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Robert V. Gallo Our current research is to investigate the involvement of endogenous opioid peptides in regulating the surge of LH release that causes ovulation. A concept has been developed in the literature that a decrease in the inhibitory influence of endogenous opioid peptides on LH secretion on the afternoon of proestrus in the rat estrous cycle is an important event contributneuroendocrine regulation of luteinizing hormone release The overall goal of my research is to understand the neuroendocrine mechanisms regulating luteinizing hormone (LH) release from the anterior pituitary. I became interested in this subject in graduate school, working in the laboratory of M.X. Zarrow at Purdue University, where I received my Ph.D. in 1968. I then spent two years of postdoctoral study at the UCLA Brain Research Institute with C.H. Sawyer. My first faculty position was at the UCSF School of Medicine in the Department of Physiology from 1970-1982. In 1982 I joined the faculty at the University of Connecticut.
ing to the occurrence of the ovulatory LH surge. This suppression is postulated to be exerted by b-endorphin originating in arcuate nucleus neurons and acting via mu-opioid receptors. However, the potential involvement of other opioid peptides and their receptors in “disinhibition” of the LH surge remained to be explored. Recent work in my laboratory suggested that a reduction in medial preoptic area (MPOA) kappaopioid receptor-mediated inhibitory tone may also be a critical event in generation of the LH surge, as pharmacological blockade of kappa-opioid receptors with norbinaltorphimine at this CNS site late on the morning of proestrus prematurely advanced the ovulatory LH surge. Dynorphin is the endogenous ligand for the kappa-opioid receptor, and very little is known about the role of the prodynorphin family of endogenous opioid peptides in reproductive neuroendocrine function. Additional studies demonstrated that prodynorphin-derived peptides, acting through kappa-opioid receptors, block the LH surge and ovulation. Dynorphin A1-17 and A1-8 are the most potent in this regard. Neutralization of these peptides, by push-pull perfusion of the MPOA on the morning of proestrus with antibodies (Ab) specific for each peptide, resulted in some animals in an advancement in the time of LH release sufficient to cause ovulation. This suggested that these two peptides might have a role in the MPOA, although a minor one, in suppressing LH secretion early on proestrus. A reduction in prodynorphin gene expression on the afternoon of proestrus may be one event involved in a possible decrease in dynorphin inhibitory tone on the ovulatory LH surge-generating signal. However, a complete loss of kappaopioid inhibition is not required for the onset of the LH surge. These experiments have broadened our understanding of the role of the prodynorphin family of opioid peptides in reproductive neuroendocrine function by clarifying their role in the mechanisms regulating the ovulatory LH surge. Selected Publications Smith, M.J., and R.V. Gallo. (1997). The effect of blockade of kappa-opioid receptors in the medial preoptic area on the luteinizing hormone surge in the proestrous rat. Brain Research 768: 111-119. Zhang, Q., and R.V. Gallo. (2002). Effect of prodynorphinderived opioid peptides on the ovulatory luteinizing hormone surge in the proestrous rat. Endocrine 18: 27-32. Zhang, Q., J. M. McCoy, and R. V. Gallo. (2002). Further studies on possible dynorphin involvement in the ovulatory luteinizing hormone surge in the proestrous rat. Endocrine 18: 231-238. Zhang, Q., and R. V. Gallo. (2003). Presence of kappa-opioid inhibitory tone at the onset of the ovulatory luteinizing hormone surge in the proestrous rat. Brain Research 980: 135-139.
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Page 3 and 4: The University About the Storrs Cam
Page 5 and 6: Graduate Program The Graduate Resea
Page 7 and 8: Faculty & Research Marie E. Cantino
Page 9 and 10: Selected Publications Cantino, M.E.
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