We found that chewing caused an increase in Fos-ir that was selective for the right hemisphere of the mPFC along with a decrease in Fos-ir that was selective for the right central nucleus of the amygdala (CeA), a region that may regulate dopamine neurotransmission in mPFC. 
We focused our study in the central nucleus of the amygdala (CeA) because it is implicated in alcohol drinking behavior as well as stress behavior.
CRF in the paraventricular nucleus of the hypothalamus (PVN) and CRF in the central nucleus of the amygdala (CeA) are involved in the regulation of stress responses, and gender differences in CRF mRNA expression in these regions in response to various stressors are controversial.
To determine neuronal activation, the expression of the immediate-early genes c-fos and activity-regulated cytoskeletal associated protein (Arc) was studied in the central nucleus of the amygdala (CeA), bed nucleus stria terminalis (BST) and paraventricular hypothalamic nucleus (PVN), which are areas involved in the neuroendocrine and central stress response.
The central nucleus of the amygdala (CeA), the nociceptive amygdala, serves as the major output nucleus of the amygdala and participates in receiving and processing pain information.
This study assessed the effect of inhibition of the central nucleus of the amygdala (CeA) and drug experience on brain regions underlying footshock-induced reinstatement of morphine-seeking behaviour in rats.
Moreover, this effect was dependent upon dopamine antagonism within the basolateral nucleus but not the central nucleus of the amygdala.
Acute stress increases amygdalar noradrenaline levels and focal application of alpha(2)-adrenoceptor agonists in the central nucleus of the amygdala (CeA) is antinociceptive.
Adrenal glucocorticoids have been implicated in the circadian regulation of clock genes expression in peripheral tissues as well as in the control of the rhythms of expression of PER2 in certain limbic forebrain regions, such as the oval nucleus of the bed nucleus of the stria terminalis (BNSTov) and central nucleus of the amygdala (CEA) in rats.
The acute pain and allodynia increased Fos-positive cells in the prefrontal cortex (PFC), basolateral nucleus (BL) and central nucleus of the amygdala (Ce), indicating that these areas are involved in pain processing.
On the other hand, the central nucleus of the amygdala directly receives afferents from the lateral nucleus of the amygdala.
The central extended amygdala (EAc) is an ensemble of highly interconnected limbic structures of the anterior brain, and forms a cellular continuum including the bed nucleus of the stria terminalis (BNST), the central nucleus of the amygdala (CeA) and the nucleus accumbens shell (AcbSh).
Acute withdrawal from all major drugs of abuse produces increases in reward thresholds, increases in anxiety-like responses, and increases in extracellular levels of CRF in the central nucleus of the amygdala.
Follow-up studies involved electrical stimulation of the central nucleus of the amygdala, a source of CRF afferents to the dorsal raphe nucleus. Activation of the central nucleus increased medial prefrontal cortex serotonin release.
As CRF expression in the central nucleus of the amygdala (CeA) is important in adaptation to chronic stress, we hypothesized that unrestrained synthesis of CRF in CeA would mimic the consequences of chronic stress exposure and cause dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis, increase emotionality and disrupt reproduction.
To gain insights into the molecular mechanisms and subregional specificity of fear conditioning, we disrupted type II glucocorticoid receptors (GRs) in the central nucleus of the amygdala (CeA) by delivering lentiviral vectors containing Cre-recombinase into floxed-GR mice.
RATIONALE: There is experimental evidence that indicates that the endogenous opioid system of the central nucleus of the amygdala (CeA) may mediate some of the reinforcing effects of ethanol.
After extinction recall, 129S1 showed reduced c-Fos and Zif268 expression in the infralimbic cortex and basolateral amygdala, and elevated c-Fos or Zif268 expression in central nucleus of the amygdala and medial paracapsular intercalated cell mass, relative to C57BL/6J.
Previous research has shown that chronic corticosterone treatment increases the expression of corticotrophin-releasing hormone (CRH) mRNA at the central nucleus of the amygdala (CeA).
Acute withdrawal from all major drugs of abuse produces increases in reward thresholds, anxiety-like responses and extracellular levels of CRF in the central nucleus of the amygdala.
Norepinephrine (NE) and corticotropin-releasing factor (CRF) signaling in the extended amygdala, including the bed nucleus of the stria terminalis, shell of the nucleus accumbens, and central nucleus of the amygdala, are generally involved in behavioral responses to environmental and internal stressors.
Preclinical research in animal models of the various aspects of nicotine dependence suggests a critical role of glutamate, gamma-aminobutyric acid (GABA), cholinergic and dopamine neurotransmitter interactions in the ventral tegmental area and possibly other brain sites, such as the central nucleus of the amygdala and the prefrontal cortex, in the effects of nicotine.
More specifically, PCP-treated animals displayed decreased AMPA receptor density in hippocampus CA1 (-16%), hippocampus CA2 (-25%), dentate gyrus (-27%), parietal cortex layers III-VI (-19%), central nucleus of the amygdala (-40%), and basolateral amygdala (-19%).
By contrast, CRF mRNA expression in the central nucleus of the amygdala and bed nuclei of the stria terminalis was unaffected by STZ treatment, but HV and CapV manipulations elevated expression in the nondiabetic, but not STZ-diabetic groups.
In the ventral forebrain, sucrose sham licking increased Fos in the bed nucleus of the stria terminalis, central nucleus of amygdala, and the shell of nucleus accumbens.
We have shown previously that unconditioned stressors inhibit neurons of the lateral/capsular division of the central nucleus of the amygdala (CEAl/c) and oval division of the bed nucleus of the stria terminalis (BSTov), which form part of the central extended amygdala.
The laterocapsular division of the central nucleus of the amygdala (CeLC) has emerged as an important site of pain-related plasticity and pain modulation.
Intercalated (ITC) amygdala neurons constitute probable mediators of extinction because they receive information about the conditioned stimulus from the basolateral amygdala (BLA), and contribute inhibitory projections to the central nucleus (CEA), the main output station of the amygdala for conditioned fear responses.
The central nucleus of the amygdala (CeA) is a critical coordinator of autonomic, behavioral, and emotional systems impacted by opioids, however there is no evidence that the essential NMDA-NR1 (NR1) subunit gene in the amygdala plays a role in opioid dependence.
