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Gunter Emons - One of the best experts on this subject based on the ideXlab platform.
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Luteinizing Hormone-Releasing Hormone Receptor-Targeted Chemotherapy Using AN-152
Neuroendocrinology, 2009Co-Authors: Gunter Emons, Andrew V. Schally, Herbert Sindermann, Jürgen Engel, Carsten GrundkerAbstract:The Luteinizing Hormone-releasing Hormone (LHRH; also known as gonadotropin-releasing Hormone) receptor can be utilized for targeted chemotherapy with cytotoxic LHRH analogues such as AN-152, in which
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expression of receptors for Luteinizing Hormone releasing Hormone in human ovarian and endometrial cancers frequency autoregulation and correlation with direct antiproliferative activity of Luteinizing Hormone releasing Hormone analogues
American Journal of Obstetrics and Gynecology, 2002Co-Authors: Peter Volker, Carsten Grundker, Oswald Schmidt, Klausdieter Schulz, Gunter EmonsAbstract:Abstract Objective: Several recent reports have demonstrated the expression of Luteinizing Hormone-releasing Hormone receptors by human ovarian and endometrial cancers. Controversy persists on the relevance of this finding, in particular whether these receptors mediate direct antiproliferative effects of Luteinizing Hormone-releasing Hormone analogues. We correlated the expression of Luteinizing Hormone-releasing Hormone receptors by well-characterized ovarian and endometrial cancer cell lines with the ability of Luteinizing Hormone-releasing Hormone analogues to reduce their proliferation and studied the autoregulation of Luteinizing Hormone-releasing Hormone receptor expression by Luteinizing Hormone-releasing Hormone agonist triptorelin and antagonist cetrorelix. The expression of Luteinizing Hormone-releasing Hormone receptors was assessed in a series of specimens from primary ovarian and endometrial cancers. Study Design: Luteinizing Hormone-releasing Hormone receptor expression was assessed by semiquantitative reverse transcriptase–polymerase chain reaction and radioligand binding assay. Antiproliferative effects were ascertained by proliferation assays in the absence or presence of Luteinizing Hormone-releasing Hormone analogues. Results: Ovarian (4/6 cell lines) and endometrial (5/6 cell lines) cancer cell lines expressed Luteinizing Hormone-releasing Hormone receptors. The proliferation of these Luteinizing Hormone-releasing Hormone receptor–positive cell lines was dose- and time-dependently reduced by agonistic and antagonistic Luteinizing Hormone-releasing Hormone analogues. Luteinizing Hormone-releasing Hormone receptor density was reduced to 80% of controls (control, 100 %; P Conclusion: These findings suggest that Luteinizing Hormone-releasing Hormone receptors that are expressed by human ovarian and endometrial cancer cell lines mediate direct antiproliferative effects of Luteinizing Hormone-releasing Hormone analogues. Because most respective primary cancers expressed Luteinizing Hormone-releasing Hormone receptors, these receptors might be used for novel antiproliferative therapeutic approaches and should be further evaluated. (Am J Obstet Gynecol 2002;186:171-9.)
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Antitumor effects of the cytotoxic Luteinizing Hormone-releasing Hormone analog AN-152 on human endometrial and ovarian cancers xenografted into nude mice.
