Oxytocin Secretion in Response to Cholecystokinin and Food: Differentiation of Nausea from Satiety

Verbalis, Joseph G.; McCann, Michael T.; McHale, Colleen M.; Stricker, Edward M.

doi:10.1126/science.3715453

Cited by 348 publications

(202 citation statements)

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“…Furthermore, preclinical data indicate that CRH may play a role in the anxiogenic (Biro et al 1993) and endocrine (Kamilaris et al 1992) effects of CCK. However, it should be noted that CCK may activate pituitary ACTH secretion, not only via CRH, but also via other neurohormones such as oxytocin and vasopressin (Carter and Lightman 1987;Verbalis et al 1986). The described association of CCK-4 induced panic attacks and an exaggerated pituitary ACTH response together with the known behavioral effects of CRH (for review see: Dunn and Berridge 1990;Holsboer et al 1992;Owens and Nemeroff 1992) are in favor of CRH mediating the panicogenic activity of CCK-4 in patients with panic disorder.…”

Section: Discussionmentioning

confidence: 99%

Increased ACTH Concentrations Associated with Cholecystokinin Tetrapeptide-Induced Panic Attacks in Patients with Panic Disorder

Ströhle

Holsboer

Rupprecht

2000

Neuropsychopharmacology

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Preclinical findings on the role of corticotropin releasing hormone (CRH) in stress and anxiety, on the interaction of CRH and cholecystokinin (CCK) in modulating anxiety, as well as the blunted corticotropin (ACTH) response to CRH in panic disorder suggest that CRH may play a role in panic disorder. To further characterize the role of the hypothalamic-pituitary-adrenocortical (HPA) system in panic disorder, we compared patients with and without CCK tetrapeptide (CCK-4) induced panic attacks. Twenty-four patients with panic disorder were given injections of CCK-4 (25 g). Panic attacks, psychopathological changes, as well as ACTH and cortisol secretion were recorded. Fifteen of the 24 patients experienced a panic attack after CCK-4. ACTH secretion was significantly higher in the patients with CCK-4-induced panic attacks than in those without such attacks. The patients without CCK-4-induced attacks had a brief but less pronounced increase in ACTH concentrations. Cortisol concentrations were not significantly increased after CCK-4 administration. The increased ACTH concentrations suggest that the activation of the HPA system in CCK-Cholecystokinin tetrapeptide (CCK-4) has been reported to have an enhanced panicogenic effect in panic disorder . Like sodium lactateand CO 2 -induced panic, CCK-4-induced attacks are accompanied by hyperventilation and resemble the pattern of panic symptoms induced by CO 2 administration . In contrast to the "respiratory" panicogens sodium lactate and CO 2 (Coplan and Klein 1996), CCK has been further reported to activate the hypothalamic-pituitary-adrenocortical (HPA) system (de Montigny 1989;Koszycki et al. 1996;Kellner et al. 1997). It has been suggested that this effect is primarily pharmacological and unrelated to the experimentally-induced panic (Abelson et al. 1994). However, in healthy control subjects, enhanced corticotropin (ACTH) and cortisol secretion has been linked recently to panic-like symptoms (Koszycki et al. 1998).To further characterize the role of the HPA system in experimentally-induced panic attacks in patients with panic disorder we compared ACTH and cortisol concentrations in patients with and without CCK-4-induced panic attacks. METHODSTwenty-four patients (nine women and fifteen men; mean age ϭ 38.1 years, SD ϭ 10.8) with a diagnosis of panic disorder but without a comorbid axis I disorder, as assessed with the Structured Clinical Interview for DSM-IV (Wittchen et al. 1997) were studied. These subjects had been medication-free for at least 10 days and had undergone thorough medical examination to rule out other illnesses, drug intake, and lifestyles that could interfere with the study. The protocol was approved by the local ethics committee for human experiments. After complete description of the study to the subjects, written informed consent was obtained.All subjects were studied from 9:00 a.m. to 1:00 p.m. in a supine position in a soundproof room with a single bed (Kellner et al. 1995(Kellner et al. , 1997Ströhle et al. 1998bStröhle et al. , 1999. Each su...

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Section: Discussionmentioning

confidence: 99%

Increased ACTH Concentrations Associated with Cholecystokinin Tetrapeptide-Induced Panic Attacks in Patients with Panic Disorder

Ströhle

Holsboer

Rupprecht

2000

Neuropsychopharmacology

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“…Systemic CCK increases pituitary hormone release via CCK-1 receptor-mediated activation of vagal afferent inputs to the caudal medulla that recruit central ascending viscerosensory pathways to the hypothalamus [43;44;45;46;47;48]. In 1986 it was reported that synthetic CCK administered peripherally at supraphysiological doses potently stimulates pituitary OT (but not AVP) secretion in rats [49]. The OT secretory responses to CCK administration were markedly attenuated after bilateral subdiaphragmatic vagotomy, after capsaicin-induced sensory vagotomy, or after systemic blockade of CCK-1 receptors [49;50].…”

Section: Viscerosensory Recruitment Of Neural Inputs To the Endocrinementioning

confidence: 99%

“…In rats, systemic CCK increases the firing rate of magnocellular OT neurons, and transiently inhibits the firing of magnocellular AVP neurons [51]. Plasma OT levels also are increased by gastric distension, which synergizes with exogenous CCK to further elevate plasma OT in rats [49]. In addition to increasing plasma OT levels, systemic CCK administration alters pituitary release of growth hormone and thyrotropin in adult male rats [52;53;54].…”

Section: Viscerosensory Recruitment Of Neural Inputs To the Endocrinementioning

confidence: 99%

Visceral sensory inputs to the endocrine hypothalamus

Rinaman

2007

Frontiers in Neuroendocrinology

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Interoceptive feedback signals from the body are transmitted to hypothalamic neurons that control pituitary hormone release. This review article describes the organization of central neural pathways that convey ascending visceral sensory signals to endocrine neurons in the paraventricular (PVN) and supraoptic nuclei (SON) of the hypothalamus in rats. A special emphasis is placed on viscerosensory inputs to corticotropin releasing factor (CRF)-containing PVN neurons that drive the hypothalamic-pituitary-adrenal axis, and on inputs to magnocellular PVN and SON neurons that release vasopressin (AVP) or oxytocin (OT) from the posterior pituitary. The postnatal development of these ascending pathways also is considered.

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“…Though the supraoptic and paraventricular nuclei themselves possess CCK receptors (Day et al, 1989;, systemically administered CCK is unlikely to access them directly, since these sites are within the blood-brain barrier. Instead CCK probably influences hormone secretion by a primary action at one of the circumventricular sites which lack an effective blood-brain barrier, or at the peripheral endings of the afferent vagus (Verbalis et al, 1986b;Carter & Lightman, 1987). Thus, it has been possible to show the induction of Fos-LI in the area postrema, a circumventricular organ, and in the dorsal vagal complex, that contains the NTS, following administration of CCK (Luckman, 1992 Luckman et al, 1993).…”

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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Oxytocin Secretion in Response to Cholecystokinin and Food: Differentiation of Nausea from Satiety

Cited by 348 publications

References 19 publications

Increased ACTH Concentrations Associated with Cholecystokinin Tetrapeptide-Induced Panic Attacks in Patients with Panic Disorder

Increased ACTH Concentrations Associated with Cholecystokinin Tetrapeptide-Induced Panic Attacks in Patients with Panic Disorder

Visceral sensory inputs to the endocrine hypothalamus

Involvement of cholecystokinin receptor types in pathways controlling oxytocin secretion

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