UII (n=12) and killed after 100 or 160 min, showed increased Fos-immunoreactivity (Fos-IR) in the nucleus of the solitary tract and the central nucleus of the amygdala (CeA) at both time points, compared with vehicle (n=11).
Many studies from our laboratories have demonstrated that circuitry that includes the amygdala central nucleus (CeA), the cholinergic neurons in the substantia innominata/nucleus basalis region and their innervation of the posterior parietal cortex is critical for this surprise-induced enhancement of attention in learning.
Punctate labeling representing spine labeling was restricted to small patches in the lateral nucleus of amygdala, intercalated cell masses (ICM), and the lateral subdivision of central nucleus. In addition, Cd, Cp, mGluR1 alpha and cortical afferents are co-distributed in the ICM distributed in the lateral nucleus and lateral capsular division of the central nucleus, and the lateral division of the central nucleus itself. Consistent with our previous studies, TrkB IR in the central nucleus was associated with Cd and Cp-immunoreactive spines whereas mGluR1 alpha IR and mGluR5 IR were almost exclusively associated with the PSDs of asymmetric synapses, in most cases apposed by cortical terminals.
The aims of the present study were to examine the role of CRH-R1 and CRH-R2 in CGRP-induced suppression of LH pulses, and to investigate the effects of CGRP on CRH expression in the paraventricular nucleus (PVN) and central nucleus of the amygdala (CeA), which have prominent CRH neurone populations that receive dense CGRP innervations.
The extracellular signal-regulated kinase (ERK) cascade has been shown to be a key modulator of pain processing in the central nucleus of the amygdala (CeA) in mice.
Sweetened milk ingestion was associated with increased numbers of c-Fos positive neurons in the caudal core and shell of the nucleus accumbens (NAc), the paraventricular thalamus (PVT), central nucleus of the amygdala (CEA), the basal lateral amygdala (BLA), in orexin-A containing neurons of the lateral hypothalamus (LH), and in cocaine and amphetamine regulated transcript (CART) neurons of the arcuate hypothalamus.
Previously, we showed that daytime restricted access to a highly palatable complete meal replacement, Ensure Plus (Ensure), shifts the rhythm of expression of the clock protein PER2 in limbic forebrain areas including the oval nucleus of the bed nucleus of the stria terminalis (BNSTov), central nucleus of the amygdala (CEA), basolateral amygdala (BLA) and dentate gyrus (DG), and induces a rhythm in the dorsomedial hypothalamic nucleus (DMH) in food deprived (restricted feeding), but not free-fed rats (restricted treat).
It has recently been reported that secretin activates gene expression in the central nucleus of the amygdala in rats.
Decreases in serotonergic activity in the central nucleus of the amygdala reduce responses to stressors, suggesting an important role for serotonin in this region of the amygdala in stress reactivity. However, it is not known whether exposure to stressors actually increases serotonin release in the central nucleus of the amygdala. The current experiment tested the hypothesis that restraint stress increases extracellular serotonin within the central nucleus of the amygdala and adjacent medial amygdala using in vivo microdialysis in awake male rats during the dark phase of the light-dark cycle. Serotonin release in the central nucleus increased immediately in response to restraint stress. Since corticotropin-releasing factor is an important mediator of both responses to stressors and serotonergic activity, subsequent experiments tested the hypothesis that central nucleus serotonergic response to restraint stress is mediated by central corticotropin-releasing factor receptors. Administration of the corticotropin-releasing factor type 1 and 2 receptor antagonist d-Phe-CRF (icv, 10 microg/5 microl) prior to restraint stress suppressed restraint-induced serotonin release in the central nucleus. The results suggest that restraint stress rapidly and selectively increases serotonin release in the central nucleus of the amygdala by the activation of central corticotropin-releasing factor receptors. Furthermore, the results imply that corticotropin-releasing factor mediated serotonergic activity in central nucleus of the amygdala may be an important component of a stress response..
This study determined the effects of mGluR7 and mGluR8 activation in the central nucleus of the amygdala (CeA) on nocifensive and affective pain responses and on pain-related anxiety-like behavior of adult rats.
Measuring fear-potentiated startle test using conditioned stimuli that vary in length we suggest that the central nucleus of the amygdala (CeA) and the lateral division of the bed nucleus of the stria terminalis (BNST(L)) are involved in short-term versus long-term fear responses we call phasic versus sustained fear, respectively.
Many labeled neurons were also consistently observed in the lateral part of the central nucleus.
The GABAergic system in the central nucleus of the amygdala (CeA) plays an important role in regulating voluntary ethanol intake.
No significant differences were found in the central nucleus of the amygdala, the piriform, and somatosensory cortices and in the hypothalamic paraventricular nucleus.
The anxiolytic effects of neuropeptide Y (NPY) are mediated in part by the central nucleus of the amygdala (CeA), a brain region involved in the regulation of alcohol-drinking behaviors.
The profile of alpha-MSH-immunoreactivity in the paraventricular (PVN), arcuate (ARC), paraventricular thalamic (PVT), dorsomedial hypothalamic-dorsal (DMNd) and -ventral (DMNv) nuclei, lateral hypothalamus (LH) and central nucleus of amygdala (CeA) was investigated with immunocytochemistry.
Information from the environment reaches the amygdaloid basolateral nucleus and after its processing is relayed to the amygdaloid central nucleus where a proper anxiogenic response is implemented.
To determine the effects of estrogen on neuronal numbers and brain region volume in MeA and central nucleus of the amygdala (CeA), we used stereology to test the effect of various estrogen regimens on the number of neuron-specific protein (NeuN)-labeled neurons and brain region volume of MeA and CeA.
METHODS: We determined the basal mRNA and protein levels of BDNF by in situ RT-PCR and immuno-histochemical procedure, respectively, in the amygdaloid [ central nucleus of amygdala (CeA), medial nucleus of amygdala (MeA), and basolateral amygdala (BLA)], nucleus accumbal (NAc shell and core), and bed nucleus of stria terminalis (BNST) [ lateral BNST (lBNST), medial BNST (mBNST), and ventral BNST (vBNST)] brain structures of P and NP rats.