American journal of obstetrics and gynecology, 2002Co-Authors: Carsten Grundker, Andrew V. Schally, Peter Volker, Frank Griesinger, Annette Ramaswamy, Attila Nagy, Gunter EmonsAbstract:Abstract Objective: Most human endometrial and ovarian cancers express receptors for Luteinizing Hormone– releasing Hormone. These receptors can be used for targeted chemotherapy with cytotoxic Luteinizing Hormone–releasing Hormone analogs such as AN-152, in which doxorubicin is linked to [D-Lys 6 ]Luteinizing Hormone–releasing Hormone. Study Design: The antitumor effects of doxorubicin and AN-152 were assessed in vivo in human Luteinizing Hormone–releasing Hormone receptor–positive HEC-1B endometrial cancers and NIH:OVCAR-3 ovarian cancers and in the Luteinizing Hormone–releasing Hormone receptor–negative SK-OV-3 ovarian line. Nude mice bearing these tumors subcutaneously were injected intravenously with saline solution (control), AN-152, or doxorubicin at equimolar doses. Luteinizing Hormone–releasing Hormone receptor expression in tumors and specimens of human reproductive (n = 5) and nonreproductive (n = 15) normal tissues and in hematopoietic stem cells were analyzed with reverse transcriptase–polymerase chain reaction and radioligand binding assay. Results: The tumor volumes of Luteinizing Hormone–releasing Hormone receptor–positive HEC-1B and NIH:OVCAR-3 cancers were reduced significantly ( P Conclusion: Targeted chemotherapeutic Luteinizing Hormone–releasing Hormone analog AN-152 is more effective and less toxic than cytotoxic radical doxorubicin on Luteinizing Hormone–releasing Hormone receptor–positive tumors. AN-152 could be considered for targeted chemotherapy in patients with ovarian or endometrial cancers. (Am J Obstet Gynecol 2002;187:528-37.)
Andrew V. Schally - One of the best experts on this subject based on the ideXlab platform.
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Combining Growth Hormone-Releasing Hormone Antagonist With Luteinizing Hormone-Releasing Hormone Antagonist Greatly Augments Benign Prostatic Hyperplasia Shrinkage
The Journal of urology, 2012Co-Authors: Ferenc G Rick, Luca Szalontay, Karoly Szepeshazi, Marta Zarandi, Norman L. Block, Andrew V. Schally, Mehrdad Nadji, Irving Vidaurre, Magdolna Kovacs, Zoltan RekasiAbstract:Purpose: Benign prostatic hyperplasia often affects aging men. Antagonists of the neuropeptide growth Hormone-releasing Hormone reduced prostate weight in an androgen induced benign prostatic hyperplasia model in rats. Luteinizing Hormone-releasing Hormone antagonists also produce marked, protracted improvement in lower urinary tract symptoms, reduced prostate volume and an increased urinary peak flow rate in men with benign prostatic hyperplasia. We investigated the influence of a combination of antagonists of growth Hormone-releasing Hormone and Luteinizing Hormone-releasing Hormone on animal models of benign prostatic hyperplasia.Materials and Methods: We evaluated the effects of the growth Hormone-releasing Hormone antagonist JMR-132, given at a dose of 40 μg daily, the Luteinizing Hormone-releasing Hormone antagonist cetrorelix, given at a dose of 0.625 mg/kg, and their combination on testosterone induced benign prostatic hyperplasia in adult male Wistar rats in vivo. Prostate tissue was examined bio...
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Luteinizing Hormone-Releasing Hormone Receptor-Targeted Chemotherapy Using AN-152
Neuroendocrinology, 2009Co-Authors: Gunter Emons, Andrew V. Schally, Herbert Sindermann, Jürgen Engel, Carsten GrundkerAbstract:The Luteinizing Hormone-releasing Hormone (LHRH; also known as gonadotropin-releasing Hormone) receptor can be utilized for targeted chemotherapy with cytotoxic LHRH analogues such as AN-152, in which
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Antitumor effects of the cytotoxic Luteinizing Hormone-releasing Hormone analog AN-152 on human endometrial and ovarian cancers xenografted into nude mice.
