Cholecystokinin Activates C‐Fos Expression in Hypothalamic Oxytocin and Corticotropin‐Releasing Hormone Neurons

Verbalis, Joseph G.; Stricker, Edward M.; Robinson, Alan G.; Hoffman, Gloria E.

doi:10.1111/j.1365-2826.1991.tb00264.x

Cited by 192 publications

(110 citation statements)

References 29 publications

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“…The biochemical coding and exact mapping of activated neurons in the PVN needs to be further characterized. Previous studies in rats showed that peripheral CCK activates oxytocinergic neurons in the PVN (62,63). The synergistic interaction between CCK and leptin may have physiological relevance.…”

Section: Discussionmentioning

confidence: 94%

Synergistic interaction between leptin and cholecystokinin to reduce short-term food intake in lean mice

Barrachina

Martı́nez

Wang

et al. 1997

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

405

256

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Leptin is a circulating protein involved in the long-term regulation of food intake and body weight. Cholecystokinin (CCK) is released postprandially and elicits satiety signals. We investigated the interaction between leptin and CCK-8 in the short-term regulation of food intake induced by 24-hr fasting in lean mice. Leptin, injected intraperitoneally (i.p.) at low doses (4-120 g͞kg), which did not influence feeding behavior for the first 3 hr postinjection, decreased food intake dose dependently by 47-83% during the first hour when coinjected with a subthreshold dose of CCK. Such an interaction was not observed between leptin and bombesin. The food-reducing effect of leptin injected with CCK was not associated with alterations in gastric emptying or locomotor behavior. Leptin-CCK action was blocked by systemic capsaicin at a dose inducing functional ablation of sensory afferent fibers and by devazepide, a CCK-A receptor antagonist but not by the CCK-B receptor antagonist, L-365,260. The decrease in food intake which occurs 5 hr after i.p. injection of leptin alone was also blunted by devazepide. Coinjection of leptin and CCK enhanced the number of Fos-positive cells in the hypothalamic paraventricular nucleus by 60%, whereas leptin or CCK alone did not modify Fos expression. These results indicate the existence of a functional synergistic interaction between leptin and CCK leading to early suppression of food intake which involves CCK-A receptors and capsaicin-sensitive afferent fibers.

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Section: Discussionmentioning

confidence: 94%

Synergistic interaction between leptin and cholecystokinin to reduce short-term food intake in lean mice

Barrachina

Martı́nez

Wang

et al. 1997

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

405

256

View full text Add to dashboard Cite

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“…The neuronal excitation (see Renaud et al, 1987;Leng & Dyball, 1991) results in an elevation of plasma oxytocin concentrations, rising 5 min after CCK injection to about 50 pg ml-' above basal levels (Verbalis et al, 1986a,b; . Systemically administered CCK also activates centrally-projecting oxytocin neurones, which form one limb of a gastric reflex arc, and also corticotrophinreleasing factor (CRF) neurones, that results in the release of ACTH (Verbalis et al, 1991b;Kamilaris et al, 1992). The profile of neuronal activation in the hypothalamus following systemic administration of CCK has been studied using products of the immediate-early gene c-fos as a marker.…”

Section: Introductionmentioning

confidence: 99%

Involvement of cholecystokinin receptor types in pathways controlling oxytocin secretion

Luckman

Hamamura

Antonijevic

et al. 1993

British J Pharmacology

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1 Intravenous administration of cholecystokinin (CCK) results in a transient activation of oxytocin neurones in the rat, and hence to oxytocin secretion: this activation is followed by expression of c-fos mRNA and of Fos-like immunoreactivity (Fos-LI) in magnocellular oxytocin neurones. Fos-like immunoreactivity is also induced in the regions of the brainstem that are thought to relay information from the periphery to the hypothalamus. 2 Administration of the selective CCKA receptor antagonist MK-329, but not the CCKB receptor antagonist L-365,260, prior to CCK injection, prevented oxytocin release as measured by radioimmunoassay and oxytocin neuronal activation as measured by electrophysiology and by the lack of induction of c-fos mRNA.3 MK-329 abolished the release of adrenocorticotrophic hormone (ACTH) following injection of CCK. 4 MK-329 prevented the expression of Fos-LI in the hypothalamic magnocellular nuclei and in the area postrema and dorsal vagal complex of the brainstem.5 L-365,260 had no effect on the expression of Fos-LI in the brainstem, but attenuated that seen in the hypothalamic magnocellular nuclei. 6 We conclude that CCK acts on CCKA receptors, either in the area postrema or on peripheral endings of the vagus nerve, to cause the release of hypothalamic oxytocin and ACTH. Information may be carried to the hypothalamus in part by CCK acting at CCKB receptors.