GR 82334 infusion into the basolateral (BLA) or the medial (MeA) nuclei of the amygdala, but not into the central nucleus of the amygdala (CeA), dose dependently reduced fear-potentiated startle.
In addition, nicotine self-administration upregulated NMDA receptor subunit expression in the central nucleus of the amygdala (CeA) and ventral tegmental area (VTA), suggesting important interactions between nicotine and the NMDA receptor.
Pain-related plasticity in the laterocapsular division of the central nucleus of the amygdala (CeLC) generates emotional-affective responses and anxiety-like behavior.
Myelin stain allowed the identification of the medial subdivision of the lateral nucleus, and resulted in intense staining of the medial subdivisions of the central nucleus.
These include: the medial preoptic nucleus; median and lateral preoptic area; medial division of the bed nucleus of stria terminalis; paraventricular nucleus; central nucleus of the amygdala; dorsal hypothalamic area/dorsomedial hypothalamus; lateral hypothalamic area; lateral, ventrolateral and dorsomedial divisions of the periaqueductal grey; dorsal raphe nuclei; parabrachial nuclei; Kölliker-Fuse nucleus; intertrigeminal region; rostral ventrolateral medulla; lateral parafacial region; and the ventral respiratory group.
A potential DYN/CRF afferent is the central nucleus of the amygdala (CeA).
The highest level of D1 mRNA was found in the central nucleus, whereas D2 mRNA was the most abundant in the basal nucleus.
Alcohol-preferring (P) rats, stereotaxically implanted with bilateral guide cannulae into the nucleus accumbens, ventral tegmental area, and the central nucleus of the amygdala were given 30% alcohol and water in a 24h voluntary two-bottle choice paradigm. The data show reduced alcohol intake by 32-49.5% after 100-pmol glycyl-glutamine into reward sites (nucleus accumbens, ventral tegmental area, and central nucleus of the amygdala), but not after injections into control sites dorsal to reward sites.
Intragastric water administration increased the number of Fos-immunoreactive cells in the infralimbic cortex and lateral part of the central nucleus of the amygdala compared with the naive group. Ethanol administration increased the number of Fos-immunoreactive cells in the infralimbic (+57.5%) and prelimbic (+105.3%) cortices, nucleus accumbens shell region (+88.2%), medial part of the central nucleus of the amygdala (+160%), and lateral part of the bed nucleus of the stria terminalis (+198.8%) compared with the water-treated group. In the nucleus accumbens shell region, central nucleus of the amygdala, and bed nucleus of the stria terminalis, more than 80% of Fos-immunoreactive neurons were GABAergic after ethanol administration.
Thereafter, changes in the expression of glutamic acid decarboxylase (GAD)67 mRNA were estimated by in situ hybridization in the central nucleus of the amygdala (CeA), basolateral amygdala (BLA), dorsolateral striatum (dLStr), nucleus accumbens shell (AcS) and core (AcC).
The present experiments demonstrated that while neither neurotoxin-induced lesions of the basolateral amygdala (BLA) nor the central nucleus of the amygdala (CeA) attenuated the display of Pavlovian conditioned disgust reactions, lesions of the BLA (but not the CeA) attenuated instrumental conditioned avoidance of the taste.
The central nucleus (CE) of the amygdala has been gaining attention for its importance in the plasticity underlying conditioned emotional responding.
Higher binding in the central nucleus of the amygdala of C.
Various classical neurotransmitters coexist with SP in mammalian brains, but there has been no information on the colocalizing substances in the central nucleus of amygdala (CeA), where both SP and its specific receptor are highly concentrated.
Moreover, presynaptic mGlu2 terminals were found in most of the forebrain structures, especially in the lateral part of the central nucleus of the amygdala, and the CA1 region of the hippocampus.
This study compared the influences of mu-opioid receptor (MOR) activation in the central nucleus of the amygdala (CEA) on unconditioned fear or anxiety-like responses in two models, the elevated plus maze, and the defensive burying test.
The latero-capsular division of the central nucleus of the amygdala (CeLC) is also important for pain modulation and pain affect.
BACKGROUND: The central extended amygdala (cEA) which includes the central nucleus of the amygdala (CeA) and the lateral posterior bed nucleus of the stria terminalis (BNSTLP), has been proposed to play a key role in excessive ethanol consumption in humans (Koob and Le Moal, 2005 Nat Neurosci 8:1442).
The intercalated islands are clusters of glutamate-responsive GABAergic neurons rich in cholecystokinin (CCK)-2 receptors which control the trafficking of nerve impulses from the cerebral cortex to the central nucleus of amygdala.
In the amygdaloid complex, GAD65 is strongly expressed in striatal-like divisions, namely, the anterior amygdaloid area, the central nucleus (CEA), the intercalated nuclei, and the dorsal part of the medial nucleus (MEA).
Rats received an anorexigenic dose of PYY(3-36), and the number of neurons expressing Fos, an indicator of neuronal activation, was determined in anterior hypothalamus (AH), arcuate nucleus (ARC), dorsomedial hypothalamus (DMH), lateral hypothalamus (LH), ventromedial hypothalamus (VMH), central nucleus of the amygdala (CeA), area postrema (AP), and caudal medial nucleus tractus solitarius (cmNTS), commissural NTS (cNTS), and gelatinosus NTS (gNTS).
Serum corticosterone level was found to increase after 30 min of restraint stress, and corticotropin-releasing factor immunoreactivity was found to be increased in the central nucleus of the amygdala.
Post mortem analyses revealed that DHS animals had a loss of oxytocin (OT)-containing cells in the paraventricular nucleus in the hypothalamus (PVN; p<0.05) as well as an increase in calcitonin-gene related peptide (CGRP; p<0.05, one tailed) processes in the central nucleus of the amygdala (CeA) on PND 198.
The amygdala, particularly the central nucleus, has high concentrations of enkephalins relative to dynorphins and has high concentrations of opioid receptors.
The posterior PVT was also found to provide a strong projection to the lateral bed nucleus of the stria terminalis (BST), interstitial nucleus of the posterior limb of the anterior commissure (IPAC), and central nucleus of the amygdala (CeA), regions associated with the extended amygdala.
Previous studies show that activation of the gustatory cortex (GC), bed nucleus of the stria terminalis (BNST), central nucleus of the amygdala (CeA), and lateral hypothalamus (LH) inhibits PBN taste responses, GABAergic neurons are present in these forebrain regions, and GABA reduces the input resistance of PBN neurons.
