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<title xml:lang="en">NEURONAL ACTIVITY AND STRESS DIFFERENTIALLY REGULATE HIPPOCAMPAL AND HYPOTHALAMIC CORTICOTROPIN-RELEASING HORMONE EXPRESSION IN THE IMMATURE RAT</title>
<author>
<name sortKey="Hatalski, C G" sort="Hatalski, C G" uniqKey="Hatalski C" first="C. G." last="Hatalski">C. G. Hatalski</name>
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<name sortKey="Brunson, K L" sort="Brunson, K L" uniqKey="Brunson K" first="K. L." last="Brunson">K. L. Brunson</name>
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<name sortKey="Tantayanubutr, B" sort="Tantayanubutr, B" uniqKey="Tantayanubutr B" first="B." last="Tantayanubutr">B. Tantayanubutr</name>
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<author>
<name sortKey="Chen, Y" sort="Chen, Y" uniqKey="Chen Y" first="Y." last="Chen">Y. Chen</name>
</author>
<author>
<name sortKey="Baram, T Z" sort="Baram, T Z" uniqKey="Baram T" first="T. Z." last="Baram">T. Z. Baram</name>
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<idno type="pmid">11113306</idno>
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<title xml:lang="en" level="a" type="main">NEURONAL ACTIVITY AND STRESS DIFFERENTIALLY REGULATE HIPPOCAMPAL AND HYPOTHALAMIC CORTICOTROPIN-RELEASING HORMONE EXPRESSION IN THE IMMATURE RAT</title>
<author>
<name sortKey="Hatalski, C G" sort="Hatalski, C G" uniqKey="Hatalski C" first="C. G." last="Hatalski">C. G. Hatalski</name>
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<name sortKey="Brunson, K L" sort="Brunson, K L" uniqKey="Brunson K" first="K. L." last="Brunson">K. L. Brunson</name>
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<name sortKey="Tantayanubutr, B" sort="Tantayanubutr, B" uniqKey="Tantayanubutr B" first="B." last="Tantayanubutr">B. Tantayanubutr</name>
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<author>
<name sortKey="Chen, Y" sort="Chen, Y" uniqKey="Chen Y" first="Y." last="Chen">Y. Chen</name>
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<author>
<name sortKey="Baram, T Z" sort="Baram, T Z" uniqKey="Baram T" first="T. Z." last="Baram">T. Z. Baram</name>
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<title level="j">Neuroscience</title>
<idno type="ISSN">0306-4522</idno>
<idno type="eISSN">1873-7544</idno>
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<date when="2000">2000</date>
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<p id="P1">Corticotropin-releasing hormone, a major neuromodulator of the neuroendocrine stress response, is expressed in the immature hippocampus, where it enhances glutamate receptor-mediated excitation of principal cells. Since the peptide influences hippocampal synaptic efficacy, its secretion from peptidergic interneuronal terminals may augment hippocampal-mediated functions such as learning and memory. However, whereas information regarding the regulation of corticotropin-releasing hormone’s abundance in CNS regions involved with the neuroendocrine responses to stress has been forthcoming, the mechanisms regulating the peptide’s levels in the hippocampus have not yet been determined. Here we tested the hypothesis that, in the immature rat hippocampus, neuronal stimulation, rather than neuroendocrine challenge, influences the peptide’s expression. Messenger RNA levels of corticotropin-releasing hormone in hippocampal CA1, CA3 and the dentate gyrus, as well as in the hypothalamic paraventricular nucleus, were determined after cold, a physiological challenge that activates the hypothalamic pituitary adrenal system in immature rats, and after activation of hippocampal neurons by hyperthermia. These studies demonstrated that, while cold challenge enhanced corticotropin-releasing hormone messenger RNA levels in the hypothalamus, hippocampal expression of this neuropeptide was unchanged. Secondly, hyperthermia stimulated expression of hippocampal immediate-early genes, as well as of corticotropin-releasing hormone. Finally, the mechanism of hippocampal corticotropin-releasing hormone induction required neuronal stimulation and was abolished by barbiturate administration.</p>
<p id="P2">Taken together, these results indicate that neuronal stimulation may regulate hippocampal corticotropin-releasing hormone expression in the immature rat, whereas the peptide’s expression in the hypothalamus is influenced by neuroendocrine challenges.</p>
</div>
</front>
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<pmc article-type="research-article" xml:lang="en">
<pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front>
<journal-meta>
<journal-id journal-id-type="nlm-journal-id">7605074</journal-id>
<journal-id journal-id-type="pubmed-jr-id">6087</journal-id>
