Abstract
We have found that exogenous prolactin (PRL) stimulates all three populations of hypothalamic neuroendocrine dopaminergic neurons. In this study, we investigated the effects of immunoneutralization of endogenous PRL on the activity of these neurons. Injection of 17β-estradiol (E2) (20 μg subcutaneously) 10 d after ovariectomy induced a proestrus-like increase in PRL in peripheral plasma the following afternoon. At 1000 h the day after E2 injection, rats received either rabbit antirat PRL antiserum (PRL-AS) (200 μL) or normal rabbit serum (NRS, 200 μL, controls) intraperitoneally. Groups of rats were then decapitated every 2 h from 1100 h to 2100 h. Trunk blood was collected and serum extracted with protein A to remove the PRL-AS/PRL complex, and the remaining free PRL was measured by radio immunoassay. Sites of neuroendocrine dopaminergic nerve terminals, the median eminence (ME), and intermediate and neural lobes of the pituitary gland were excised and stored for determination of dopamine (DA) and 3,4-dihydroxyphenyl acetic acid (DOPAC) concentrations by high-performance liquid chromatography electrochemical detection (EC). In addition, the anterior lobe of the pituitary gland, the locus of DA action, was collected. The concentration of PRL in NRS-treated animals increased by 1500 h, peaked by 1700 h, and returned to low levels by 2100 h. PRL-AS prevented the increase in PRL secretion in response to E2. The turnover of DA (DOPAC:DA ratio; an index of dopaminergic neuronal activity) in the ME of NRS-treated animals increased at 1500 h and rapidly returned to basal levels. Treatment with PRL-AS prevented the increase in DA turnover in the ME. DA turnover in the intermediate lobe increased coincident with the peak of PRL in serum of NRS-treated rats. PRL-AS administration prevented increased DA turnover in the intermediate lobe. The turnover of DA in the neural lobe increased by 1300 h and decreased steadily through 2100 h. However, administration of PRL-AS minimally suppressed the turnover of DA in the neural lobe. Moreover, administration of PRL-AS attenuated the rise of DA in the anterior lobe associated with the waning phase of the E2-induced PRL surge. These results clearly indicate that endogenous PRL regulates its own secretion by activating hypothalamic neuroendocrine dopaminergic neurons.
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DeMaria, J. E., Zelena, D., Vescernyés, M., Nagy, G. M., and Freeman, M. E. (1998). Brain Res. 806, 89–94.
Fuxe, K. and Hokfelt, T. (1966). Acta Physiol. Scand. 66, 245.
Fuxe, K. (1964). Acta Physiol. Scand. 58, 383–384.
Bjorklund, A., Moore, R. Y., Nobin, A., and Stenevi, U. (1973). Brain Res. 51, 171–191.
Goudreau, J. L., Lindley, S. E., Lookingland, K. J., and Moore, K. E. (1992). Neuroendocrinology 56, 100–105.
Goudreau, J. L., Falls, W. M., Lookingland, K. J., and Moore, K. E. (1995). Neuroendocrinology 62, 147–154.
Ben-Jonathan, N. (1985). Endocr. Rev. 6, 564–589.
Ben-Jonathan, N. and Peters, L. L. (1982). Endocrinology 110, 1861–1865.
Murai, I. and Ben-Jonathan, N. (1986). Neuroendocrinology 43, 453–458.
Murai, I., Garris, P. A., and Ben-Jonathan, N. (1989). Endocrinology 124, 2343–2349.
Peters, L. A., Hoefer, M. T., and Ben-Jonathan, N. (1981). Science 213, 659–661.
DeMaria, J. E., Livingstone, J. D., and Freeman, M. E. (1998). Neuroendocrinology 67, 377–383.
DeMaria, J. E., Nagy, G. M., Lerant, A. A., Fekete, M. I. E., Levenson, C. W., and Freeman, M. E. (2000). Endocrinology 141, 366–374.
DeMaria, J. E., Lerant, A., and Freeman, M. E. (1999). Brain Res. 837, 236–241.
Nagy, G. M., DeMaria, J. E., and Freeman, M. E. (1998). Brain Res. 790, 315–317.
Lerant, A., Herman, M. E., and Freeman, M. E. (1996). Endocrinology 137, 3621–3628.
Lerant, A. and Freeman, M. (1997). Neuroendocrinology 65, 436–445.
Chiu, S., Koos, R. D. and Wise, P. M. (1992). Endocrinology 130, 1747–1749.
Chiu, S. and Wise, P. M. (1994). J. Neuroendocrinol. 6, 191–199.
Crumeyrolle-Arias, M., Latouche, J., Jammes, H., Djiane, J., Kelly, P. A., Reymond, M. J., and Haour, F. (1993). Neuroendocrinology 57, 457–466.
Meister, B., Jacobsson, G., and Elde, R. (1992). Acta Physiol. Scand. 146, 533–534.
Muccioli, G. and Di Carlo, R. (1994). Brain Res. 663, 244–250.
