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      Immortalized Gonadotropin-Releasing Hormone Neurons (GT1-7 Cells) Exhibit Synchronous Bursts of Action Potentials

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          Abstract

          Although it has been assumed that synchronized firing of gonadotropin-releasing hormone (GnRH) neurons is necessary for pulsatile GnRH secretion, there is no clear evidence for this. In the present study we simultaneously recorded spontaneous action potentials from multiple cells. Immortalized GnRH neurons (GT1-7 cells) were cultured on a multi-electrode dish (MED) and action potentials recorded by an extracellular recording method. One to two weeks after the beginning of culture, spontaneous action potentials appeared, exhibiting bursts composed of 5–10 action potentials. Burst activity was intermittent and periodic with mean burst intervals of 13.3 s. Furthermore, burst activity was recorded almost simultaneously from several micro-electrodes, suggesting that electrical activities of GT1-7 cells were synchronized with each other. Periodic bursts were completely and reversibly blocked by 1–5 µ M tetrodotoxin, indicating that voltage-dependent Na<sup>+</sup> channels are involved in their generation. γ-Aminobutyric acid (GABA) given at a 10-µ M concentration shortened inter-burst intervals, whereas 10 µ M bicuculline lengthened them. Finally, the gap junctional blockers n-octyl alcohol (1 m M) and carbenoxolone (100 µ M) reversibly blocked periodic burst activity. The present study provides direct evidence that the electrical activity of GT1-7 cells exhibits synchronous and periodic bursts composed of action potentials. In addition, endogenous GABA is involved in GT1-7 cells in determining burst frequency. Although the precise mechanism of synchronized burst activities needs to be clarified, gap junctional communications among GT1-7 cells are at least partially involved.

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          Most cited references 4

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          Segmentation and the origin of regional diversity in the vertebrate central nervous system

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            Pulsatile Gonadotropin-Releasing Hormone (GnRH) Secretion Is an Inherent Function of GnRH Neurons, as Revealed by the Culture of Medial Olfactory Placode Obtained from Embryonic Rats

            To determine whether gonadotropin-releasing hormone (GnRH) neurons in culture without the hypothalamus secrete GnRH in a pulsatile fashion, the nasal placode (NAP) was obtained at day 13.5 of gestation and cultured by a roller tube method. If the GnRH release occurs in a pulsatile fashion, it can be said that the pulse generator of GnRH exists inherently in each cell or community of cells in the culture. The concentration of GnRH in the NAP culture medium collected at 8-min intervals for 160 min after 2- to 4-week cultures showed that GnRH release occurred in a pulsatile fashion with a mean interpulse interval of 29.8 ± 2.3 min (n = 9). When the NAP was cultured with tissues of the forebrain vesicle (n = 3) or the hypothalamus (n = 4), GnRH was also released in a pulsatile fashion with similar intervals (27.3 ± 1.0 min for the NAP+forebrain vesicle culture and 36.0 ± 6.3 min for the NAP+hypothalamus culture) as those in cultures without brain tissues. It is concluded that pulsatile GnRH release is an inherent function of GnRH neurons.
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              Identification of Gap Junctional Connexin-32 mRNA and Protein in Gonadotropin-Releasing Hormone Neurons of the Female Rat

              Pulsatile gonadotropin-releasing hormone (GnRH) release from the median eminence is critical for the appropriate function of the pituitary gonadotropes and for the generation of a preovulatory gonadotropin surge. The mechanisms by which many GnRH axon terminals are synchronized to release GnRH in a coordinated fashion into the capillaries of the primary plexus are unknown as are the anatomical sites at which the regulation of GnRH neurons takes place. While many neurotransmitters have been shown to influence GnRH release, it is not clear if such neurotransmitters regulate GnRH neurons directly through synaptic interactions or through intermediate neurons. An alternative mechanism of interneuronal communication is provided by gap junctions which allow a rapid, bidirectional exchange of signals. In order to explore if GnRH neurons synthesize the appropriate proteins to form gap junctions with adjacent cells we used double immunohistochemistry for GnRH and connexins-26, -32 or -43 as well as dual in situ hybridization to identify GnRH mRNA and connexin-32 mRNA. The results show that all GnRH neurons contain connexin-32 immunoreactive puncta at their perikarya and, occasionally, at their axon terminals in the median eminence while connexin-26 and -43 immunoreactivity was absent in GnRH neurons. In addition, connexin-32 mRNA was detected in GnRH mRNA containing neurons. However, gap junctional connections between adjacent GnRH neurons were not observed. The data suggest that gap junctional coupling of GnRH neurons with neighboring non-GnRH containing cells may occur and may represent a mechanism by which GnRH neurons can be synchronized or by which hormonal or neurotransmitter signals can be conveyed to the GnRH neurons.
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                Author and article information

                Journal
                NEN
                Neuroendocrinology
                10.1159/issn.0028-3835
                Neuroendocrinology
                S. Karger AG
                0028-3835
                1423-0194
                2001
                March 2001
                02 April 2001
                : 73
                : 3
                : 157-165
                Affiliations
                Departments of aPhysiology, and bGynecology and Obstetrics, Yokohama City University School of Medicine, Yokohama, Japan
                Article
                54632 Neuroendocrinology 2001;73:157–165
                10.1159/000054632
                11307034
                © 2001 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: 4, References: 33, Pages: 9
                Categories
                Gonadotropin Regulation: Properties of GnRH Neurons

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