Cholecystokinin in Discrete Rat Brain Regions as a Function of Sex and Estrous Cycle

Siegel, Richard A.; Frankfurt, Maya; Pahnke, Ulrich; Wuttke, W.

doi:10.1111/j.1749-6632.1985.tb29977.x

Cited by 13 publications

(6 citation statements)

References 4 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has been suggested also that the level of oestradiol influences the satiating effect of CCK-SS (Butera et al 1993;Geary et al 1994). In addition, it has been shown that CCK concentrations are higher in all hypothalamic areas in female than in male rats (McLaughlin et al 1985) and that these vary in several brain regions during the cycle in female rats (Siegel et al 1985). These findings thus confirm the impact of sex hormones on the control of food intake by CCK.…”

Section: Discussionsupporting

confidence: 77%

Obesity induced by unspecific early postnatal overfeeding in male and female rats: hypophagic effect of CCK-8S

Voits

Forster

Rödel

et al. 1996

Naunyn-Schmiedeberg's Arch Pharmacol

View full text Add to dashboard Cite

The response to cholecystokinin (CCK) as a satiety peptide in obesity or anorexia has been tested mainly in extreme models of food intake control. In the present study, the effect of CCK-8S on food intake was investigated in a nongenetic and less-stressful model of obesity due to unspecific early postnatal overfeeding in male and female rats. Reducing the normal litter size of ten to three newborn rats on day 3 of life led to an enhanced food intake resulting in an increased body weight until adulthood. Freely fed male and female, normal and obese rats were given 10 micrograms/kg CCK-8S i.p. on day 41 and 40 micrograms/kg CCK-8S on day 91 of life and food intake was measured for 24 h. Compared with treatment with saline (i.p.) 1 day before the test, the lower dose of 10 micrograms/kg CCK-8S reduced food intake for 2 h in normal, but not in obese rats. Conversely, the higher dose of 40 micrograms/kg CCK-8S reduced food intake in both normal and obese rats for 2 h, but this effect was more evident in the obese rats. Moreover, the satiating effect of CCK-8S was more pronounced and longer lasting in male than in female rats. In summary, the data suggest that the response to CCK-8S differs in normal and obese rats and depends on sex.

show abstract

Section: Discussionsupporting

confidence: 77%

Obesity induced by unspecific early postnatal overfeeding in male and female rats: hypophagic effect of CCK-8S

Voits

Forster

Rödel

et al. 1996

Naunyn-Schmiedeberg's Arch Pharmacol

View full text Add to dashboard Cite

show abstract

“…The VMH has been re ported to contain higher levels of CCK in females ran domly sampled during the estrous cycle when compared with males [31], while Siegel et al [37] found the VMH of males to contain more CCK than the VMH of diestrus fe males. While it is currently unclear why these findings di verge.…”

Section: Discussionmentioning

confidence: 99%

“…1986 Accepted after revision: October 14, 1986 CCK release. Moreover, the CCK content of the VMH va ries between male and female rats and fluctuates during the estrous cycle [12,30,37], suggesting that levels of CCK in the VMH may be affected by fluctuations in circulating lev els of steroid hormones.…”

mentioning

confidence: 99%

Estrous Cyclicity of <sup>125</sup>I-Cholecystokinin Octapeptide Binding in the Ventromedial Hypothalamic Nucleus

