Organization of peptidergic and catecholaminergic efferents from the nucleus of the solitary tract to the rat amygdala

Zardetto-Smith, Andrea M.; Gray, Thackery S.

doi:10.1016/0361-9230(90)90183-z

Cited by 130 publications

(68 citation statements)

References 83 publications

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“…Immunocytochemical studies of the rat brainstem have shown that a 2A receptors are found on the axon terminals and dendrites of noradrenergic locus coeruleus neurons that project to the lateral and basolateral amygdala nuclei (Lee et al, 1998). Noradrenergic neurons within the nucleus tractus solitarius (NTS) project to the central nucleus (Asan, 1998), and the activation of the NTS (Zardetto-Smith and Gray, 1990) contributes to an increased norepinephrine release in the amygdala and enhances memory (Williams et al, 2000). Norepinephrine release from the ascending noradrenergic tracts is also under presynaptic control of both a 2C and a 2A ARs (Bucheler et al, 2002), where they act as an autoreceptors on noradrenergic terminals.…”

Section: Discussionmentioning

confidence: 99%

Activation of α2 Adrenergic Receptors Suppresses Fear Conditioning: Expression of c-Fos and Phosphorylated CREB in Mouse Amygdala

Davies

Tsui

Flannery

et al. 2003

Neuropsychopharmacol

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a 2 adrenergic agonists such as dexmedetomidine generally suppress noradrenergic transmission and have sedative, analgesic, and antihypertensive properties. Considering the importance of the neurotransmitter norepinephrine in forming memories for fearful events, we have investigated the acute and chronic effects of dexmedetomidine on discrete cue and contextual fear conditioning in mice. When administered before training, dexmedetomidine (10-20 mg/kg, i.p.) selectively suppressed discrete cue fear conditioning without affecting contextual memory. This behavioral change was associated with a decrease in memory retrieval-induced expression of c-Fos and P-CREB in the lateral, basolateral, and central nuclei of the amygdala. Dexmedetomidine's action on discrete cue memory did not occur in a 2A adrenoceptor knockout (KO) mice. When dexmedetomidine was administered after training, it suppressed contextual memory, an effect that did not occur in a 2A adrenoceptor KO mice. We conclude that dexmedetomidine, acting at a 2A adrenoceptors, must be present during the encoding process to decrease discrete cue fear memory; however, its ability to suppress contextual memory is likely the result of blocking the consolidation process. The ability of a 2 agonists to suppress fear memory may be a valuable property clinically in order to suppress the formation of memories during stressful situations.

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Section: Discussionmentioning

confidence: 99%

Activation of α2 Adrenergic Receptors Suppresses Fear Conditioning: Expression of c-Fos and Phosphorylated CREB in Mouse Amygdala

Davies

Tsui

Flannery

et al. 2003

Neuropsychopharmacol

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“…Since a similar colo caliza. tion seems to be present in the central amygdaloid nucleus (Zardetto-Smith and Gray 1990;Riche et al 1990), NPY could exert its anxiolytic-like effect on this structure in an analogous manner. However, NPYin the amygdala also coexists with somatostatin and gamma-aminobutyric acid in a population of intrinsic interneurons similar to those seen in the neocortex and striatum (McDonald 1989;McDonald and Pearson 1989).…”

Section: Discussionmentioning

confidence: 99%

“…Conversely, the amygdaloid complex and in particular the central nucleus of the amygdala are known to be important for emotionality, and the central nucleus receives a dense NPY -ergic innervation (Chronwall et al 1985;Zardetto Smith and Gray 1990). The present study was under taken to examine the question of whether orexigenic and anxiolytic-like effects of NPY can be anatomically dissociated, and to test the hypothesis that anxiolytic like effects of NPY are produced in the amygdaloid com plex.…”

Section: Rkusmentioning

confidence: 93%

Anxiolytic-Like Action of Neuropeptide Y: Mediation by Y1 Receptors in Amygdala, and Dissociation from Food Intake Effects

