{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,10]],"date-time":"2026-06-10T16:28:43Z","timestamp":1781108923488,"version":"3.54.1"},"reference-count":54,"publisher":"National Academy of Sciences","issue":"20","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2008,5,20]]},"abstract":"<jats:p>\n                    Estrogens act within the ventromedial nucleus of the hypothalamus (VMN) to facilitate lordosis behavior. Estradiol treatment\n                    <jats:italic>in vivo<\/jats:italic>\n                    induces \u03b1\n                    <jats:sub>1b<\/jats:sub>\n                    -adrenoreceptor mRNA and increases the density of \u03b1\n                    <jats:sub>1B<\/jats:sub>\n                    -adrenoreceptor binding in the hypothalamus. Activation of hypothalamic \u03b1\n                    <jats:sub>1<\/jats:sub>\n                    -adrenoceptors also facilitates estrogen-dependent lordosis. To investigate the cellular mechanisms of adrenergic effects on VMN neurons, whole-cell patch-clamp recordings were carried out on hypothalamic slices from control and estradiol-treated female rats. In control slices, bath application of the \u03b1\n                    <jats:sub>1<\/jats:sub>\n                    -agonist phenylephrine (PHE; 10 \u03bcM) depolarized 10 of 25 neurons (40%), hyperpolarized three neurons (12%), and had no effect on 12 neurons (48%). The depolarization was associated with decreased membrane conductance, and this current had a reversal potential close to the K\n                    <jats:sup>+<\/jats:sup>\n                    equilibrium potential. The \u03b1\n                    <jats:sub>1b<\/jats:sub>\n                    -receptor antagonist chloroethylclonidine (10 \u03bcM) blocked the depolarization produced by PHE in all cells. From estradiol-treated rats, significantly more neurons in slices depolarized (71%) and fewer neurons showed no response (17%) to PHE. PHE-induced depolarizations were significantly attenuated with 4-aminopyridine (5 mM) but unaffected by tetraethylammonium chloride (20 mM) or blockers of Na\n                    <jats:sup>+<\/jats:sup>\n                    and Ca\n                    <jats:sup>2+<\/jats:sup>\n                    channels. These data indicate that \u03b1\n                    <jats:sub>1<\/jats:sub>\n                    -adrenoceptors depolarize VMN neurons by reducing membrane conductance for K\n                    <jats:sup>+<\/jats:sup>\n                    . Estradiol amplifies \u03b1\n                    <jats:sub>1b<\/jats:sub>\n                    -adrenergic signaling by increasing the proportion of VMN neurons that respond to stimulation of \u03b1\n                    <jats:sub>1b<\/jats:sub>\n                    -adrenergic receptors, which is expected in turn to promote lordosis.\n                  <\/jats:p>","DOI":"10.1073\/pnas.0802760105","type":"journal-article","created":{"date-parts":[[2008,5,14]],"date-time":"2008-05-14T21:10:01Z","timestamp":1210799401000},"page":"7333-7338","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":19,"title":["Estradiol modulation of phenylephrine-induced excitatory responses in ventromedial hypothalamic neurons of female rats"],"prefix":"10.1073","volume":"105","author":[{"given":"Anna W.","family":"Lee","sequence":"first","affiliation":[{"name":"*Laboratory of Neurobiology and Behavior, The Rockefeller University, New York, NY 10065; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andreas","family":"Kyrozis","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, Albert Einstein College of Medicine, Bronx, NY 10461"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vivien","family":"Chevaleyre","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, Albert Einstein College of Medicine, Bronx, NY 10461"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lee-Ming","family":"Kow","sequence":"additional","affiliation":[{"name":"*Laboratory of Neurobiology and Behavior, The Rockefeller University, New York, NY 10065; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nino","family":"Devidze","sequence":"additional","affiliation":[{"name":"*Laboratory of Neurobiology and Behavior, The Rockefeller University, New York, NY 10065; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qiuyu","family":"Zhang","sequence":"additional","affiliation":[{"name":"*Laboratory of Neurobiology and Behavior, The Rockefeller University, New York, NY 10065; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anne M.","family":"Etgen","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, Albert Einstein College of Medicine, Bronx, NY 10461"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Donald W.","family":"Pfaff","sequence":"additional","affiliation":[{"name":"*Laboratory of Neurobiology and Behavior, The Rockefeller University, New York, NY 10065; and"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2008,5,20]]},"reference":[{"key":"e_1_3_3_1_2","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-4613-8084-9"},{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2826.1996.04716.x"},{"key":"e_1_3_3_3_2","doi-asserted-by":"crossref","first-page":"381","DOI":"10.1016\/B978-012532104-4\/50048-2","volume-title":"Hormones, Brain, and Behavior","author":"Etgen AM","year":"2002","unstructured":"AM Etgen, Estrogen regulation of neurotransmitter and growth factor signaling in the brain. 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