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“…After 20 d of the second restricted-food process, rats were killed at the moment of food arrival to analyze c-Fos immuno-reactivity in the brain. Because c-Fos protein takes between 60 and 90 min to be expressed after the activation of a neuron (24), this time point reflects the neuronal activation during FAA, at least 60 min before expected food arrival.…”

mentioning

confidence: 99%

Interaction between hypothalamic dorsomedial nucleus and the suprachiasmatic nucleus determines intensity of food anticipatory behavior

Acosta-Galvan

Vliet

et al. 2011

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

162

131

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Food anticipatory behavior (FAA) is induced by limiting access to food for a few hours daily. Animals anticipate this scheduled meal event even without the suprachiasmatic nucleus (SCN), the biological clock. Consequently, a food-entrained oscillator has been proposed to be responsible for meal time estimation. Recent studies suggested the dorsomedial hypothalamus (DMH) as the site for this food-entrained oscillator, which has led to considerable controversy in the literature. Herein we demonstrate by means of c-Fos immunohistochemistry that the neuronal activity of the suprachiasmatic nucleus (SCN), which signals the rest phase in nocturnal animals, is reduced when animals anticipate the scheduled food and, simultaneously, neuronal activity within the DMH increases. Using retrograde tracing and confocal analysis, we show that inhibition of SCN neuronal activity is the consequence of activation of GABA-containing neurons in the DMH that project to the SCN. Next, we show that DMH lesions result in a loss or diminution of FAA, simultaneous with increased activity in the SCN. A subsequent lesion of the SCN restored FAA. We conclude that in intact animals, FAA may only occur when the DMH inhibits the activity of the SCN, thus permitting locomotor activity. As a result, FAA originates from a neuronal network comprising an interaction between the DMH and SCN. Moreover, this study shows that the DMH-SCN interaction may serve as an intrahypothalamic system to gate activity instead of rest overriding circadian predetermined temporal patterns. P hysiology and behavior of all mammals is organized in an alternating pattern of rest and activity cycles, whereby the endogenous and light-induced daily neuronal activity of the suprachiasmatic nucleus (SCN) signals rest in nocturnal rodents and activity in diurnal primates, such as humans (1, 2). Restricting food access to a short and predictable episode during the rest phase changes this behavioral pattern, such that an animal becomes active and for up to several hours anticipates the upcoming feeding event. This food anticipatory activity (FAA) is even exhibited without the known circadian oscillator, the SCN (3), and thus may rely on a different circadian pacemaker.In search of the location of this so-called "food entrained oscillator" (FEO), two recent studies have claimed that its position is within the dorsomedial nucleus of the hypothalamus (DMH) (4, 5). The designation of the DMH as master clock for food entrainment is, however, controversial because some groups reported unimpaired FAA despite large lesions of the DMH (6, 7); others have shown that lesions of the DMH disturb and diminish the intensity of FAA (6). The possible participation of other brain structures in FAA is evident from studies that demonstrate modulation of neuronal activity and induction of clock-gene rhythmicity in hypothalamic and limbic structures by feeding schedules (8-11). Thus, it has been suggested that FAA depends on a multioscillatory system comprised of a complex and redundant neuronal netwo...

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Cholecystokinin Activates C‐Fos Expression in Hypothalamic Oxytocin and Corticotropin‐Releasing Hormone Neurons

Cited by 192 publications

References 29 publications

Synergistic interaction between leptin and cholecystokinin to reduce short-term food intake in lean mice

Synergistic interaction between leptin and cholecystokinin to reduce short-term food intake in lean mice

Involvement of cholecystokinin receptor types in pathways controlling oxytocin secretion

Interaction between hypothalamic dorsomedial nucleus and the suprachiasmatic nucleus determines intensity of food anticipatory behavior

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