Previous lesion studies have implicated the central nucleus of the amygdala (CN) and basal forebrain corticopetal cholinergic system in mediating surprise-induced changes in attention.
Corticotropin-releasing factor (CRF) is a peptide neurotransmitter with high numbers of cell bodies found in limbic regions of the rat brain including the oval nucleus of the bed nucleus of the stria terminalis (BNSTov) and central nucleus of the amygdala (CeA) as well as in the paraventricular nucleus of the hypothalamus (PVN).
Neurophysiological and histochemical experiments on rats were performed to study the effects of the central nucleus of the amygdala on the activity of cells in various areas of the hypothalamus. A series of histochemical studies following activation of the central nucleus demonstrated increases in the quantity and optical densities of NADP diaphorase (NADP-d)-positive neurons in the parvocellular zone of the paraventricular nucleus of the hypothalamus and the medial part of the lateral hypothalamic area.
Also, CRH fibers were immunostained in the central nucleus of the amygdala and the area of immunostaining was obtained. In the central nucleus of the amygdala, the area of CRH fiber staining was significantly higher in the SS group than in the MSR or HSR groups (p < 0.05, SNK).
Additionally, we mapped Fos induction in rats treated with scopolamine and/or Ro 4368554; scopolamine increased Fos expression in the central nucleus of the amygdala and this was attenuated by Ro 4368554.
In addition, THC promoted a greater increase in c-Fos expression in Nrg1 HET mice than WT mice in the central nucleus of the amygdala, the bed nucleus of the stria terminalis and the paraventricular nucleus of the hypothalamus.
The purpose of the current study was to relate basal corticotropin-releasing factor (CRF) mRNA level in the central nucleus of the amygdala (CeA) with anxiety-like behavior using three strains of rat reported to exhibit a range of behavioral and neuroendocrine responses to stress.
The effect of MCAO on autonomic tone was assessed by monitoring vagal and renal efferent nerve activities before and following systemic administration of either estrogen or saline and the bilateral microinjection of the estrogen receptor antagonist, ICI 182, 780, into several autonomic nuclei (the intrathecal space of the spinal cord, nucleus tractus solitarius, nucleus ambiguus, rostral ventrolateral medulla, parabrachial nucleus, central nucleus of the amygdala or ventral posteromedial thalamus). The presence of ICI 182, 780 in the intrathecal space of the spinal cord, nucleus ambiguous, nucleus tractus solitarius, rostral ventrolateral medulla, parabrachial nucleus, or central nucleus of the amygdala prior to the administration of estrogen resulted in a significant attenuation (ranging from 79% to 94 %) in the estrogen-induced recovery of autonomic function following MCAO.
RESULTS AND DISCUSSION: The greatest number of galanin-immunoreactive neurons were identified in the medial part of the central nucleus and in the dorsal part of the medial nucleus. VIP-immunoreactive fibers were observed in the lateral part oJ'the central nucleus, while long and radially oriented fibers were present in the frontal and dorsal cortical nucleus. CONCLUSION: By distribution analysis of GAL and VIP immunoreactive neurons and fibers, and according to literature data, it can be assumed that the medial part of the central nucleus receives VIP fibers from other parts of the amygdaloid body, and then sends GAL fibers to the medial nucleus..
Lard-associated changes in c-Fos(+) cell numbers were observed in the nucleus of the tractus solitarius, lateral parabrachial nucleus, central nucleus of the amygdala, ventral tegmental area, nucleus accumbens shell and the prefrontal cortex, and were associated with lower levels of triglycerides and free fatty acids.
The capacity of rats with BLA lesions to acquire fear memory may be mediated by the central nucleus of the amygdala (CEA).
Recent work shows that, as in the primate, the subdivisions of the rat orbitofrontal cortex issue different patterns of projections to the amygdala, with intriguing variations in the relative distribution of projections to the sensory-related basal areas compared with output areas, such as the central nucleus.
Within most amygdalar nuclei, a moderate BDNF mRNA expression was found; however, BDNF mRNA was virtually absent from the central nucleus.
Both Devalue and Maintain rats showed greater FOS expression than control rats in amygdala central nucleus, GC, and both subregions of ACBs.
The lateral subdivision of the central nucleus of the amygdala (CeA) comprises two groups of gamma-aminobutyric acid (GABA) neurons that express corticotrophin-releasing hormone (CRH) and enkephalin.
Compared to wild-type mice, mice lacking apoE and apoE4 mice showed pathological alterations in the central nucleus of the amygdala, which is involved in regulation of anxiety.
Bilateral microinjection of clonidine into the central nucleus of the amygdala (CeA) resulted in a significant, dose-dependent increase in TFL.
In adult rats, exposure to unpredictable stress reduced Bcl-2 mRNA levels in the central nucleus of the amygdala (CeA), cingulate (Cg), and frontal (Fr) cortices.
Earlier work demonstrated involvement of the primate central nucleus of the amygdala (CeA) in mediating anxious temperament.
High concentrations of pituitary adenylate cyclase-activating polypeptide (PACAP) nerve fibers are present in the central nucleus of amygdala (CeA), a brain region implicated in the control of fear-related behavior.
The main area of the forebrain of FLT rats sacrificed at R + 1, showing an increased expression of Fos, was the central nucleus of the amygdala (CeA) (cf.
We studied the involvement of cocaine- and amphetamine-regulated transcript peptide (CART) in the central nucleus of amygdala (CeA), lateral bed nucleus of the stria terminalis (BNSTl) and nucleus accumbens shell (AcbSh) in generation of ethanol withdrawal symptoms, with particular focus on anxiety-like behavior using a social interaction test.
The other pathway innervates the central nucleus of the amygdala, and can lead to downstream inhibition of central autonomic structures, resulting in autonomic homeostasis.
Elevations in CRH hnRNA were also identified in hippocampus, the lateral bed nucleus of the stria terminalis (BNST) and globus pallidus at 60 and 120 min following KA and in the piriform cortex, and central nucleus of the amygdala at 120 min after KA.