<journal-id journal-id-type="nlm-ta">Neuroscience</journal-id>
<journal-title-group>
<journal-title>Neuroscience</journal-title>
</journal-title-group>
<issn pub-type="ppub">0306-4522</issn>
<issn pub-type="epub">1873-7544</issn>
</journal-meta>
<article-meta>
<article-id pub-id-type="pmid">11113306</article-id>
<article-id pub-id-type="pmc">3129847</article-id>
<article-id pub-id-type="manuscript">NIHMS306763</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Article</subject>
</subj-group>
</article-categories>
<title-group>
<article-title>NEURONAL ACTIVITY AND STRESS DIFFERENTIALLY REGULATE HIPPOCAMPAL AND HYPOTHALAMIC CORTICOTROPIN-RELEASING HORMONE EXPRESSION IN THE IMMATURE RAT</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname>HATALSKI</surname>
<given-names>C. G.</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>BRUNSON</surname>
<given-names>K. L.</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>TANTAYANUBUTR</surname>
<given-names>B.</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>CHEN</surname>
<given-names>Y.</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>BARAM</surname>
<given-names>T. Z.</given-names>
</name>
<xref ref-type="corresp" rid="CR1">*</xref>
</contrib>
<aff id="A1">Department of Anatomy & Neurobiology and Pediatrics, University of California, Irvine, CA 92697-4475, USA</aff>
</contrib-group>
<author-notes>
<corresp id="CR1">
<label>*</label>
To whom correspondence should be addressed. Tel.: + 1-949-824-1064; fax: + 1-949-824-1106.
<email>tallie@uci.edu</email>
(T. Z. Baram).</corresp>
</author-notes>
<pub-date pub-type="nihms-submitted">
<day>27</day>
<month>6</month>
<year>2011</year>
</pub-date>
<pub-date pub-type="ppub">
<year>2000</year>
</pub-date>
<pub-date pub-type="pmc-release">
<day>5</day>
<month>7</month>
<year>2011</year>
</pub-date>
<volume>101</volume>
<issue>3</issue>
<fpage>571</fpage>
<lpage>580</lpage>
<permissions>
<copyright-statement>© 2000 IBRO. Published by Elsevier Science Ltd. All rights reserved.</copyright-statement>
<copyright-year>2000</copyright-year>
</permissions>
<abstract>
<p id="P1">Corticotropin-releasing hormone, a major neuromodulator of the neuroendocrine stress response, is expressed in the immature hippocampus, where it enhances glutamate receptor-mediated excitation of principal cells. Since the peptide influences hippocampal synaptic efficacy, its secretion from peptidergic interneuronal terminals may augment hippocampal-mediated functions such as learning and memory. However, whereas information regarding the regulation of corticotropin-releasing hormone’s abundance in CNS regions involved with the neuroendocrine responses to stress has been forthcoming, the mechanisms regulating the peptide’s levels in the hippocampus have not yet been determined. Here we tested the hypothesis that, in the immature rat hippocampus, neuronal stimulation, rather than neuroendocrine challenge, influences the peptide’s expression. Messenger RNA levels of corticotropin-releasing hormone in hippocampal CA1, CA3 and the dentate gyrus, as well as in the hypothalamic paraventricular nucleus, were determined after cold, a physiological challenge that activates the hypothalamic pituitary adrenal system in immature rats, and after activation of hippocampal neurons by hyperthermia. These studies demonstrated that, while cold challenge enhanced corticotropin-releasing hormone messenger RNA levels in the hypothalamus, hippocampal expression of this neuropeptide was unchanged. Secondly, hyperthermia stimulated expression of hippocampal immediate-early genes, as well as of corticotropin-releasing hormone. Finally, the mechanism of hippocampal corticotropin-releasing hormone induction required neuronal stimulation and was abolished by barbiturate administration.</p>
<p id="P2">Taken together, these results indicate that neuronal stimulation may regulate hippocampal corticotropin-releasing hormone expression in the immature rat, whereas the peptide’s expression in the hypothalamus is influenced by neuroendocrine challenges.</p>
</abstract>
<kwd-group>
<kwd>hippocampus</kwd>
<kwd>corticotropin-releasing factor</kwd>
<kwd>c-
<italic>fos</italic>
</kwd>
<kwd>rat</kwd>
<kwd>hypothalamus</kwd>
<kwd>stress</kwd>
</kwd-group>
<funding-group>
<award-group>
<funding-source country="United States">National Institute of Neurological Disorders and Stroke : NINDS</funding-source>
<award-id>R01 NS035439-03 || NS</award-id>
</award-group>
<award-group>
<funding-source country="United States">National Institute of Neurological Disorders and Stroke : NINDS</funding-source>
<award-id>R01 NS028912-06 || NS</award-id>
</award-group>
</funding-group>
</article-meta>
</front>
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