0
views
0
recommends
+1 Recommend
1 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found

      Lordosis of Rats Is Modified by Neurosteroidogenic Effects of Membrane Benzodiazepine Receptors in the Ventral Tegmental Area

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Progestins modulate lordosis through actions in the ventral tegmental area (VTA). Whether neurosteroidogenesis of 5α-pregnan-3α-ol-20-one (3α,5α-THP), involving mitochondrial benzodiazepine receptors (MBR), is important for lordosis was investigated. Ovariectomized (Ovx), hormone-primed rats (experiments 1, 3, 5, 6) and rats in behavioral estrus (experiments 2 and 4) were unilaterally infused via chronic guide cannula to the VTA with a MBR agonist, N,N-dihexyl-2-(4-fluorophenyl) indole-30-acetamide (FGIN 1–27) or antagonist 1-(2-chlorophenyl)-N-methyl-N-(1-methylpropyl)-3-isoquinolinecarboximide (PK-11195). Experiment 1: Estradiol benzoate (EB)-primed (25 µg) rats administered 0 or 25 µg progesterone (P<sub>4</sub>) SC showed increased lordosis when infused with 5.0 µg FGIN 1–27 to the VTA; those administered 100 or 200 µg P<sub>4</sub> SC exhibited greater lordosis when infused with 2.5 or 5.0 µg FGIN, relative to saline-infused rats. Experiment 2: Rats, near the termination of behavioral estrus, infused with 2.5 or 5.0 µg of FGIN 1–27 to the VTA, showed increased lordosis compared to that seen following vehicle administration. Experiment 3: EB-primed rats administered 200 or 500 µg P<sub>4</sub> SC showed decreased lordosis when infused with 100, 200, or 400 ng PK-11195, relative to saline-infused rats. Experiment 4: Rats infused at the peak of behavioral estrus with 100, 200, or 400 ng PK-11195 to the VTA exhibited reduced lordosis compared to that seen following vehicle administration. Experiment 5: 3α,5α-THP (100 ng) infusions to the VTA reinstated lordosis of hormone-primed rats infused with PK-11195 (100 ng) to the VTA. Experiment 6: FGIN 1–27 (5.0 µg) and PK-11195 (100 ng) infusions aimed at the VTA respectively increased and decreased midbrain levels of 3α,5α-THP compared to vehicle. Notably, the specific effects observed with infusions to the VTA were not seen with infusions to the control site, the substantia nigra. These data suggest that neurosteroidogenesis involving MBRs in the VTA mediates lordosis of hormone-primed or behavioral estrous rats.

          Related collections

          Most cited references 21

          • Record: found
          • Abstract: not found
          • Article: not found

          Peripheral benzodiazepine receptor in cholesterol transport and steroidogenesis

           H. Li,  B Vidic,  A.S. Brown (1997)
            Bookmark
            • Record: found
            • Abstract: not found
            • Article: not found

            Female sex steroid hormones: from receptors to networks to performance--actions on the sensorimotor system.

             Sheryl Smith (1994)
              Bookmark
              • Record: found
              • Abstract: not found
              • Article: not found

              The neurosteroids, progesterone and 3α,5α-THP, enhance sexual motivation, receptivity, and proceptivity in female rats

                Bookmark

                Author and article information

                Journal
                NEN
                Neuroendocrinology
                10.1159/issn.0028-3835
                Neuroendocrinology
                S. Karger AG
                0028-3835
                1423-0194
                2003
                January 2003
                10 March 2003
                : 77
                : 1
                : 71-82
                Affiliations
                aDepartment of Psychology, bBiological Sciences, cCenter for Neuroscience Research, The University at Albany-SUNY, Albany, N.Y., USA
                Article
                68338 Neuroendocrinology 2003;77:71–82
                10.1159/000068338
                12624543
                © 2003 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 6, References: 72, Pages: 12
                Categories
                Reproductive Neuroendocrinology

                Comments

                Comment on this article