The descending afferent connections of the paraventricular nucleus of the hypothalamus (PVN)

Silverman, Ann‐Judith; Hoffman, Donald L.; Zimmerman, Earl A.

doi:10.1016/s0361-9230(81)80068-8

Cited by 316 publications

(120 citation statements)

References 65 publications

Supporting

Mentioning

107

Contrasting

Unclassified

Order By: Relevance

“…Neurons of the subfornical organ (SFO), a circumventricular organ lacking a BBB, have ghrelin receptors, and ghrelin affects the electrical activity of SFO neurons (31). The SFO projects to hypothalamic nuclei, such as the arcuate (32), paraventricular, supraoptic nuclei, and lateral hypothalamus (33)(34)(35), and these are possible sites for the effects of peripheral ghrelin on the brain.…”

Section: Summary Of Resultsmentioning

confidence: 99%

Stomach ghrelin-secreting cells as food-entrainable circadian clocks

LeSauter

Hoque

Weintraub

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

278

267

View full text Add to dashboard Cite

Increases in arousal and activity in anticipation of a meal, termed “food anticipatory activity” (FAA), depend on circadian food-entrainable oscillators (FEOs), whose locations and output signals have long been sought. It is known that ghrelin is secreted in anticipation of a regularly scheduled mealtime. We show here that ghrelin administration increases locomotor activity in nondeprived animals in the absence of food. In mice lacking ghrelin receptors, FAA is significantly reduced. Impressively, the cumulative rise of activity before food presentation closely approximates a Gaussian function ( r = 0.99) for both wild-type and ghrelin receptor knockout animals, with the latter having a smaller amplitude. For both groups, once an animal begins its daily anticipatory bout, it keeps running until the usual time of food availability, indicating that ghrelin affects response threshold. Oxyntic cells coexpress ghrelin and the circadian clock proteins PER1 and PER2. The expression of PER1, PER2, and ghrelin is rhythmic in light–dark cycles and in constant darkness with ad libitum food and after 48 h of food deprivation. In behaviorally arrhythmic-clock mutant mice, unlike control animals, there is no evidence of a premeal decrease in oxyntic cell ghrelin. Rhythmic ghrelin and PER expression are synchronized to prior feeding, and not to photic schedules. We conclude that oxyntic gland cells of the stomach contain FEOs, which produce a timed ghrelin output signal that acts widely at both brain and peripheral sites. It is likely that other FEOs also produce humoral signals that modulate FAA.

show abstract

Section: Summary Of Resultsmentioning

confidence: 99%

Stomach ghrelin-secreting cells as food-entrainable circadian clocks

LeSauter

Hoque

Weintraub

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

278

267

View full text Add to dashboard Cite

show abstract

“…Furthermore, BNST inactivation during the stressor did not prevent the corticosterone response. These results are somewhat unexpected given the projections from the BNST to hypothalamic and brainstem areas associated with the stress response (Gray, Carney, & Magnuson, 1989;Gray & Magnuson, 1987;Han & Ju, 1990;Moga, Saper, & Gray, 1989;Sawchenko & Swanson, 1983;Silverman, Hoffman, & Zimmerman, 1981;Sofroniew, 1983). Moreover, others have shown that electrical stimulation of the BNST can alter plasma corticosterone levels (Dunn, 1987), and that lesions of the BNST prevent the corticosterone response in contextual, but not cued, fear conditioning (Sullivan, Apergis, Bush, Johnson, Hou, & LeDoux, 2004).…”

Section: Discussionmentioning

confidence: 99%

The bed nucleus of the stria terminalis is critically involved in enhancing associative learning after stressful experience.

Bangasser

Santollo

Shors³

2005

Behavioral Neuroscience

View full text Add to dashboard Cite

Exposure to an acute stressful event enhances trace eyeblink conditioning in male rats, even when rats begin training days after the stressor (Shors, 2001). The authors examined whether the bed nucleus of the stria terminalis (BNST), an area involved in stress and anxiety, is critically involved in this effect and, if so, when. The authors found that excitotoxic lesions to the BNST prevented the enhanced conditioning after stressor exposure. In addition, temporary inactivation of the BNST during the stressor did not alter enhanced responding, whereas inactivation during training prevented the enhancement. These data indicate that stressful experience induces persistent changes in the BNST that are necessary for enhancing learning well after the stressful event has ceased.

show abstract

“…Anatomical and functional interconnections between the two sides of the PVH, and/or between the PVH and SON, may account for their bilateral activation (Silverman et al, 1981;Belin et al, 1984;Belin and Moos, 1986;Saphier and Feldman, 1987;Boudaba and Tasker, 2006). Also, NE recruitment of PVH projections to hindbrain cell groups (Swanson and Kuypers, 1980;Sawchenko and Swanson, 1982;SchwanzelFukuda et al, 1984;van der Kooy et al, 1984) may, in turn, have engaged SO neurons via ascending relays (Raby and Renaud, 1989).…”

Section: Interpreting the Effects Of Central Ne Microinjection Evidenmentioning

confidence: 99%

Catecholaminergic Control of Mitogen-Activated Protein Kinase Signaling in Paraventricular Neuroendocrine NeuronsIn VivoandIn Vitro: A Proposed Role during Glycemic Challenges

Khan¹,

Ponzio²,

Sanchez‐Watts³

et al. 2007

J. Neurosci.

View full text Add to dashboard Cite

We show that systemic insulin and 2-DG, and PVH-targeted NE microinjections, rapidly elevated PVH phospho-ERK1/2 levels. NE increased Crh and c-fos expression, together with circulating ACTH/corticosterone. However, because injections also increased c-Fos mRNA in other brain regions, we used hypothalamic slices maintained in vitro to clarify whether NE activates PVH neurons without contribution of inputs from distal regions. In slices, bath-applied NE triggered robust phospho-ERK1/2 immunoreactivity in PVH (including CRH) neurons, which attenuated markedly in the presence of the ␣ 1 adrenoceptor antagonist, prazosin, or the MAP kinase kinase (MEK) inhibitor, U0126 (1,4-diamino-2,3-dicyano-1,4-bis[2-aminophenylthio]butadiene). Therefore, at a systems level, local PVH delivery of NE is sufficient to account for hindbrain activation of CRH neuroendocrine neurons during glycemic challenge. At a cellular level, these data provide the first demonstration that MAP kinase signaling cascades (MEK3 ERK) are intracellular transducers of noradrenergic signals in CRH neurons, and implicate this transduction mechanism as an important component of central neuroendocrine responses during glycemic challenge.

show abstract

The descending afferent connections of the paraventricular nucleus of the hypothalamus (PVN)

Cited by 316 publications

References 65 publications

Stomach ghrelin-secreting cells as food-entrainable circadian clocks

Stomach ghrelin-secreting cells as food-entrainable circadian clocks

The bed nucleus of the stria terminalis is critically involved in enhancing associative learning after stressful experience.

Catecholaminergic Control of Mitogen-Activated Protein Kinase Signaling in Paraventricular Neuroendocrine NeuronsIn VivoandIn Vitro: A Proposed Role during Glycemic Challenges

Contact Info

Product

Resources

About