Cholecystokinin stimulates and inhibits lordosis behavior in female rats

Bloch, George J.; Babcock, Alex M.; Gorski, Roger A.; Micevych, Paul E.

doi:10.1016/0031-9384(87)90012-6

Cited by 63 publications

(28 citation statements)

References 36 publications

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“…These studies support the hypothesis that the estrogen activation of MOP is part of the mechanism involved in the normal facilitation of lordosis by estrogen and progesterone. Unlike the rat, however, maximal lordosis behavior is not induced by prolonged superphysiological estrogen priming in mice [17,18], indicating that activation of progesterone receptors in the mouse is obligatory for maximal sexual receptivity. Thus, one possible mechanism for the role of MOP is that estrogen-induced MOP activation may be involved in the estrogen-induced upregulation of progesterone receptors through which progesterone acts to facilitate lordosis.…”

Section: Discussionmentioning

confidence: 95%

Sexual receptivity is reduced in the female mu-opioid receptor knockout mouse

Sinchak¹,

Shahedi²,

Dewing³

et al. 2005

NeuroReport

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Activation of mu-opioid receptors is critical to steroid regulation of female sexual behavior, lordosis, in rodents. Estrogen treatment activates mu-opioid receptors in the medial preoptic area inhibiting lordosis, but ultimately appears important for progesterone facilitation of lordosis. We investigated the role of mu-opioid receptors in the expression of sexual receptivity in mice lacking mu-opioid receptors. Although estrogen and progesterone facilitated lordosis in mu-opioid receptor knockout mice, they exhibited deficits in lordosis quotient and score compared with wild-type females, indicating reduced sexual receptivity. In contrast, wild-type and mu-opioid receptor knockout female mice did not differ in either active or passive avoidance of the male. These data are most consistent with the hypothesis that mu-opioid receptor activation is necessary for estrogen and progesterone to maximally facilitate lordosis.

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Section: Discussionmentioning

confidence: 95%

Sexual receptivity is reduced in the female mu-opioid receptor knockout mouse

Sinchak¹,

Shahedi²,

Dewing³

et al. 2005

NeuroReport

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“…Our present results provide direct evidence in support of this mechanism for OT pathways as well, and strongly suggest that CCK causes a widespread activation of oxytocinergic neurons within the brain in addition to its obvious effects to stimulate pituitary OT secretion. In this regard, it is also interesting that recent studies have demonstrated that systemic CCK stimulates maternal behavior (28), and under some circumstances lordosis behavior (29), in rats. In conjunction with the well-known effects of central OT injections to stimulate both of these behaviors (30,31), these findings further suggest that systemic CCK administration stimulates secretion of OT from terminals within the CNS.…”

