Identification of urocortin 3 afferent projection to the ventromedial nucleus of the hypothalamus in rat brain

Chen, Peilin; Lin, David T.S.; Giesler, Jessica; Li, Chien

doi:10.1002/cne.22620

Cited by 33 publications

(43 citation statements)

References 55 publications

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“…The VMH, which is densely innervated by Ucn3-positive fibers [8,37], expresses CRF 2 receptor mRNA [5]. The CRF 2 receptor-expressing glutamatergic neurons of the VMH project to the ARC, and stimulate production of an anorectic neuropeptide, proopiomelanocortin [10].…”

Section: Discussionmentioning

confidence: 99%

Regulation of corticotropin-releasing factor and urocortin 2/3 mRNA by leptin in hypothalamic N39 cells

et al. 2013

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Corticotropin-releasing factor (CRF) activates the pituitary-adrenal axis during stress, and shows anorectic effects via CRF type 1 receptors in the hypothalamus.Both urocortin (Ucn) 2 and Ucn3 also act as anorectic neuropeptides via CRF type 2 receptors. Leptin, a product of the obesity gene secreted mainly from adipose tissue, reduces food intake and increases energy expenditure. A possible interaction between leptin and CRF/Ucns has been suggested, as leptin can regulate expression and activation of CRF and Ucns in the hypothalamus. This study aimed to explore the possible function of leptin in the hypothalamus, and its effects in regulating CRF and Ucns. The study identified mRNA expression of the leptin receptor (Ob-R) and its subtypes, CRF, and Ucn2/3 in mouse hypothalamic N39 cells. Leptin stimulated signal transducer and activators of transcription type 3 (STAT3) phosphorylation, directly increased the mRNA levels of both CRF and Ucn2/3 in hypothalamic cells, and increased Ob-Rb mRNA levels. A Janus kinase inhibitor inhibited the leptin-mediated increase in STAT3 phosphorylation, and then the increases in CRF and Ucn2/3 mRNA levels. Leptin may contribute to a stress response or anorectic effect via the regulation 2 of CRF and Ucn2/3 in the hypothalamus.

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Section: Discussionmentioning

confidence: 99%

Regulation of corticotropin-releasing factor and urocortin 2/3 mRNA by leptin in hypothalamic N39 cells

et al. 2013

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“…Using optogenetic and in vivo recording methods, a distinct region within the HAA, the ventrolateral subdivision of the ventromedial hypothalamic nucleus (VMHvl), was recently shown to be necessary and sufficient for offensive aggression in mice (Lin et al, 2011). Afferents to the VMH are also numerous, and include other hypothalamic nuclei, the bed nucleus of stria terminalis , lateral septum, and amygdala (Berk and Finkelstein, 1981; Chen et al, 2011; Luiten and Room, 1980). The substantial connections of the VMH suggest that there are multiple nodes of neuromodulatory control over agonistic behaviors.…”

Section: Introductionmentioning

confidence: 99%

Mood and anxiety regulation by nicotinic acetylcholine receptors: A potential pathway to modulate aggression and related behavioral states

et al. 2015

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The co-morbidity between smoking and mood disorders is striking. Preclinical and clinical studies of nicotinic effects on mood, anxiety, aggression, and related behaviors, such as irritability and agitation, suggest that smokers may use the nicotine in tobacco products as an attempt to self-medicate symptoms of affective disorders. The role of nicotinic acetylcholine receptors (nAChRs) in circuits regulating mood and anxiety are beginning to be elucidated in animal models, but the mechanisms underlying the effects of nicotine on aggression-related behavioral states (ARBS) are still not understood. Clinical trials of nicotine or nicotinic medications for neurological and psychiatric disorders have often found effects of nicotinic medications on ARBS, but few trials have studied these outcomes systematically. Similarly, the increase in ARBS resulting from smoking cessation can be resolved by nicotinic agents, but the effects of nicotinic medications on these types of mental states and behaviors in non-smokers are less well understood. Here we review the literature on the role of nAChRs in regulating mood and anxiety, and subsequently on the closely related construct of ARBS. We suggest avenues for future study to identify how nAChRs and nicotinic agents may play a role in these clinically important areas.

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“…Our previous anatomical study showed that the main source of Ucn 3 input into the VMH originates in the PVHap and the adjacent BSTp. The MEA provides moderate Ucn 3 afferent projections (Chen et al, 2011). Ucn 3 cells in the median preoptic nucleus supply negligible input into the nucleus (Chen et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

“…The MEA provides moderate Ucn 3 afferent projections (Chen et al, 2011). Ucn 3 cells in the median preoptic nucleus supply negligible input into the nucleus (Chen et al, 2011). Interestingly, Ucn 3 neurons in the rostral perifornical hypothalamus just caudal and lateral to the PVHap area do not project to the VMH; these cells instead send projections to the LS (Chen et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Stress-activated afferent inputs into the anterior parvicellular part of the paraventricular nucleus of the hypothalamus: Insights into urocortin 3 neuron activation

van-Hover

2015

Brain Research

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Urocortin 3 (Ucn 3) is a member of the corticotropin-releasing factor family, which plays a major role in coordinating stress responses. Ucn 3 neurons in the anterior parvicellular part of the paraventricular nucleus of the hypothalamus (PVHap) provide prominent input into the ventromedial nucleus of the hypothalamus (VMH), a well known satiety center, where Ucn 3 acts to suppress feeding and modulate blood glucose levels. In the present study, we first determined that Ucn 3 expression in the PVHap was stimulated by acute restraint stress. We then performed retrograde tracing with fluorogold (FG) combined with immunohistochemistry for Fos as a marker for neuronal activation after restraint stress to determine the stress-activated afferent inputs into the PVHap. Substantial numbers of FG/Fos double labeled cells were found in the bed nucleus of the stria terminalis, lateral septal nucleus, the medial amygdala, and a number of nuclei in the hypothalamus including the VMH, the arcuate nucleus, the posterior nucleus, and the ventral premammillary nucleus. In the brainstem, FG/Fos positive cells were found in the periaqueductal gray, the nucleus of the solitary tract, and the ventrolateral medulla. In conclusion, the present study showed that acute stress rapidly stimulates Ucn 3 expression in the PVHap and identified specific stress-sensitive brain areas that project to the PVHap. These areas are potentially important in mediating the stress-induced activation of Ucn 3 neurons in the PVHap.

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Identification of urocortin 3 afferent projection to the ventromedial nucleus of the hypothalamus in rat brain

Cited by 33 publications

References 55 publications

Regulation of corticotropin-releasing factor and urocortin 2/3 mRNA by leptin in hypothalamic N39 cells

Regulation of corticotropin-releasing factor and urocortin 2/3 mRNA by leptin in hypothalamic N39 cells

Mood and anxiety regulation by nicotinic acetylcholine receptors: A potential pathway to modulate aggression and related behavioral states

Stress-activated afferent inputs into the anterior parvicellular part of the paraventricular nucleus of the hypothalamus: Insights into urocortin 3 neuron activation

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