Cholecystokinin B Receptor Gene Expression in Hypothalamic Neurosecretory Neurons after Experimental Manipulations

Meister, Björn; Broberger, Christian; Villar, Marcelo J.; Hökfelt, Tomas

doi:10.1159/000126782

Cited by 20 publications

(6 citation statements)

References 46 publications

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“…The expression of peptides and their receptors shows a high degree of plasticity as reported in the brain, including magnocellular hypothalamic neurons (Hinks et al, 1995;Larsen et al, 1992aLarsen et al, ,b, 1993Meister et al, 1990Meister et al, , 1994Villar et al, 1990) and in the periphery . The present results clearly demonstrate that GAL-R1-Rs in the magnocellular hypothalamic neurons can also be regulated by various types of manipulations (Fig.…”

Section: Regulation and Functional Role Of Gal-r1 Receptors And Galaninmentioning

confidence: 88%

Galanin-R1 receptor in anterior and mid-hypothalamus: Distribution and regulation

1998

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The distribution and regulation of galanin-R1 receptor (GAL-R1-R) mRNA has been studied in the anterior and mid-diencephalon by using in situ hybridization. Moreover, possible colocalization of GAL-R1-R mRNA and prepro-galanin or vasopressin mRNAs has been analyzed at the cellular level using double in situ hybridization methodology. Many nuclei in the hypothalamus expressed GAL-R1-R mRNA, including the paraventricular nucleus (PVN) and the supraoptic nucleus (SON). Strong expression was also seen in the same sections in various areas outside of the diencephalon. The distribution patterns are similar to those described in earlier studies. Double labeling experiments showed GAL-R1-R mRNA in vasopressin neurons in the PVN and SON. Moreover, GAL-R1-R mRNA and prepro-galanin mRNA were colocalized in several hypothalamic nuclei. GAL-R1-R mRNA levels showed a high degree of plasticity. Thus, salt loading resulted in a marked increase in GAL-R1-R mRNA levels in the PVN and SON and a moderate decrease was seen during lactation. In contrast, hypophysectomy caused a decrease in GAL-R1-R mRNA levels. Differential effects of colchicine were recorded with a decrease of GAL-R1-R mRNA in the magnocellular hypothalamic neurons. After salt loading or during lactation, GAL-R1-R mRNA and prepro-galanin mRNA were regulated in parallel, whereas their levels changed in opposite directions after hypophysectomy and colchicine injection. In conclusion, GAL-R1-Rs are present in several hypothalamic nuclei, partly in neurons synthesizing galanin. The receptors are regulated in a specific fashion in the various nuclei, depending on the stimulus applied. The results suggest that the effect of galanin in the hypothalamus partly depends on the state of receptor expression.

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Section: Regulation and Functional Role Of Gal-r1 Receptors And Galaninmentioning

confidence: 88%

Galanin-R1 receptor in anterior and mid-hypothalamus: Distribution and regulation

1998

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“…Further, in vitro autoradiography proved the presence of CCK receptors in the PVN and studies using quantitative in situ hybridization unveiled nutrient dependent changes in the synthesis of the CCK-B receptor in the PVN [17, 18]. These neuroanatomical observations and the lack of effect of the CCK-A receptor antagonist on colonic transit when microinfused into the PVN in the present study indicate, that CCK released from terminal endings of neurons in the PVN which subsequently acts on CCK-B receptors within this brain area is involved in the CNS regulation of colonic motility.…”

Section: Discussionmentioning

confidence: 99%

“…Experimental evidence has been provided that CCK is released in the PVN in response to a meal, and that CCK in the periphery may also induce release of this peptide in hypothalamic regions including the PVN [31]. Further, the PVN is well established to play a role in CNS regulation of GI motility and feeding, and nutrient dependent changes in the synthesis of the CCK-B but not the CCK-A receptor have been demonstrated in the PVN [11, 14, 18]. Also, endogenous CCK causes satiety by an agonist action on CCK-B receptors in the brain [28], and it has been shown that activation of hypothalamic but not brainstem neurons induced by CCK administered systemically could be attenuated by central application of a CCK-B receptor antagonist [33].…”