Akesson¹,

Mantyh²,

Mantyh³

et al. 1987

Neuroendocrinology

View full text Add to dashboard Cite

Although there is a good correlation between the levels of gonadal steroids and sex differences in reproductive behavior and food intake, the neurochemical mechanisms by which a gonadal steroid may regulate these behaviors remain unknown. An important central nervous site for steroid modulation of food intake and reproduction is the ventromedial nucleus of the hypothalamus (VMH). Recently it has been suggested that some of the activities of the VMH are dependent on the neuroactive peptide cholecystokinin octapeptide (CCK). High levels of CCK in the VMH have been measured by radioimmunoassay, and immunohistochemical analysis has revealed a dense plexus of CCK fibers and terminals which appose and make synaptic contact with VMH neurons. There is, however, a paucity of information concerning the presence of CCK-binding sites in the VMH. This study demonstrates high levels of ¹²⁵I-CCK8 binding in the VMH of male and female rats. Tissue sampled on the morning of estrus revealed depressed levels of CCK binding, and, while ovariectomy itself did not affect binding, ovariectomy followed by estrogen replacement depressed CCK binding. These results provide evidence for an estrogenic effect on CCK-binding sites that may help elucidate a role of CCK in the VMH.

show abstract

“…Signeau, and Gepts, 1975) and this distribution is sexually dimorphic in the limbic-hypothalamic continuum (Frankfurt, Siegel, Sim. and Wuttke, 1985;Micevych, Matt, and Go, 1988;Siegel, Frankfurt, Pahnke, and Wuttke, 1985). Sex differences in the number of CCK-im-munoreactive cells have been described in the bed nucleus of the stria terminalis, medial preoptic nucleus, preoptic periventricular nucleus, posterior magnocellular subdivision of the paraventricular hypothalamic nucleus, and the ventromedial nucleus of the hypothalamus (VMN) ( Micevych, Park, Akesson, and Eldc, 1987;Micevych, Akesson, and Elde, 1988).…”

Section: Introductionmentioning

confidence: 99%

Role of postnatal androgens in sexual differentiation of the lordosis‐inhibiting effect of central injections of cholecystokinin

Ulibarri¹,

Popper²,

Micevych³

1990

J. Neurobiol.

View full text Add to dashboard Cite

The neuropeptide cholecystokinin (CCK) inhibits lordosis behavior when infused into the ventromedial nucleus of the hypothalamus (VMN) of female rats and has no effect when infused into the VMN of male rats. To test whether this sex difference develops under the control of perinatal steroids, male rats were castrated or given sham surgeries within 3 h of birth and female rats were injected with either 0 or 100 micrograms testosterone propionate on postnatal day 5. As adults, these rats were castrated as necessary, implanted with unilateral cannulae directed at the VMN, and tested for their ability to display female sexual behavior and to respond to CCK. Neonatal castration of males prevented defeminization of this response. When treated with 5 micrograms estradiol benzoate (EB), neonatally castrated males showed both lordosis behavior and a profound inhibition of that behavior after infusions of CCK. Neonatally castrated males did not display lordosis behavior when treated with 2 micrograms EB. Control males showed no lordosis behavior and, therefore, no response to CCK. Both doses of EB induced lordosis behavior in neonatally androgenized females. Significantly, these neonatally androgenized females were less responsive to CCK's inhibition of lordosis and were also anovulatory. These results imply that androgens alter the development of CCK responsive circuits as well as defeminize cyclic gonadotropin release. Levels of 125I-sCCK-8 binding in the VMN were correlated closely with an individual's ability to respond to sCCK-8. In summary, the inhibition of female sexual behavior caused by exogenously administered CCK in normal adult female rats appears to be controlled at least partially by levels of CCK receptors in the VMN and to differentiate under the control of perinatally present testosterone.

show abstract

Cholecystokinin in Discrete Rat Brain Regions as a Function of Sex and Estrous Cycle

Cited by 13 publications

References 4 publications

Obesity induced by unspecific early postnatal overfeeding in male and female rats: hypophagic effect of CCK-8S

Obesity induced by unspecific early postnatal overfeeding in male and female rats: hypophagic effect of CCK-8S

Estrous Cyclicity of <sup>125</sup>I-Cholecystokinin Octapeptide Binding in the Ventromedial Hypothalamic Nucleus

Role of postnatal androgens in sexual differentiation of the lordosis‐inhibiting effect of central injections of cholecystokinin

Contact Info

Product

Resources

About