Finally, MS subjects had significantly more stress-induced Fos positive cells, an estimate of neuronal activation, in the central nucleus of the amygdala (CeA), paraventricular nucleus of the hypothalamus (PVN), and the bed nucleus of the stria terminalis (BNST), each of which plays an important role in organizing the biobehavioral response to stress.
Consistent with these data, histamine immunohistochemistry revealed lower total and synaptic histamine levels in the central nucleus of the amygdala of Apoe-/- than wild-type mice.
The current study examined if the central nucleus of the amygdala (ACe) contributes to the elevated response for amphetamine in HR rats.
Accordingly the current study examined the stress modulation of extracellular glutamate levels in the basolateral nucleus (BLA) and the central nucleus (CeA) of the amygdala by in vivo microdialysis.
Third, pretreatment with D-cycloserine did not increase c-Fos induction by either LiCl or vehicle injection in central visceral relays (the nucleus of the solitary tract, the parabrachial nucleus, the central nucleus of the amygdala, the supraoptic nucleus, and the paraventricular nucleus).
Inhibition of neurons in the central nucleus of the amygdala suppressed conditioned responses to both ambiguous and nonambiguous cues.
A selective CRF1 receptor antagonist (NBI27914) or vehicle was administered systemically (i.p.) or into the central nucleus of the amygdala (CeA, by microdialysis).
Here, we studied the effects of a daily restricted presentation of highly palatable complete meal replacement, chocolate Ensure Plus (Ensure) in food-deprived (restricted feeding, RF) and free-fed (restricted treat, RT) rats, on the expression of the clock protein, Period2 (PER2) in regions of the brain involved in motivational and emotional regulation; these include the oval nucleus of the bed nucleus of the stria terminalis (BNSTov), the central nucleus of the amygdala (CEA), the basolateral amygdala (BLA), the dentate gyrus (DG) and the dorsomedial hypothalamus (DMH).
Furthermore, ICER staining was significantly increased in the perinuclear zone of the supraoptic nucleus, supraoptic nucleus, median preoptic nucleus, OVLT, medial preoptic area, central nucleus of the amygdala, and medial nucleus of the solitary tract.
Interestingly, there was no increase of corticotrophin-releasing factor (CRF) mRNA expression in the PVN and central nucleus of the amygdala of Sprague-Dawley rats subjected to the AA treatment.
CRF(1) receptor-specific antagonists, administered systemically, and CRF receptor subtype nonspecific antagonists, administered into the central nucleus of the amygdala (CeA), selectively decrease the anxiety-like behaviors and increased ethanol self-administration associated with ethanol withdrawal.
Here, we study the neuroanatomical and cellular substrates of the hypergrooming induced by administration of OT in the central nucleus of amygdala (CeA).
Reports, as reviewed here, suggest that two important regions of the limbic system, the central nucleus of the amygdala (CeA) and the bed nucleus of the stria terminalis (BNST), control different aspects of emotional behaviour.
MATERIALS AND METHODS: In situ hybridization was used to measure proenkephalin mRNA expression in adult VPA rats' central nucleus of the amygdala, the dorsal striatum, and the nucleus accumbens. RESULTS: Prenatal exposure to VPA decreased proenkephalin mRNA expression in the dorsal striatum and the nucleus accumbens but not in the central nucleus of the amygdala.
Microinjection of glutamate into the central nucleus of the amygdala produced a dose-related inhibition of the discharge rate of LC neurons in nerve-injured animals but no significant effect on discharge rates in control groups.
Low levels of c-Fos expression in the central nucleus of the amygdala (CE) were observed throughout EXT with little change in expression detectable following SR.
central nucleus of the amygdala is involved in cardiovascular regulation. A cannula was implanted bilaterally into the central nucleus of the amygdala. Mean arterial pressure and heart rate were directly measured via indwelling femoral artery cannula post bilateral intra central nucleus of the amygdala microinjection of renin substrate.
Recent evidence suggests that the amygdala central nucleus (CeA) and midbrain-striatal dopamine systems are critically involved in the alteration of attentional and emotional processing of initially neutral stimuli by associative learning.
The central nucleus and bed nucleus of the stria terminalis responded more to averted than directed-gaze faces. Independent behavioral measures confirmed that faces with averted gaze were more arousing, suggesting the activity in the central nucleus may be related to attention and arousal..
In a second study, the effect of bilateral infusions of the corticotropin-releasing factor (CRF) receptor antagonist D-Phe-CRF(12-41) (0.25 microg/0.5 microL) into the central nucleus of the amygdala (CeA) on ethanol intake was compared in vapor-exposed animals and air controls.
We previously reported a decrease in the basal level of CRH immunoreactivity in the central nucleus of the amygdala and the tyrosine hydroxylase immunoreactivity in the locus coeruleus after chronic variable stress (CVS), whereas both responses were augmented by a novel stress (footshock). Since the acoustic startle reflex (ASR) can be enhanced by the CRH neuronal activity in the central nucleus of the amygdala, we examined the influence of footshock on ASR in rats exposed to CVS.
The laterocapsular division of the central nucleus of the amygdala (CeLC) is important for the modulation of pain affect.
Galanin induced a significant increase in c-Fos levels relative to saline-treated controls in dorsomedial hypothalamus and in the central nucleus of the amygdala.
Our previous studies showed that pain-related audible and ultrasonic vocalizations are modulated by the central nucleus of the amygdala (CeA).
The present study examined the effects of neurotoxic lesions of the central nucleus (CNA) and basolateral complex (BLA) of the amygdala on conditioned taste aversion (CTA) in a latent inhibition design.
Similarly, lesions of the amygdala central nucleus (CeA) have been found to impair attentional function in some circumstances.
Previous studies showed that a circuit including the amygdala central nucleus (CEA) and the cholinergic substantia innominata/nucleus basalis magnocellularis (SI/nBM) is important for both sustained attention guiding action in a five-choice serial reaction time (5CSRT) task and for enhanced new learning about less predictive cues in a serial conditioning task.
The LV system comprises the neurons in the central nucleus of the amygdala that excite DA cells.
Other structures such as the central tegmental field/subparafascicular nucleus of the thalamus, central nucleus of the amygdala, and medial amygdala, also important in the display of male copulatory behavior, were less reliably labeled.