American journal of obstetrics and gynecology, 2002Co-Authors: Carsten Grundker, Andrew V. Schally, Peter Volker, Frank Griesinger, Annette Ramaswamy, Attila Nagy, Gunter EmonsAbstract:Abstract Objective: Most human endometrial and ovarian cancers express receptors for Luteinizing Hormone– releasing Hormone. These receptors can be used for targeted chemotherapy with cytotoxic Luteinizing Hormone–releasing Hormone analogs such as AN-152, in which doxorubicin is linked to [D-Lys 6 ]Luteinizing Hormone–releasing Hormone. Study Design: The antitumor effects of doxorubicin and AN-152 were assessed in vivo in human Luteinizing Hormone–releasing Hormone receptor–positive HEC-1B endometrial cancers and NIH:OVCAR-3 ovarian cancers and in the Luteinizing Hormone–releasing Hormone receptor–negative SK-OV-3 ovarian line. Nude mice bearing these tumors subcutaneously were injected intravenously with saline solution (control), AN-152, or doxorubicin at equimolar doses. Luteinizing Hormone–releasing Hormone receptor expression in tumors and specimens of human reproductive (n = 5) and nonreproductive (n = 15) normal tissues and in hematopoietic stem cells were analyzed with reverse transcriptase–polymerase chain reaction and radioligand binding assay. Results: The tumor volumes of Luteinizing Hormone–releasing Hormone receptor–positive HEC-1B and NIH:OVCAR-3 cancers were reduced significantly ( P Conclusion: Targeted chemotherapeutic Luteinizing Hormone–releasing Hormone analog AN-152 is more effective and less toxic than cytotoxic radical doxorubicin on Luteinizing Hormone–releasing Hormone receptor–positive tumors. AN-152 could be considered for targeted chemotherapy in patients with ovarian or endometrial cancers. (Am J Obstet Gynecol 2002;187:528-37.)
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treatment of uterine leiomyomas with Luteinizing Hormone releasing Hormone antagonist cetrorelix
Human Reproduction, 1997Co-Authors: David Gonzalezbarcena, Raquel Banuelos Alvarez, Elizabeth Pere Ochoa, Imelda Cardenas Cornejo, Ana Maria Comaruschally, Juergen Engel, Thomas Reissmann, Andrew V. Schally, Hilde RiethmullerwinzenAbstract:The efficacy of the Luteinizing Hormone-releasing Hormone antagonist Cetrorelix (SB-75) in the medical management of uterine leiomyomas (fibromas) was evaluated. Cetrorelix was administered to 18 pre-menopausal women with myomas with a mean age of 33.3 years, who had been candidates for hysterectomy. The initial dose of Cetrorelix was 5 mg twice daily s.c. for the first 2 days and thereafter 0.8 mg was given twice daily s.c. for at least 3 months. The mean duration of the treatment was 4.4 months. Before the therapy with Cetrorelix, the mean uterine volume, measured by ultrasonography, was 395.4 ± 69.2 ml (range 89-1166). Sixteen patients showed a progressive reduction in uterine volume from 410.4 ± 77.1 to a mean of 230.8 ± 52.6 ml at 3 months. All patients became amenorrhoeic and had hot flushes. After treatment with Cetrorelix, a surgical myomectomy was performed in 12 women. One of the patients subjected to myomectomy after therapy with Cetrorelix became pregnant. These patients have been followed for up to 25 months and only in one case has the uterine volume increased after therapy. Three patients had good responses to therapy with Cetrorelix and it was decided to follow them only by observation. One patient became pregnant 2 months later. In the other patient, the uterine volume remained unchanged for the duration of the follow-up of 2 years and the third patient showed an increase after 21 months. In three patients, it was necessary to perform total hysterectomy. In 14 patients, serum concentrations of Luteinizing Hormone, follicle stimulating Hormone and oestradiol decreased after the administration of the first dose of Cetrorelix and continued at subnormal values throughout therapy. In 15 patients who were not subjected to total hysterectomy, menstrual function returned at 1 month after cessation of treatment. Overall results support the use of Cetrorelix for the management of uterine leiomyomas.
