaviors.

160 plasticity by driving synaptic excitation of CeA neurons.

161 sed the effect of reversible inactivation of CeA or BLA by GABAA+GABAB receptor agonists (muscimol+ba

162 Furthermore, inhibition of CeA GABAA receptors mimicked the pain effect, rendering

163 morphine withdrawal, and viral knockdown of CeA GluA1 eliminated the morphine-seeking behavior in wi

164 Adenoviral knockdown of CeA GluA2 subunits facilitated CPP acquisition, but did

165 Furthermore, viral overexpression of CeA MeCP2 repressed the GluA1 level and eliminated the m

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 reby disinhibiting the medial subdivision of CeA and releasing fear expression.

171 r alterations in selective subpopulations of CeA neurons may lead to unbalanced CeA processing, thus

172 paths and concise orbitofrontal cortex (OFC)-CeA-driven extra-amygdaloid connectivity.

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

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

175 ight into the specific effects of ethanol on CeA microcircuitry.

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

177 We previously demonstrated that rat CeA GABAergic transmission is enhanced by acute and chro

178 Previously, we reported that in the rat CeA, acute and chronic ethanol exposures significantly d

179 Moreover, we found reduced CeA/LA activity in HAB mice, which responded with decrea

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

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

182 ELS was associated with extensive and robust CeA-facilitated intra- and extra-amygdaloid paths.

183 Fos neurons here and in the rostral CeA were highly correlated with quinine-elicited gapes.

184 -stimulated labeled cells in the rostralmost CeA and in the subregion approximating the dysgranular g

185 In addition, Tac2-CeA neurons were shown to co-express striatal-enriched p

186 in nonvomiting laboratory rodents) and that CeA NMDA receptor blockade attenuates cisplatin-induced

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

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

189 tamatergic synapses in the CeA and find that CeA neurons exhibit multiple mechanistically and tempora

190 In CeA neurons, we found that CeA GluA1 expression was significantly increased 2 h aft

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

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

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

194 behavioral/pharmacological data showed that CeA AMPA/kainate receptor blockade attenuates cisplatin-

195 Our results suggest that CeA dopamine function is involved in modulation of disen

196 These results suggest that CeA neurons can be a cellular target for cocaine to resh

197 ry work in animals collectively suggest that CeA structure and function are altered in individuals wi

198 d after cisplatin treatment, suggesting that CeA glutamate receptor signaling plays a role in mediati

199 paired external food reward, suggesting that CeA photo-excitation specifically transformed the value

200 This pattern suggests that CeA photo-excitation specifically enhances and narrows i

201 The CeA consists of the lateral (CeL) and medial (CeM) subdi

202 The CeA is also a constituent region of a conceptual macrost

203 The CeA is therefore identified as a key node in the circuit

204 The CeA receives dense inputs from cortical regions, is the

205 The CeA receives excitatory and inhibitory inputs from the b

206 The CeA was subsequently targeted with bilateral infusions o

207 ole for NE signaling within the BNST and the CeA in the anxiogenic actions of cocaine.

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

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

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

213 ted that site-specific KOR antagonism in the CeA ameliorated escalated alcohol self-administration du

214 lcohol acutely increases GABA release in the CeA and alcohol dependence is characterized by increased

215 c machinery at glutamatergic synapses in the CeA and find that CeA neurons exhibit multiple mechanist

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

217 a suggest that activation of PKCtheta in the CeA and hypothalamus have different effects on energy ba

218 tion of the CRF1 receptor transcripts in the CeA and in the BLA after body restraint.

219 acetylation of H3-K9 but not H3-K14, in the CeA and medial nucleus of amygdala compared with NP rats

220 acute stress increases N/OFQ systems in the CeA and that N/OFQ has antistress properties.

221 Glutamatergic synapses, in the CeA and throughout the brain, are very sensitive to etha

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

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

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

225 We discuss neurotransmission in the CeA as a potential integrative hub between anxiety disor

226 isposing the inhibitory GABA function in the CeA circuitry involved in the behavior of opioid reward.

