Effects of preoptic injections of gastrin, cholecystokinin, secretin, vasoactive intestinal peptide and PHI on the secretion of luteinizing hormone and prolactin in ovariectomized estrogen-primed rats

Kimura, Fukuko; Mitsugi, Naoto; Ai, Jun; Akema, Tatsuo; Yoshida, Kumiko

doi:10.1016/0006-8993(87)90330-1

Cited by 56 publications

(32 citation statements)

References 26 publications

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“…Interestingly, co-expression of secretin and secretin receptor is also detected in chicken testis, suggesting that secretin may act as an autocrine/paracrine factor involved in the regulation of testis functions (Wang et al 2012), similar to what is observed in rat (Chow et al 2004). In ovariectomized estrogen-primed rats, secretin injection into the preoptic nucleus could increase the circadian rise of luteinizing hormone release (Kimura et al 1987). In human, secretin has been suggested to be involved in the stimulation of ovulation as a concurrent surge of plasma secretin and serum estradiol has been observed (Holst et al 1989a), and it inhibits prolactin release during follicular and luteal phases of the menstrual cycle (Holst et al 1991).…”

Section: Secretin In Other Peripheral Organssupporting

confidence: 59%

MOLECULAR EVOLUTION OF GPCRS: Secretin/secretin receptors

Tam

Lee

Jin

et al. 2014

Journal of Molecular Endocrinology

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In mammals, secretin is a 27-amino acid peptide that was first studied in 1902 by Bayliss and Starling from the extracts of the jejunal mucosa for its ability to stimulate pancreatic secretion. To date, secretin has only been identified in tetrapods, with the earliest diverged secretin found in frogs. Despite being the first hormone discovered, secretin's evolutionary origin remains enigmatic, it shows moderate sequence identity in nonmammalian tetrapods but is highly conserved in mammals. Current hypotheses suggest that although secretin has already emerged before the divergence of osteichthyans, it was lost in fish and retained only in land vertebrates. Nevertheless, the cognate receptor of secretin has been identified in both actinopterygian fish (zebrafish) and sarcopterygian fish (lungfish). However, the zebrafish secretin receptor was shown to be nonbioactive. Based on the present information that the earliest diverged bioactive secretin receptor was found in lungfish, and its ability to interact with both vasoactive intestinal peptide and pituitary adenylate cyclase-activating polypeptide potently suggested that secretin receptor was descended from a VPAC-like receptor gene before the Actinopterygii-Sarcopterygii split in the vertebrate lineage. Hence, secretin and secretin receptor have gone through independent evolutionary trajectories despite their concurrent emergence post-2R. A functional secretin-secretin receptor axis has probably emerged in the amphibians. Although the pleiotropic actions of secretin are well documented in the literature, only limited information of its physiological functions in nonmammalian tetrapods have been reported. To decipher the structural and functional divergence of secretin and secretin receptor, functional characterization of the ligandreceptor pair in nonmammals would be the next perspective for investigation.

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Section: Secretin In Other Peripheral Organssupporting

confidence: 59%

MOLECULAR EVOLUTION OF GPCRS: Secretin/secretin receptors

Tam

Lee

Jin

et al. 2014

Journal of Molecular Endocrinology

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“…The secretory activity of lactotrope cells is also regulated by various hypothalamic neuropeptides (Ruberg et al, 1981;Hinuma et al, 1998;Galas et al, 2009). In particular, VIP and to a lesser extent PHI and secretin stimulate PRL secretion (Vijayan et al, 1979;Enjalbert et al, 1980;Kimura et al, 1987;Muratori et al, 1994;Judd, 1995;Youngren et al, 1998). In fact, PACAP is more potent than other members of the family in stimulating PRL secretion because intrave- Miyata et al, 1989;Culler and Paschall, 1991;Canny et al, 1992;Gracia-Navarro et al, 1992;Leonhardt et al, 1992;Perrin et al, 1993;Rawlings et al, 1993;Hashizume et al, 1994;Garrel et al, 2002 Somatotrope cells 1 cAMP, 1 ͓Ca 2ϩ ͔ i 1/3 GH release Miyata et al, 1989;Canny et al, 1992;Goth et al, 1992;Gracia-Navarro et al, 1992;Hart et al, 1992;Jarry et al, 1992;Leonhardt et al, 1992;Nagy et al, 1993;Rawlings et al, 1993;Wei et al, 1993;Yada et al, 1993;Hashizume et al, 1994;Velkeniers et al, 1994;Rousseau et al, 1999;Wong et al, 2005; Miyata et al, 1989;Gracia-Navarro et al, 1992;Hart et al, 1992;Jarry et al, 1992;<...>…”

Section: B Effects Of Pituitary Adenylate Cyclase-activating Polypepmentioning

confidence: 99%

Pituitary Adenylate Cyclase-Activating Polypeptide and Its Receptors: 20 Years after the Discovery

et al. 2009

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“…With use of the general method outlined by Kimura et al (1987), the ovaries were resected bilaterally at 6 weeks of age. Each rat was anesthetized with ethyl ether before being placed on its ventral surface without restraint.…”

Section: Animalsmentioning

confidence: 99%

17β-Estradiol Mediates the Sex Difference in Capsaicin-Induced Nociception in Rats

Lu¹,

Chen²,

Wang³

et al. 2009

J Pharmacol Exp Ther

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We have previously shown that the male sex steroid testosterone inhibits slightly, but the female sex steroid 17␤-estradiol (E 2 ) potentiates dramatically, the capsaicin receptor-mediated current in rat dorsal root ganglion (DRG) neurons. Here, we used pharmacological methods and the nociceptive behavioral test to determine whether there is a sex difference in capsaicininduced acute pain in rats in vivo and what mechanism underlies this sex difference. Results revealed that intradermal injection of capsaicin induced a dose-dependent nocifensive response in males and females, with the dose required to produce a comparable level of nociception being approximately 3-to 4-fold higher in males than in females. In addition, females during the proestrus stage exhibited significantly greater capsaicin-induced nocifensive responses compared with the estrus stage. Moreover, the female's enhanced sensitivity to the capsaicin-induced nocifensive response was completely reversed by ovariectomy 6 weeks before capsaicin injection. It is noteworthy that intradermal coinjection of E 2 but not progesterone with capsaicin potentiated the capsaicininduced nocifensive response in ovariectomized rats. Likewise, intradermal E 2 injection dose-dependently potentiated the capsaicin-induced nocifensive response in male rats. Furthermore, potentiation by E 2 of the capsaicin-induced nocifensive response in male rats was not significantly reduced by a selective protein kinase C (PKC) inhibitor or by a selective protein kinase A (PKA) inhibitor, indicating that neither PKC nor PKA was involved in the effect of E 2 . These data demonstrate that E 2 mediates the female's enhanced sensitivity to capsaicin-induced acute pain, consistent with potentiation by E 2 of the capsaicin receptor-mediated current in rat DRG neurons.

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Effects of preoptic injections of gastrin, cholecystokinin, secretin, vasoactive intestinal peptide and PHI on the secretion of luteinizing hormone and prolactin in ovariectomized estrogen-primed rats

Cited by 56 publications

References 26 publications

MOLECULAR EVOLUTION OF GPCRS: Secretin/secretin receptors

MOLECULAR EVOLUTION OF GPCRS: Secretin/secretin receptors

Pituitary Adenylate Cyclase-Activating Polypeptide and Its Receptors: 20 Years after the Discovery

17β-Estradiol Mediates the Sex Difference in Capsaicin-Induced Nociception in Rats

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