Section: Discussionmentioning

confidence: 99%

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

Verbalis

Stricker

Robinson

et al. 1991

J Neuroendocrinology

192

101

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The effect of systemically-administered cholecystokinin octapeptide (CCK) on hypothalamic oxytocin, vasopressin, and corticotropinreleasing hormone neurons was studied by analysis of c-fos antigen expression in immunocytochemically-characterized neurons in the supraoptic and paraventricular nuclei. CCK (100 pglkg intraperitoneally) caused a marked increase in nuclear c-fos immunocytochemical staining, which peaked at 60 to 90 min after injection. C-fos expression was found in most magnocellular oxytocin neurons in the supraoptic nucleus and in all magnocellular subdivisions of the paraventricular nucleus, but in no vasopressin neurons in either area. C-fos expression was also found in several parvocellular subdivisions of the paraventricular nucleus: in oxytocin neurons within the medial and lateral, but not the dorsal, parvocellular subdivisions, and in corticotropinreleasing hormone neurons in the medial parvocellular subdivision. Injection of lower doses of CCK showed that c-fos expression closely paralleled the pattern of pituitary oxytocin secretion in response to CCK, with a threshold for activation at 1 pglkg, near maximal responses by lopglkg, and maximal responses by 100pglkg. These studies demonstrate that the pattern of c-fos expression in hypothalamic magnocellular neurons following systemic CCK administration mirrors the neurosecretory response of these neurons, both with regard to specificity for the peptides secreted as well as intensity of secretion. They also demonstrate that systemic CCK administration activates c-fos expression in parvocellular oxytocin and corticotropin-releasing hormone neurons, and therefore likely causes secretion of oxytocin and corticotropin-releasing hormone within the brain at the terminal fields of these neurons.Previous studies from this and other laboratories have shown that systemic administration of cholecystokinin (CCK) stimulates pituitary secretion of oxytocin (OT) but not vasopressin (AVP) in rats (1, 2). Electrophysiological recordings from hypothalamic supraoptic nucleus (SON) neurons have confirmed that CCK causes activation of magnocellular neurons rather than simply releasing OT from pituitary axon terminals (3). Additional studies have demonstrated that the well-known effects of CCK to inhibit food intake (4) and gastric emptying and motility (5-7) are correlated with its effects to stimulate pituitary OT secretion (1, 5, 7-10). However, because peripheral infusions of OT do not affect either food intake (10) or gastric motility (11) in rats, we have postulated that centrally-projecting parvocellular OT neurons may be activated in concert with the pituitary-projecting magnocellular neurons to produce or modulate these diverse behavioral and physiological effects (8, 12).Recent studies have demonstrated that the antigen of the protooncogene c-fos is expressed in the nucleus of many activated neurons, including those in the hypothalamus (13). The present studies utilized immunohistochemical staining for c-fos antigen (14) to identify those hypothal...

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“…Considerable experimental evidence suggests that the medial amygdala and bed nucleus of the stria terminalis, particularly the region of the BSTe, exert facilitory influences on luteinizing hormone secretion [15, 26. CCK has also been implicated in the control of female copulatory behavior. Systemic treatments of estrogenprimed, progesterone-treated female rats with CCK octapeptide have been shown both to stimulate [38] or to inhibit [7] lordosis responses, depending on the timing and dosage of the administered steroid. While there is general agreement that the MPNc functions to suppress the expres sion of lordosis [see ref.…”

Section: Discussionmentioning

confidence: 99%

Estrous Cycle Variations in Levels of Cholecystokinin Immunoreactivity within Cells of Three Interconnected Sexually Dimorphic Forebrain Nuclei

1988

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The central part of the medial preoptic nucleus (MPNc), the encapsulated part of the bed nucleus of the stria terminalis (BSTe), and the posterodorsal part of the medial nucleus of the amygdala (MeAp) are all thought to be involved in the neural control of female reproductive behavior, as well as other neuroendocrine mechanisms. Although the developmental importance of gonadal steroids during the perinatal period on these sexual dimorphisms is well known, an understanding of possible activational effects on these cell groups of circulating gonadal steroids in the adult is less clear. In the present study we evaluated the number of cholecystokinin (CCK)-immunoreactive cells present within MPNc, BSTe, and MeAp of regularly cycling female rats over the estrous cycle. In addition, the effects of ovariectomy and estrogen replacement on CCK staining were also examined. The number of CCK-immunoreactive cells within each cell group varied over the estrous cycle with the fewest cells present in animals sacrificed while in diestrus. Proestrous female rats showed a greater number of cells within each nucleus, while intermediate numbers were found for animals in estrus. These changes appear to be due, at least in part, to changes in levels of circulating estrogen, since subcutaneous implants of estradiol prevented the decline in the number of CCK-stained cells within MPNc, BSTe, and MeAp that was seen in untreated, ovariectomized female rats. Thus, the present findings support the hypothesis that levels of CCK within cells of these three sexually dimorphic cell groups are regulated by circulating gonadal steroids within a physiologically relevant time frame and may possibly contribute to the activation of female reproductive behavior as well as other neuroendocrine functions.

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Cholecystokinin stimulates and inhibits lordosis behavior in female rats

Cited by 63 publications

References 36 publications

Sexual receptivity is reduced in the female mu-opioid receptor knockout mouse

Sexual receptivity is reduced in the female mu-opioid receptor knockout mouse

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

Estrous Cycle Variations in Levels of Cholecystokinin Immunoreactivity within Cells of Three Interconnected Sexually Dimorphic Forebrain Nuclei

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