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fibrocystic disease of the breast in premenopausal women histohormonal correlation and response to Luteinizing Hormone releasing Hormone analog treatment
American Journal of Obstetrics and Gynecology, 1991Co-Authors: Joseph Monsonego, Ana Maria Comaruschally, Marie Dominique Destable, Georges De Saint Florent, Jacques Amouroux, Jean Claude Kouyoumdjian, Jean Luc Breau, Lucien Israel, Andrew V. SchallyAbstract:Sixty-six patients with fibrocystic mastopathy were enrolled in the trial after being selected according to clinical, radioultrasonographic, and histologic criteria. No characteristic hormonal profile was noted in most patients (52%). Estrogen receptors or progesterone receptors, or both, were found in 57% of patients. Hormone receptor levels were correlated with atypical proliferative mastopathy (87.5%). Mastopathy was associated with a uterine fibroma or a fibromatous uterus in 73% of cases. All patients received intramuscular injections of a sustained delivery system (microcapsules) of Luteinizing Hormone releasing Hormone agonist [d-Trp 6 ]-LHRH, Ipsen-Biotech, Paris) for 3 to 6 months. In case of partial response at 3 months, an antiestrogen (tamoxifen, 40 mg/day, for estrogen receptor-predominant lesions) or a progestin (cyproterone acetate, 50 mg/day, for progesterone receptor-predominant lesions) was added to the Luteinizing Hormone releasing Hormone agonist. A complete response was observed in more than half of the patients ( n = 35, 53%) treated by [d-Trp 6 ]-LHRH alone ( n = 29) or associated with tamoxifen ( n = 4) or cyproterone acetate ( n = 2). A significant partial response was observed in 30 other patients (45%). Additionally, half of them received inhibitory drugs. The best responses were seen with cyst reformation (complete response, 100%) and fibrous block. Clinical responses to treatment with [d-Trp 6 ]-LHRH alone were independent of Hormone receptor status, but synergistic effects occurred with concomitant use of the corresponding inhibitory drugs. We conclude that chronic mastopathy, particularly when associated with uterine fibroma, can be successfully treated by Luteinizing Hormone releasing Hormone analogs in premenopausal women.
Carsten Grundker - One of the best experts on this subject based on the ideXlab platform.
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Luteinizing Hormone-Releasing Hormone Receptor-Targeted Chemotherapy Using AN-152
Neuroendocrinology, 2009Co-Authors: Gunter Emons, Andrew V. Schally, Herbert Sindermann, Jürgen Engel, Carsten GrundkerAbstract:The Luteinizing Hormone-releasing Hormone (LHRH; also known as gonadotropin-releasing Hormone) receptor can be utilized for targeted chemotherapy with cytotoxic LHRH analogues such as AN-152, in which
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expression of receptors for Luteinizing Hormone releasing Hormone in human ovarian and endometrial cancers frequency autoregulation and correlation with direct antiproliferative activity of Luteinizing Hormone releasing Hormone analogues
American Journal of Obstetrics and Gynecology, 2002Co-Authors: Peter Volker, Carsten Grundker, Oswald Schmidt, Klausdieter Schulz, Gunter EmonsAbstract:Abstract Objective: Several recent reports have demonstrated the expression of Luteinizing Hormone-releasing Hormone receptors by human ovarian and endometrial cancers. Controversy persists on the relevance of this finding, in particular whether these receptors mediate direct antiproliferative effects of Luteinizing Hormone-releasing Hormone analogues. We correlated the expression of Luteinizing Hormone-releasing Hormone receptors by well-characterized ovarian and endometrial cancer cell lines with the ability of Luteinizing Hormone-releasing Hormone analogues to reduce their proliferation and studied the autoregulation of Luteinizing Hormone-releasing Hormone receptor expression by Luteinizing Hormone-releasing Hormone agonist triptorelin and antagonist cetrorelix. The expression of Luteinizing Hormone-releasing Hormone receptors was assessed in a series of specimens from primary ovarian and endometrial cancers. Study Design: Luteinizing Hormone-releasing Hormone receptor expression was assessed by semiquantitative reverse transcriptase–polymerase chain reaction and radioligand binding assay. Antiproliferative effects were ascertained by proliferation assays in the absence or presence of Luteinizing Hormone-releasing Hormone analogues. Results: Ovarian (4/6 cell lines) and endometrial (5/6 cell lines) cancer cell lines expressed Luteinizing Hormone-releasing Hormone receptors. The proliferation of these Luteinizing Hormone-releasing Hormone receptor–positive cell lines was dose- and time-dependently reduced by agonistic and antagonistic Luteinizing Hormone-releasing Hormone analogues. Luteinizing Hormone-releasing Hormone receptor density was reduced to 80% of controls (control, 100 %; P Conclusion: These findings suggest that Luteinizing Hormone-releasing Hormone receptors that are expressed by human ovarian and endometrial cancer cell lines mediate direct antiproliferative effects of Luteinizing Hormone-releasing Hormone analogues. Because most respective primary cancers expressed Luteinizing Hormone-releasing Hormone receptors, these receptors might be used for novel antiproliferative therapeutic approaches and should be further evaluated. (Am J Obstet Gynecol 2002;186:171-9.)
