CCK-8S activates c-Fos in a dose-dependent manner in nesfatin-1 immunoreactive neurons in the paraventricular nucleus of the hypothalamus and in the nucleus of the solitary tract of the brainstem

Noetzel, Steffen; Stengel, Andreas; Inhoff, Tobias; Goebel, Miriam; Wisser, Anna-Sophia; Bannert, Norbert; Wiedenmann, Bertram; Klapp, Burghard F.; Taché, Yvette; Mönnikes, Hubert; Kobelt, Peter

doi:10.1016/j.regpep.2009.06.009

Cited by 58 publications

(42 citation statements)

References 48 publications

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“…Conversely, it has been reported that peripheral administration of CCK stimulates c-Fos expression in nesfatin-1-containing neurons in the hypothalamic PVN and brain stem NTS [13]. These data by us and others, taken together,, raise the possibility that peripheral and central nesfatin-1 could have a strong connection with the neurons that respond to peripheral CCK with respect to the regulation of food intake.…”

mentioning

confidence: 57%

Nesfatin-1 evokes Ca2+ signaling in isolated vagal afferent neurons via Ca2+ influx through N-type channels

Iwasaki

Nakabayashi

Kakei

et al. 2009

Biochemical and Biophysical Research Communications

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mentioning

confidence: 57%

Nesfatin-1 evokes Ca2+ signaling in isolated vagal afferent neurons via Ca2+ influx through N-type channels

Iwasaki

Nakabayashi

Kakei

et al. 2009

Biochemical and Biophysical Research Communications

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“…First, there is a critical time in which c-Fos is maximally expressed in response to a stimulus. In our experiments, animals were studied 90 min after CCK administration, since maximal c-Fos expression in response to a stimulus (32), or specifically CCK, has been shown to be between 90 and 120 min (37,52,89). Second, exposure to stress induces c-Fos expression, so it is important to adapt the animals to handling and manipulation to decrease the levels of basal c-Fos expression.…”

Section: Discussionmentioning

confidence: 99%

The subfornical organ: a novel site of action of cholecystokinin

Ahmed

Dai

et al. 2014

American Journal of Physiology-Regulatory, Integrative and Comp

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The subfornical organ (SFO) is an important sensory circumventricular organ implicated in the regulation of fluid homeostasis and energy balance. We investigated whether the SFO is activated by the hormone cholecystokinin (CCK). CCK₁ and CCK₂ receptors were identified in the SFO by RT-PCR. Dissociated SFO neurons that responded to CCK (40/77), were mostly depolarized (9.2 ± 0.9 mV, 30/77), but some were hyperpolarized (-7.3 ± 1.1 mV, 10/77). We next examined the responses of SFO neurons in vivo to CCK (16 μg/kg ip), in the presence and absence of CCK₁ or CCK₂ receptor antagonists (devazepide; 600 μg/kg and L-365,260; 100 μg/kg, respectively), using the functional activation markers c-Fos and phosphorylated extracellular signal-related kinase (p-ERK). The nucleus of the solitary tract (NTS) served as a control for CCK-induced activity. There was a significant increase in c-Fos expression in the NTS (259.2 ± 20.8 neurons) compared with vehicle (47.5 ± 2.5). Similarly, in the SFO, c-Fos was expressed in 40.5 ± 10.6 neurons in CCK-treated compared with 6.6 ± 2.7 in vehicle-treated rats (P < 0.01). Devazepide significantly reduced the effects of CCK in the NTS but not in SFO. L-365,260 blocked the effects of CCK in both brain regions. CCK increased the number of p-ERK neurons in NTS (27.0 ± 4.0) as well as SFO (18.0 ± 4.0), compared with vehicle (8.0 ± 2.6 and 4.3 ± 0.6, respectively; P < 0.05). Both devazepide and L-365,260 reduced CCK-induced p-ERK in NTS, but only L-365,260 reduced it in the SFO. In conclusion, the SFO represents a novel brain region at which circulating CCK may act via CCK₂ receptors to influence central autonomic control.

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“…Yet, to our knowledge, no report has been published on the direct effects of leptin on the hypothalamic expression of NUCB2/nesfatin-1, or its potential alterations in conditions of leptin deficiency. On the contrary, the anorectic hormone, cholecystokinin, has been shown to activate nesfatin-1 neurons at the PVN and NTS, thus suggesting the involvement of these neuronal populations in mediating the satiating effects of this gut-derived peptide (Noetzel et al 2009. Co-expression analyses of NUCB2/nesfatin-1 at specific hypothalamic nuclei, coupled with functional studies, have shed light into the potential neuroendocrine mechanisms and pathways for the anorectic effects of nesfatin-1.…”

Section: Reproductive Organsmentioning

confidence: 99%

Expanding roles of NUCB2/nesfatin-1 in neuroendocrine regulation

García-Galiano

Navarro

Gaytán

et al. 2010

Journal of Molecular Endocrinology

121

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Nesfatin-1 was originally identified as a hypothalamic neuropeptide, derived from the precursor NEFA (for DNA binding/EF-hand/acidic protein)/nucleobindin 2 (NUCB2), with the ability to suppress food intake, acting in a leptin-independent manner. Departing from this seminal finding, the patterns of expression of NUCB2/nesfatin-1 have been thoroughly characterized in different hypothalamic nuclei and brain areas with proven roles in energy homeostasis, and its potential interactions with other key neuropeptide regulators of appetite have been documented. Intriguingly, recent experimental evidence suggests that NUCB2/nesfatin-1 is also expressed in peripheral tissues with relevant metabolic functions, such as the pancreas, the adipose, and the gut. In addition, evidence is mounting that nesfatin signaling may participate in adaptative responses and in the control of body functions gated by the state of energy reserves, such as puberty onset. Altogether, these observations have broadened our perception of the biological profile of nesfatin-1 that, rather than a simple anorectic signal in the hypothalamus, might operate at different tissues as an integral regulator of energy homeostasis and closely related neuroendocrine functions.

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CCK-8S activates c-Fos in a dose-dependent manner in nesfatin-1 immunoreactive neurons in the paraventricular nucleus of the hypothalamus and in the nucleus of the solitary tract of the brainstem

Cited by 58 publications

References 48 publications

Nesfatin-1 evokes Ca2+ signaling in isolated vagal afferent neurons via Ca2+ influx through N-type channels

Nesfatin-1 evokes Ca2+ signaling in isolated vagal afferent neurons via Ca2+ influx through N-type channels

The subfornical organ: a novel site of action of cholecystokinin

Expanding roles of NUCB2/nesfatin-1 in neuroendocrine regulation

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