227 he recruitment of a neuronal ensemble in the CeA during abstinence from alcohol is causally related t

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

229 We also demonstrate that PACAP in the CeA exerts its anorectic effects via local melanocortin

230 ied KOR-related physiological changes in the CeA following escalation of cocaine self-administration

231 ntly decreased GABAergic transmission in the CeA from naive rats but increased it in LgA rats.

232 d GABAergic transmission was enhanced in the CeA from ShA and LgA rats compared with cocaine-naive ra

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

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

235 ing that glutamate receptor signaling in the CeA is critical for the energy balance dysregulation cau

236 es evidence that local MMP-9 activity in the CeA is crucial for the appetitive, but not for aversive,

237 n the modulation of synaptic efficacy in the CeA is not well understood.

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

239 hat focusing on the neuronal ensemble in the CeA may lead to a better understanding of the etiology o

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

241 y mainly decreasing glutamate release in the CeA of naive rats.

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

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

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

245 is present at the excitatory synapses in the CeA with its activity greatly enhanced after the appetit

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

247 of CRF significantly increased IPSPs in the CeA, and this enhancement was blocked by N/OFQ.

248 nimals that were injected with Daun02 in the CeA.

249 n of GR and subsequent CRF expression in the CeA.

250 ate N-arachidonoylethanolamine levels in the CeA.

251 ncy, revealing tonic ghrelin activity in the CeA.

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

253 nfused with PACAP (0-1 mug per rat) into the CeA and home-cage food intake, body weight change, micro

254 of a histone deacetylase inhibitor into the CeA attenuated anxiety-like behavior as well as somatic

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

256 betaxolol and ICI 118551 or vehicle into the CeA or BNST.

257 f amplicons for TLR4 or MCP-1 siRNA into the CeA or VTA from the P rats inhibited target gene express

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

259 rats received D1 or D2 antagonists into the CeA unilaterally prior to behavioral tests.

260 int rats after N/OFQ microinjection into the CeA.

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

262 ry neurons in the lateral subdivision of the CeA (CeL).

263 1+ and CRF1- neurons that project out of the CeA and into the bed nucleus of the stria terminalis.

264 esulting in an increase in the output of the CeA and the CRF1 receptor system, in particular.

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

266 exposure is an increase in the output of the CeA CRF1 system, a neuroadaptation that may contribute t

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

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

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

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

271 We found that inactivation of the CeA neuronal ensemble during abstinence significantly de

272 nd pain induced by prolonged exposure of the CeA to CORT.

273 x vivo) brain, electrical stimulation of the CeA, or the neighboring bed nucleus of the stria termina

274 g changes in local inhibitory control of the CeA, resulting in an increase in the output of the CeA a

275 ory hM4 receptor in GABAergic neurons of the CeA.

276 convergent viscerosensory signals reach the CeA.

277 rmation followed separate lines to reach the CeA.

278 previous studies, results indicate that the CeA has a critical role in incubation of both drug and n

279 These results indicate that the CeA is one of the brain areas through which the PACAP sy

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

281 ons in the lPBN) neurons that project to the CeA, outlining a neuroanatomical circuit that is activat

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

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

284 creases in Group1 mGluR signaling within the CeA as a neuroadaptation maintaining excessive alcohol i

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

286 i) the 2-AG-CB(1) receptor system within the CeA is recruited during abstinence from palatable diet c

287 We focally manipulated activity within the CeA or BLA in macaques by intracerebral microinjection o

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

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

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

291 Therefore, CeA rats chose and intensely pursued only the laser-pair

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

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

294 CBs in the modulation of excitatory drive to CeA neurons and provide insight into the mechanisms by w

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

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

297 ations of CeA neurons may lead to unbalanced CeA processing, thus contributing to the progressive agg

298 decreased the firing discharge of unlabeled CeA neurons.

299 ectrophysiological techniques in an in vitro CeA slice preparation, we investigated the effects of no

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