In contrast, there was a diminished response in juvenile/adolescent ventral CPu and in juvenile central nucleus of the amygdala, and an increased response in juvenile/adolescent cortex.
We confirmed that ovalbumin challenge in allergic mice leads to increased activity in the paraventricular nucleus of the hypothalamus and central nucleus of the amygdala, and avoidance behavior towards an allergen-associated compartment.
One neural site linked to a sense of adversity is the amygdala, and one neuropeptide, corticotropin-releasing hormone (CRH), is localized within the central nucleus of the amygdala.
Bilateral focal microinjection of a NMDA antagonist, 2-amino-7-phosphonoheptanoate (AP7), into either central nucleus or lateral nucleus of the amygdala (LAMG) significantly reduced AGS.
Nicotine induced c-fos expression in the bed nucleus of the stria terminalis, the central nucleus of the amygdala (CeA), nucleus accumbens, and the superior colliculus (SC) at both ages, whereas it activated the hypothalamic paraventricular nucleus (PVN) and consequent corticosterone secretion only in adults.
We therefore explored ALLO effects on GABA neurotransmission in the central nucleus (Ce) of the amygdala, a major output nucleus involved in fear and anxiety.
FRA expression affected also at the reentry pontine and diencephalic structures, such as the lateral parabrachial nucleus and the central nucleus of the amygdala, which are known to contribute to the occurrence of pontine waves and the related bursts of REM.
Electrical stimulation of the medial area of the central nucleus caused obvious excitatory neuronal reactions within the medial part of the paraventricular nucleus and rostral portion of the lateral hypothalamic area. The nistochemical study revealed that the central nucleus stimulation caused an increase in number and optical density of the NADPH-d-positive cells within the parvicellular zone of the paraventricular nucleus and in the medial part of the lateral hypothalamic area.
The central nucleus of the amygdala (CeA) plays a critical role in positive emotional responses that involve stimulus-reward learning and are induced by the reinforcing effects of many drugs of abuse, including alcohol.
At 30 days of age (first isolation), higher plasma corticosterone and corticotrophin-releasing hormone (CRH) mRNA expression in the paraventricular nucleus (PVN) of the hypothalamus and in the central nucleus of the amygdala (CeA) were found in males caged with a new partner (SS) after isolation than those returned to their original partner (ISO).
The results replicated previous findings of significant c-Fos expression in the parabrachial nucleus, the central nucleus of the amygdala and the basolateral amygdala.
In this series of studies we show that after oral or nasal ovalbumin (OVA) challenge, allergic mice present increased Fos expression in the paraventricular nucleus of the hypothalamus (PVN) and in the central nucleus of the amygdala (CeA).
These neurons were found in the central nucleus of the amygdala, the nucleus that receives inputs from other amygdala nuclei and in turn sends outputs to other emotion-related brain areas.
Fluorogold was iontophoresed into the bed nucleus of stria terminalis (BST), central nucleus of the amygdala (CEA), paraventricular nucleus of the hypothalamus (PVN), and the pontine lateral parabrachial nucleus (PBL; an important component of ascending viscerosensensory pathways) followed 2 weeks later by intraperitoneal injection of lipopolysaccharide (LPS, 0.1 mg/kg) or saline.
In the age of 90 - 100 days, all rats were implanted electrodes into lateral hypothalamus and cannulas into the central nucleus of amygdala.
We also report that reconsolidation of CS-withdrawal memories upregulates Zif268 protein in the basolateral but not central nucleus of the amygdala and that Zif268 knockdown occurs selectively in the BLA.
During fear expression, the LA is thought to engage the central nucleus of the amygdala (CE), which serves as the principal output nucleus for the expression of conditioned fear responses.
22 +/- 3) parts of the central nucleus of the amygdala also showed increased nNOS-ir in dehydrated rats.
In contrast, Fos expression in stress-associated brain areas, including the ventral lateral bed nucleus of the stria terminalis (VL-BNST), central nucleus of the amygdala (CE), and noradrenergic (A2) neurons in the nucleus tractus solitarius (NTS) was significantly elevated only in morphine-abstinent animals.
We examined the central nucleus of amygdala (CeA) because the CeA is implicated in alcohol reinforcement (Koob et al., 1998).
We wished to determine whether neurones of the nucleus of the solitary tract (NTS) or ventrolateral medulla (VLM) convey visceral afferent information to the central nucleus of the amygdala (CeA) or periaqueductal grey region (PAG), structures that play a key role in adaptive autonomic responses triggered by stress or fear.
Among a variety of brain regions including the parabrachial nucleus, amygdala, insular cortex, supramammillary nucleus, nucleus accumbens, and ventral pallidum that are involved in different phases of CTA expression, the enhanced taste sensitivity to facilitate detection of the conditioned stimulus may originate in the central nucleus of the amygdala and the hedonic shift, from positive to negative, may originate in the basolateral nucleus of the amygdala..
The effects of systemically administered diazepam are also blocked by injections of naltrexone into the central nucleus of the amygdala.
In rats chronically treated with corticosterone this effect was attenuated in the mPVN and DG, enhanced in the M1, and additionally observed in the CA1, CA2 layers of the hippocampus, and in the central nucleus of amygdala (CeA), in comparison to control animals not subjected to contextual fear test.
Brain microinjection studies have revealed that the positive-linked receptors are located in eight to nine brain regions spanning the neuraxis including the secondary motor cortex, piriform cortex, nucleus accumbens, preoptic area, lateral hypothalamic area, vermis cerebellum, locus coeruleus, dorsal raphe and possibly the C1 nucleus of the ventrolateral medulla, whereas the stress-linked receptors are present in at least three areas including the paraventricular nucleus of the hypothalamus, central nucleus of the amygdala and bed nucleus of the stria terminalis.
LiCl did not increase Fos above control levels in the central nucleus of the amygdala, bed nucleus of the stria terminalis (BNST), or paraventricular nucleus of the hypothalamus on P0 but did on P7 and later.
The present study was designed to explore the brain sites within the extended amygdala [ central nucleus of the amygdala (CeA), lateral bed nucleus of the stria terminalis (BNST), and nucleus accumbens shell (NAcSh)] that mediate the increased ethanol self-administration observed during withdrawal.