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Antitumor effects of the cytotoxic Luteinizing Hormone-releasing Hormone analog AN-152 on human endometrial and ovarian cancers xenografted into nude mice.
American journal of obstetrics and gynecology, 2002Co-Authors: Carsten Grundker, Andrew V. Schally, Peter Volker, Frank Griesinger, Annette Ramaswamy, Attila Nagy, Gunter EmonsAbstract:Abstract Objective: Most human endometrial and ovarian cancers express receptors for Luteinizing Hormone– releasing Hormone. These receptors can be used for targeted chemotherapy with cytotoxic Luteinizing Hormone–releasing Hormone analogs such as AN-152, in which doxorubicin is linked to [D-Lys 6 ]Luteinizing Hormone–releasing Hormone. Study Design: The antitumor effects of doxorubicin and AN-152 were assessed in vivo in human Luteinizing Hormone–releasing Hormone receptor–positive HEC-1B endometrial cancers and NIH:OVCAR-3 ovarian cancers and in the Luteinizing Hormone–releasing Hormone receptor–negative SK-OV-3 ovarian line. Nude mice bearing these tumors subcutaneously were injected intravenously with saline solution (control), AN-152, or doxorubicin at equimolar doses. Luteinizing Hormone–releasing Hormone receptor expression in tumors and specimens of human reproductive (n = 5) and nonreproductive (n = 15) normal tissues and in hematopoietic stem cells were analyzed with reverse transcriptase–polymerase chain reaction and radioligand binding assay. Results: The tumor volumes of Luteinizing Hormone–releasing Hormone receptor–positive HEC-1B and NIH:OVCAR-3 cancers were reduced significantly ( P Conclusion: Targeted chemotherapeutic Luteinizing Hormone–releasing Hormone analog AN-152 is more effective and less toxic than cytotoxic radical doxorubicin on Luteinizing Hormone–releasing Hormone receptor–positive tumors. AN-152 could be considered for targeted chemotherapy in patients with ovarian or endometrial cancers. (Am J Obstet Gynecol 2002;187:528-37.)
Peter Volker - One of the best experts on this subject based on the ideXlab platform.
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expression of receptors for Luteinizing Hormone releasing Hormone in human ovarian and endometrial cancers frequency autoregulation and correlation with direct antiproliferative activity of Luteinizing Hormone releasing Hormone analogues
American Journal of Obstetrics and Gynecology, 2002Co-Authors: Peter Volker, Carsten Grundker, Oswald Schmidt, Klausdieter Schulz, Gunter EmonsAbstract:Abstract Objective: Several recent reports have demonstrated the expression of Luteinizing Hormone-releasing Hormone receptors by human ovarian and endometrial cancers. Controversy persists on the relevance of this finding, in particular whether these receptors mediate direct antiproliferative effects of Luteinizing Hormone-releasing Hormone analogues. We correlated the expression of Luteinizing Hormone-releasing Hormone receptors by well-characterized ovarian and endometrial cancer cell lines with the ability of Luteinizing Hormone-releasing Hormone analogues to reduce their proliferation and studied the autoregulation of Luteinizing Hormone-releasing Hormone receptor expression by Luteinizing Hormone-releasing Hormone agonist triptorelin and antagonist cetrorelix. The expression of Luteinizing Hormone-releasing Hormone receptors was assessed in a series of specimens from primary ovarian and endometrial cancers. Study Design: Luteinizing Hormone-releasing Hormone receptor expression was assessed by semiquantitative reverse transcriptase–polymerase chain reaction and radioligand binding assay. Antiproliferative effects were ascertained by proliferation assays in the absence or presence of Luteinizing Hormone-releasing Hormone analogues. Results: Ovarian (4/6 cell lines) and endometrial (5/6 cell lines) cancer cell lines expressed Luteinizing Hormone-releasing Hormone receptors. The proliferation of these Luteinizing Hormone-releasing Hormone receptor–positive cell lines was dose- and time-dependently reduced by agonistic and antagonistic Luteinizing Hormone-releasing Hormone analogues. Luteinizing Hormone-releasing Hormone receptor density was reduced to 80% of controls (control, 100 %; P Conclusion: These findings suggest that Luteinizing Hormone-releasing Hormone receptors that are expressed by human ovarian and endometrial cancer cell lines mediate direct antiproliferative effects of Luteinizing Hormone-releasing Hormone analogues. Because most respective primary cancers expressed Luteinizing Hormone-releasing Hormone receptors, these receptors might be used for novel antiproliferative therapeutic approaches and should be further evaluated. (Am J Obstet Gynecol 2002;186:171-9.)