Pi, X. J. and Grattan, D. R. (1998). J. Compar. Neurol. 394, 462–474.
Lerant, A., and Freeman, M. E. (1998). Brain Res. 802, 141–154.
Demarest, K., Riegle, G., and Moore, K. (1984). Neuroendocrinology 38, 467–475.
Demarest, K. T., Duda, N. J., Riegle, G. D., and Moore, K. E. (1983). Brain Res. 272, 175–178.
Demarest, K. T., Moore, K. E., and Riegle, G. D. (1987). Neuroendocrinology 45, 227–232.
Demarest, K. T., Moore, K. E., and Riegle, G. D. (1983). Neuroendocrinology 36, 371–375.
Demarest, K. T., and Moore, K. E. (1981). Neuroendocrinology 33, 230–234.
Gudelsky, G. A. and Porter, J. C. (1980). Endocrinology 106, 526–529.
Hokfelt, T. and Fuxe, K. (1972). Neuroendocrinology 9, 100–122.
Koike, K., Kadowaki, K., Hirota, K., Ohmichi, M., Ikegami, H., Sawada, T., Miyake, A., and Tanizawa, O., (1993). Acta Endocrinol. 129, 548–553.
Lee, Y. S. and Voogt, J. L. (1999). Endocrinology 140, 2159–2166.
Gregerson, K. A., and Selmanoff, M. (1989). J. Neurosci. 8, 2477–2484.
Selmanoff, M. (1985). Endocrinology 116, 1943–1952.
Arita, J. and Kimura, F. (1986). Endocrinology 119, 1666–1672.
Moore, K. E. (1987). Biol. Reprod. 36, 47–58.
Lerant, A., Kanyicska, B., and Freeman, M. E. (1999). Proc. Ann. Mtg. Society for Neuroscience 25, 1186 (abstract).
Demarest, K. T., Riegle, G. D., and Moore, K. E. (1985). Neuroendocrinology 40, 369–376.
Demarest, K. T., Riegle, G. D., and Moore, K. E. (1984). Neuroendocrinology 38, 467–475.
Arbogast, L. A. and Voogt, J. L. (1991). Endocrinology 128, 997–1005.
Hentschel, K., Fleckenstein, A. E., Toney, T. W., Lawson, D. M., Moore, K. E., and Lookingland, K. J. (2000). Brain Res. 852, 28–36.
Demarest, K. T., Riegle, G. D., and Moore, K. E. (1984). Endocrinology 115, 2091–2097.
Lookingland, K., Jarry, H. D., and Moore, K. E. (1987). Brain Res. 419, 303–310.
Lindley, S. E., Gunnet, J. W., Lookingland, K. J., and Moore, K. E. (1990). Brain Res. 506, 133–138.
Cramer, O. M., Parker, R., and Porter, J. C. (1979). Endocrinology 104, 419–422.
Cramer, O. M., Parker, R., and Porter, J. C. (1979). Endocrinology 105, 929–933.
Arbogast, L. A. and Voogt, J. L. (1993). Neuroendocrinology 58, 501–510.
Huang, S. K. and Pan, J. T. (1996). Neuroendocrinology. 64, 208–214.
Carretero, J., Vazquez, R. J., Santos, M., Cacicedo, L., Rubio, M., Sanchez-Franco, F. and Vazquez, R. (1996). Neuropeptides 30, 81–86.
Yuan, Z. F. and Pan, J.-T. (1996). Endocrinology. 137, 4120–4125.
Crowley, W. R., Parker, S. L., Armstrong, W. E., Wang, W., and Grosvenor, C. E. (1991). Neuroendocrinology. 53, 493–502.
Horvath, T. L. (1998). J. Neurosci. 18, 1546–1558.
Arey, B. J., Averill, R. L., and Freeman, M. E. (1989). Endocrinology 124, 119–123.
Arey, B. J. and Freeman, M. E. (1989). Endocrinology 124, 878–883.
Arey, B. J. and Freeman, M. E. (1990). Endocrinology 126, 279–284.
Arey, B. J. and Freeman, M. E. (1992). Endocrinology 131, 736–742.
Arey, B. J. and Freeman, M. E. (1992). Endocrinology, 130, 126–132.
Arey, B. J., Kanyicska, B., and Freeman, M. E. (1991). Neuroendocrinology 53, 35–40.
Kanyicska, B., Lerant, A., and Freeman, M. E. (1998). Endocrinology 139, 5164–5173.
Freeman, M. E. and Sterman, J. R. (1978). Endocrinology 102, 1915–1920.
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DeMaria, J.E., Nagy, G.M. & Freeman, M.E. Immunoneutralization of prolactin prevents stimulatory feedback of prolactin on hypothalamic neuroendocrine dopaminergic neurons. Endocr 12, 333–337 (2000). https://doi.org/10.1385/ENDO:12:3:333
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DOI: https://doi.org/10.1385/ENDO:12:3:333