A moderate number of strongly stained neurons appeared in the medial division of the central nucleus, and a larger accumulation of strongly positive cells was present in the lateral and the capsular divisions.
Neurons in the latero-capsular part of the central nucleus of the amygdala (CeA), a region now called the "nociceptive amygdala", receive predominantly nociceptive information from the dorsal horn through afferent pathways relayed at the nucleus parabrachialis (PB).
MATERIALS AND METHODS: The effects of these compounds on contextual and cued fear conditioning were assessed after direct bilateral infusions into the prelimbic (PrL) cortex, infralimbic (IL) cortex or central nucleus of the amygdala (CeA).
Atipamezole, an alpha(2)-adrenoceptor antagonist, or saline was administered systemically or microinjected into the locus coeruleus, the lateral parabrachial nucleus, the central nucleus of the amygdala, the midbrain periaqueductal gray, and/or through an intrathecal (i.t.) catheter to the spinal cord.
Post-training opioid receptor antagonism (odor aversion) prevented the learning-induced changes in the anterior piriform cortex and also induced significant changes in Fos protein expression in the central nucleus of the amygdala.
These effects were accompanied by modulation of c-fos expression in the hippocampus, central nucleus of the amygdala, bed nucleus of the stria terminalis, and medial parvocellular paraventricular nucleus of the hypothalamus.
Evidence suggests that the 'anxiety-like' behaviour and stress associated with protracted withdrawal may be mediated by increased corticotropin-releasing factor (CRF) in the central nucleus of the amygdala (CeA), a part of the limbic circuitry engaged in the coding and transmission of stimulus-reward associations.
To study this issue, we assessed in rats the effect of thyroidectomy/parathyrodectomy (TPX) on the expression of the clock protein, PER2, in the suprachiasmatic nucleus (SCN), the master circadian clock, and in a number of key limbic forebrain structures, the oval nucleus of the bed nucleus of the stria terminalis (BNSTov), the central nucleus of the amygdala (CEA), the basolateral amygdala (BLA) and the dentate gyrus (DG).
Previous independent studies have demonstrated efferent projections from the NTS to the nucleus paragigantocellularis (PGi) and the central nucleus of the amygdala (CNA) in rat brain.
Alcohol has been shown to affect glutamate (GLU) and dopamine (DA) release and their correlated receptors in the key reward center--extended amygdala--which includes the shell of nucleus accumbens (sNAc) and central nucleus of amygdala (cAmg).
They also send minor axonal projections to the midbrain ventral tegmental area, lateral and paraventricular hypothalamic nuclei, central nucleus of the amygdala, and periaqueductal gray matter.
NADPH-d and noxious-stimuli induced Fos staining were also examined in tissue containing PB cells labeled by the retrograde transport of fluogold (FG) injected into the central nucleus of the amygdala (CeA).
Moreover, MPTP treatment caused prominent reductions of TH-positive fiber densities in the basolateral, lateral and central nucleus of the amygdala (about -20%).
These include pyramidal cells of the hippocampal CA1 and CA2 regions and dentate gyrus granule cells, cerebellar Purkinje neurons, cortical pyramidal neurons, neurons of the central nucleus of the amygdala and parvocellular neurons of the hypothalamic paraventricular nucleus.
Additionally, single Cdk5 IR revealed a 42% increase in the central nucleus of the amygdala (CNA).
Previous research from this laboratory showed that a neural circuit that includes the amygdala central nucleus (CeA), substantia nigra pars compacta (SNc) and dorsolateral striatum (DLS) is essential for the learning and expression of one example of conditioned orienting, the rearing of rats to visual stimuli paired with food.
The astressin blockade of extrahypothalamic corticoliberin receptors in the central nucleus of amygdala modified the effects of various narcogens on self-stimulation reaction. The astressin-induced enhancement of the inhibiting action of leu-enkephalin on cerebral self-stimulation is probably related to a temporary switch-off of the activating influence of the central nucleus of amygdala on hypothalamus..
The PVN represents the central nucleus of the brain's stress systems, the hypothalamus-pituitary-adrenal (HPA) axis and the sympathetic nervous system (SNS).
In contrast to 4 months old animals, 12 months old transgenic mice showed alpha-synucleinopathy in several brain regions, including the central nucleus of the amygdala, which is involved in cognitive behavior of mice, and is susceptible to alphaSYN pathology in human patients.
Five micrograms per kilogram decreased intake and increased the number of CFLI cells in four subnuclei of the nucleus tractus solitarius (NTS), in arcuate nucleus (ARC), and in central nucleus of the amygdala (CeA).
The amygdaloid complex was outlined on coronal sections then partitioned into five reliably defined subdivisions: (1) lateral nucleus, (2) basal nucleus, (3) accessory basal nucleus, (4) central nucleus, and (5) remaining nuclei.
We examined sleep and the encephalogram for 8 h following bilateral microinjections into the central nucleus of the amygdala (CNA) of the cholinergic agonist, carbachol (CARB(L): 0.3 microg; CARB(H): 3.0 microg), the acetylcholinesterase inhibitor, neostigmine (NEO(L): 0.3 microg; NEO(H): 3.0 microg), the muscarinic antagonist, scopolamine (SCO(L): 0.3 microg; SCO(H): 1.0 microg), the nicotinic antagonist, mecamylamine (MEC(L): 0.3 microg; MEC(H): 1.0 microg) and saline (SAL, 0.2 microl) alone.
Given the role of noradrenergic circuitry of the extended amygdala in opioid withdrawal, we examined adrenergic receptor gene expression in the bed nucleus of stria terminalis (BST) and central nucleus of the amygdala.
WR animals also had significantly higher levels of neuronal activation, as indicated by Fos expression in the central nucleus of the amygdala, but less activation in the basolateral nucleus, compared to sedentary controls.
The central nucleus of the amygdala (CeA) orchestrates autonomic and other behavioral and physiological responses to conditioned stimuli that are aversive or elicit fear.
Group I mGluRs contribute to pain-related sensitization and synaptic plasticity of neurons in the laterocapsular division of the central nucleus of the amygdala (CeLC), although the roles of groups II and III mGluRs are not known.
The central nucleus of the amygdala (CeA) has been shown to modulate salt intake in response to aldosterone, so we investigated the connections between these two sites.