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Antitumor effects of the cytotoxic Luteinizing Hormone-releasing Hormone analog AN-152 on human endometrial and ovarian cancers xenografted into nude mice.
American journal of obstetrics and gynecology, 2002Co-Authors: Carsten Grundker, Andrew V. Schally, Peter Volker, Frank Griesinger, Annette Ramaswamy, Attila Nagy, Gunter EmonsAbstract:Abstract Objective: Most human endometrial and ovarian cancers express receptors for Luteinizing Hormone– releasing Hormone. These receptors can be used for targeted chemotherapy with cytotoxic Luteinizing Hormone–releasing Hormone analogs such as AN-152, in which doxorubicin is linked to [D-Lys 6 ]Luteinizing Hormone–releasing Hormone. Study Design: The antitumor effects of doxorubicin and AN-152 were assessed in vivo in human Luteinizing Hormone–releasing Hormone receptor–positive HEC-1B endometrial cancers and NIH:OVCAR-3 ovarian cancers and in the Luteinizing Hormone–releasing Hormone receptor–negative SK-OV-3 ovarian line. Nude mice bearing these tumors subcutaneously were injected intravenously with saline solution (control), AN-152, or doxorubicin at equimolar doses. Luteinizing Hormone–releasing Hormone receptor expression in tumors and specimens of human reproductive (n = 5) and nonreproductive (n = 15) normal tissues and in hematopoietic stem cells were analyzed with reverse transcriptase–polymerase chain reaction and radioligand binding assay. Results: The tumor volumes of Luteinizing Hormone–releasing Hormone receptor–positive HEC-1B and NIH:OVCAR-3 cancers were reduced significantly ( P Conclusion: Targeted chemotherapeutic Luteinizing Hormone–releasing Hormone analog AN-152 is more effective and less toxic than cytotoxic radical doxorubicin on Luteinizing Hormone–releasing Hormone receptor–positive tumors. AN-152 could be considered for targeted chemotherapy in patients with ovarian or endometrial cancers. (Am J Obstet Gynecol 2002;187:528-37.)
Janice H. Urban - One of the best experts on this subject based on the ideXlab platform.
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steroid modulation of neuropeptide y induced Luteinizing Hormone releasing Hormone release from median eminence fragments from male rats
Neuroendocrinology, 1996Co-Authors: Janice H. Urban, Indranil Das, Jon E. LevineAbstract:Neuropeptide Y (NPY) has been shown to stimulate hypothalamic release of Luteinizing Hormone-releasing Hormone (LHRH) both in vitro and in vivo. In female rats, NPY facilitation of LHRH release is gre
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AMPLITUDE AND FREQUENCY MODULATION OF PULSATILE Luteinizing Hormone-RELEASING Hormone RELEASE
Cellular and molecular neurobiology, 1995Co-Authors: Jon E. Levine, Patrick E. Chappell, Leslie M. Besecke, Angela C. Bauer-dantoin, Andrew Wolfe, Tarja Porkka-heiskanen, Janice H. UrbanAbstract:1. A variety of neuroendocrine approaches has been used to characterize cellular mechanisms governing Luteinizing Hormone-releasing Hormone (LHRH) pulse generation. We review recentin vivo microdialysis,in vitro superfusion, andin situ hybridization experiments in which we tested the hypothesis that the amplitude and frequency of LHRH pulses are subject to independent regulation via distinct and identifiable cellular pathways.