Heilig

McLeod²,

Brot

et al. 1993

Neuropsychopharmacol

345

195

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from animal and human studies suggests that eropeptide Y (NPY) may be a potent endogenous .my tie. The anatomic structures mediating this action �fht peptide remain unknown. Furthermore, in addition �iIs anxiolytic-like effects, intracerebroventricular ""istration of NPY induces food intake through IIJpothalamic me chanisms, making the anxiolytic-like • of the peptide more difficult to interpret. The JI1JIOSi of this study was to examine the anatomic _rate for the effects of NPY on anxiety, and to _ferize the NPY receptors mediating these effects. lItrIctrebroventricular injection of NPY produced irrmse d food intake in free-feeding animals, and dose Itpmdent anticonflictlanxiolytic-like effects in an IIIbI ished animal model of anxiety, the Geller-Seifter Mlished by Elsevier Science Publishing Co., Inc.• Avenue of the Americas, New York, NY 10010 punished responding test. In contrast, microinjection of NPY into the central nucleus of the amygdala did not increase food intake in free-feeding animals, did not affect unpunished lever pressing for food, but did reproduce the anticonflictlanxiolytic-like effect with high potency. The selective NPY-YI agonist, p[Leu 31 ,Pro 3 4]NPY was approximately equipotent with native NPY in the conflict paradigm, and markedly more potent than the Y2 agonist, NPY 13 -3 6. Intrastriatal injections had no effect on conflict behavior. Thus, activation of YI receptors in the central nucleus of the amygdala produces effects similar to established anxiolytics without affecting food intake, suggesting that YI-receptors in the amygdala may be a substrate for anxiolytic actions of NPY.

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“…The neurotransmitters involved in these brainstem pathways include particularly norepinephrine and serotonin. [43][44][45] Recent studies utilizing the age-specific stress paradigm of maternal separation have yielded important evidence supporting the role of CRH, acting via the CRF 2 receptor, in transducing and integrating somatosensory, gustatory, and visceral signals received in brainstem nuclei, such as the NTS and Barrington's nucleus, with the neuroendocrine stress response (Figure 1c). 46 CRH is highly expressed in neurons residing in Barrington's nucleus, 47 as well as in ACe.…”

Section: Molecular Psychiatrymentioning

confidence: 98%

Neurobiology of the stress response early in life: evolution of a concept and the role of corticotropin releasing hormone

et al. 2001

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Over the last few decades, concepts regarding the presence of hormonal and molecular responses to stress during the first postnatal weeks in the rat and the role of the neuropeptide corticotropin releasing hormone (CRH) in these processes, have been evolving. CRH has been shown to contribute critically to molecular and neuroendocrine responses to stress during development. In turn the expression of this neuropeptide in both hypothalamus and amygdala is differentially modulated by single and recurrent stress, and is determined also by the type of stress (eg, psychological or physiological). A likely transcriptional regulatory factor for modulating CRH gene expression, the cAMP responsive element binding protein CREB, is phosphorylated (activated) in the developing hypothalamus within seconds of stress onset, preceding the transcription of the CRH gene and initiating the activation of stress-induced cellular and neuroendocrine cascades. Finally, early life stress may permanently modify the hypothalamic pituitary adrenal axis and the response to further stressful stimuli, and recent data suggest that CRH may play an integral role in the mechanisms of these long-term changes. Molecular Psychiatry (2001) 6, 647-656.

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Organization of peptidergic and catecholaminergic efferents from the nucleus of the solitary tract to the rat amygdala

Cited by 130 publications

References 83 publications

Activation of α2 Adrenergic Receptors Suppresses Fear Conditioning: Expression of c-Fos and Phosphorylated CREB in Mouse Amygdala

Activation of α2 Adrenergic Receptors Suppresses Fear Conditioning: Expression of c-Fos and Phosphorylated CREB in Mouse Amygdala

Anxiolytic-Like Action of Neuropeptide Y: Mediation by Y1 Receptors in Amygdala, and Dissociation from Food Intake Effects

Neurobiology of the stress response early in life: evolution of a concept and the role of corticotropin releasing hormone

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