Nicotine has been shown to activate stress-related brain nuclei, including the paraventricular nucleus of the hypothalamus (PVN) and the central nucleus of the amygdala (CEA), through complex mechanisms involving direct and indirect pathways.
Previous reports from our laboratories demonstrated that circuitry, including the amygdala central nucleus (CeA), the cholinergic neurons of the substantia innominata/nucleus basalis region, and their innervation of the posterior parietal cortex, is critical to these surprise-induced enhancements of attention in associative learning.
The effects of corticotrophin-releasing factor administration to the serotonin cell body regions of the dorsal raphe nucleus on fear behavior, behavioral activity, and extracellular serotonin levels were assessed in freely moving rats with microdialysis probes implanted into the central nucleus of the amygdala and the medial prefrontal cortex. Infusion of corticotrophin-releasing factor (0.5 microg) into the dorsal raphe rapidly induced freezing behavior, which was positively correlated with an immediate increase in serotonin release in the central nucleus of the amygdala.
They also send minor axonal projections to the midbrain ventral tegmental area, lateral and paraventricular hypothalamic nuclei, central nucleus of the amygdala, and periaqueductal gray matter.
BACKGROUND: The latero-capsular part of the central nucleus of the amygdala (CeLC) is the target of the spino-parabrachio-amygdaloid pain pathway.
We investigated the involvement of the adrenal glucocorticoid, corticosterone, in the control of the rhythmic expression of the circadian clock protein, Period2, in forebrain nuclei known to be sensitive to glucocorticoids, stressors and drugs of abuse, the oval nucleus of the bed nucleus of the stria terminalis and the central nucleus of the amygdala. We now show that, in rats, in the absence of the adrenals, corticosterone replacement via the drinking water, which is associated with daily fluctuations in corticosterone levels, restores the rhythm of Period2 in the oval nucleus of the bed nucleus of the stria terminalis and central nucleus of the amygdala. These results underscore the importance of circadian glucocorticoid signaling in Period2 rhythms in the oval nucleus of the bed nucleus of the stria terminalis and central nucleus of the amygdala and suggest a novel mechanism whereby stressors, drugs of abuse, and other abnormal states that affect the patterns of circulating glucocorticoids can alter the functional output of these nuclei..
Compared to the normal DCE, atropine-induced disruption of the DCE was associated with an increase of the amount of Fos immunoreactive neurons within the central nucleus of the amygdala.
Rat dams with no gestational drug treatment that received an infusion of an OT antagonist directly into the central nucleus of the amygdala (CeA) exhibited similarly high levels of maternal aggression towards intruders.
Three extrahypothalamic areas, the nucleus of the tractus solitari (NTS), the central nucleus of the amygdala (CeA) and the dorsal raphe nucleus (DRN), all potentially involved in peripheral ghrelin signalling of appetite control mediated by the glucose levels were examined.
(5) Individual nuclei begin to be detectable at stages 17-21, the central nucleus at stage 23 and the lateral nucleus shortly thereafter.
The current experiment investigated the predictive role of anxiety-like behaviors in ethanol self-administration and the relationship of NPY in the central nucleus of the amygdala (CeA) with anxiety and ethanol self-administration.
In the deprived animals 5-hydroxytryptamine-immunoreactive fiber densities were increased in the core region of the nucleus accumbens (up to 126%), in the central nucleus of the amygdala (up to 112%) and in the outer subregion of the dentate gyrus stratum moleculare (up to 149%), whereas decreased fiber densities were detected in the dentate subgranular layer (down to 86%) and in the stratum lacunosum of the hippocampal cornu ammonis region 1 (down to 86%).
OBJECTIVE: To investigate the cardiovascular responses induced by activation of the paraventricular nucleus of hypothalamus (PVN) and the roles of the central nucleus of amygdala (CeA) on this effect.
central nucleus of the amygdala, bed nucleus of the stria terminalis and shell of the nucleus accumbens) have been implicated in the aversive aspects of withdrawal from chronic opiate administration. On either the first or second day of testing, the basolateral amygdala, central nucleus of the amygdala, bed nucleus of the stria terminalis, or nucleus accumbens was temporarily inactivated immediately prior to naloxone injection by microinfusion of the glutamatergic alpha-amino-3-hydroxy-5-methyl-4-isoxazole proprionic acid receptor antagonist 1,2,3,4-tetrahydro-6-nitro-2,3-dioxo-benzo(f)quinoxaline-7-sulfonamide (3 microg/0.5 microl). On the first day, inactivation of the basolateral amygdala, central nucleus of the amygdala, or bed nucleus of the stria terminalis, but not the nucleus accumbens blocked withdrawal-potentiated startle, a behavioral measure of the anxiogenic effects of withdrawal. On the second day, inactivation of the nucleus accumbens, but not the basolateral amygdala, central nucleus of the amygdala, or bed nucleus of the stria terminalis disrupted the withdrawal effect. A fear-potentiated startle procedure provided functional confirmation of correct cannulae placement in basolateral amygdale- and central nucleus of the amygdala-implanted animals.
A series of reports from our laboratories demonstrated that these surprise-induced enhancements of stimulus associability depend on circuitry that includes the amygdala central nucleus (CeA), the cholinergic neurons in the sublenticular substantia innominata/nucleus basalis magnocellularis (SI/nBM), as well as certain cortical projections of these latter neurons.
Since the central nucleus of the amygdala (CeA) plays a role in mediating an individual's behavioral and physiological reactivity to stress, we investigated, in rhesus monkeys, whether selective lesions of the CeA altered the gene expression of chemokines (IL-8 and MIP-1alpha) that are associated with early dermal healing.
Retrograde tracing with CTb confirmed this topography and revealed little hippocampal innervation of the central nucleus of the amygdala.
We investigated the possible involvement of nicotinic and dopaminergic signalling in the central nucleus of the amygdala (CeA) and dorsolateral bed nucleus of the stria terminalis (dlBNST) in the anhedonic depression-like effect of precipitated nicotine withdrawal in rats.
Here we identify an influence on the circadian oscillation of the clock protein PER2, endogenous changes in ovarian steroids, within two nuclei of the limbic forebrain: the oval nucleus of the bed nucleus of the stria terminalis and central nucleus of the amygdala.
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