Section: Discussionmentioning

confidence: 99%

“…Morphological studies revealed the presence of CCK-like immunoreactivity (LI) positive nerves and fibers as well as CCK receptors in the PVN, and physiological experiments indicate that CCK released in this brain area plays a role in CNS control of food intake [13, 16, 17, 18]. Further, there is considerable evidence suggesting that CCK acts on oxytocin neurons in the hypothalamic paraventricular nucleus to modulate upper GI tract motility [19].…”

Section: Introductionmentioning

confidence: 99%

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Involvement of CCK in the Paraventricular Nucleus of the Hypothalamus in the CNS Regulation of Colonic Motility

Mönnikes

Tebbe²,

Grote³

et al. 2000

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The effects of cholecystokinin octapeptide (CCK₈), the CCK-A receptor antagonist, MK-329, and the CCK-B receptor antagonist, L-365, 260, microinfused into the paraventricular nucleus of hypothalamus (PVN) on colonic motor function was investigated in awake rats, chronically implanted with a microinjection cannula into the PVN and a catheter into the proximal colon. In fasted rats, bilateral microinfusion of CCK₈ at doses of 1.5 and 3.0 μg/rat into the PVN stimulated colonic transit, as shown by a significant increase in the geometric center by 47 and 54%, respectively. This effect of CCK₈ was site-specific to the PVN, since microinjection of the peptide into sites outside of but adjacent to PVN had no effect. In non-fasted rats, L-365,260 bilaterally microinjected into the PVN at a dose of 1.5 μg/rat inhibited propulsive colonic motor function; colonic transit time significantly increased by 73% in comparison to the control condition. Microinfusion of the CCK-A antagonist into in the PVN did not affect colonic transit. These results show that the PVN is a responsive site for the central CCK₈-induced modulation of colonic motility. The data suggest, that endogenous CCK in the paraventricular nucleus of the hypothalamus unfolds a stimulatory effect on colonic transit through action on CCK-B receptors.

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“…In the hypothalamus, both CCK‐A and CCK‐B receptor gene expression has been detected in the paraventricular nucleus (PVN) (Meister et al ., 1994). In addition, intraperitoneal administration of CCK‐8 activates catecholaminergic neurons in the caudal medulla projecting to the PVN (Rinaman et al ., 1995).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of the hypothalamic‐pituitary‐adrenal axis in food‐deprived rats by a CCK‐A receptor antagonist

Ruiz‐Gayo

Garrido

Fuentes

2000

British J Pharmacology

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1 The circadian activity of the hypothalamic-pituitary-adrenal (HPA) axis is regulated by caloric ow in rats. During the dark cycle, it has been shown that, in fasted rats, the time-course pro®le of plasma concentrations of adrenocorticotropin (ACTH) and corticosterone parallels the pro®le of food intake in ad libitum fed animals. 2 Cholecystokinin (CCK) is involved in regulating food intake in rodents. CCK-8 reduces food intake by acting on CCK-A receptors subtype. 3 This work aims at establishing an eventual relationship between the modulatory role of CCK on food intake and its eect on HPA axis activity during fasting. 4 We studied the eect of CCK-A and CCK-B receptor antagonists on food intake during the ®rst period of the dark cycle. Under these conditions we observed that the CCK-A receptor antagonist, SR-27897 (0.3 mg kg 71), but not the CCK-B receptor antagonist, L-365260 (1 mg kg 71 ), increases food-intake. 5 In a second series of experiments we observed that the increase of both ACTH and corticosterone plasma level elicited by fasting, was prevented by SR-27897, but not by L-365260. 6 These results indicate that CCK-A receptor blockade during fasting prevents the activation of the HPA axis.

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Cholecystokinin B Receptor Gene Expression in Hypothalamic Neurosecretory Neurons after Experimental Manipulations

Cited by 20 publications

References 46 publications

Galanin-R1 receptor in anterior and mid-hypothalamus: Distribution and regulation

Galanin-R1 receptor in anterior and mid-hypothalamus: Distribution and regulation

Involvement of CCK in the Paraventricular Nucleus of the Hypothalamus in the CNS Regulation of Colonic Motility

Inhibition of the hypothalamic‐pituitary‐adrenal axis in food‐deprived rats by a CCK‐A receptor antagonist

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