The role of brain histamine in acute and chronic stresses
Identifieur interne : 001507 ( Main/Exploration ); précédent : 001506; suivant : 001508The role of brain histamine in acute and chronic stresses
Auteurs : C. Ito [Japon]Source :
- Biomedicine & Pharmacotherapy [ 0753-3322 ] ; 2000.
English descriptors
- Entity :
- org : Japan Summary.
- KwdEn :
- Teeft :
- Accumbens, Acute increaseof, Acute stress, Agonist, Antagonist, Anterior pituitary hormone, Behavioral sensitization, Biogenic amine, Brain histamine, Chronic restraint stress, Chronic stress, Diencephalon, Discrepant result, Edition scientifiques, Fisher rat, Histamine, Histamine agonist, Histamine turnover, Histaminergic, Histaminergic neuron system, Histidine decarboxylase, Important role, Limbic system, Mammalian brain, Medicales elsevier, Neuron, Nucleus accumbens, Pharmacol, Pharmacol biochem behav, Presynaptic histamine, Receptor, Receptor agonist, Receptor antagonist, Stress vulnerability, Striatum, Turnover.
Abstract
Summary: As a neurotransmitter or neuromodulator, brain histamine has a variety of physiological roles in brain functions. Acute stress increases the histamine turnovers in the diencephalon, nucleus accumbens and striatum. Histamine regulates anterior pituitary hormones. Anxiolytic drugs also decrease brain histamine turnover. Histamine H1 receptor antagonists and H3 receptor agonists decrease the anxiety state. These findings show that acute stresses increase brain histamine turnover, especially in the diencephalon, which would be partly related to the pathology of anxiety. Moreover, chronic restraint stress continued to increase the histamine turnovers in the nucleus accumbens and striatum, not in the diencephalon. Chronic administration of psychostimulants also increase the striatal histamine release. Histamine agonists prevent psychostimulant-induced behavior and the development of behavioral sensitization. These results indicate that chronic stress continues to increase the histamine turnovers in the nucleus accumbens and striatum, which would have a role of preventing stress vulnerability. Moreover, histamine H3 receptor antagonists have antidepressive effects. Therefore, no increase of histamine turnover in the diencephalon is related to the pathology of depressive state.
Url:
DOI: 10.1016/S0753-3322(00)80069-4
Affiliations:
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Ito</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Psychiatry, Tohoku Graduate University School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai 980-8574</wicri:regionArea><wicri:noRegion>Sendai 980-8574</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Biomedicine & Pharmacotherapy</title><title level="j" type="abbrev">BIOPHA</title><idno type="ISSN">0753-3322</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="2000">2000</date><biblScope unit="volume">54</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="263">263</biblScope><biblScope unit="page" to="267">267</biblScope></imprint><idno type="ISSN">0753-3322</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0753-3322</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Entity" type="org" xml:lang="en"><term>Japan Summary</term></keywords><keywords scheme="KwdEn" xml:lang="en"><term>acute stress</term><term>brain histamine</term><term>chronic stress</term></keywords><keywords scheme="Teeft" xml:lang="en"><term>Accumbens</term><term>Acute increaseof</term><term>Acute stress</term><term>Agonist</term><term>Antagonist</term><term>Anterior pituitary hormone</term><term>Behavioral sensitization</term><term>Biogenic amine</term><term>Brain histamine</term><term>Chronic restraint stress</term><term>Chronic stress</term><term>Diencephalon</term><term>Discrepant result</term><term>Edition scientifiques</term><term>Fisher rat</term><term>Histamine</term><term>Histamine agonist</term><term>Histamine turnover</term><term>Histaminergic</term><term>Histaminergic neuron system</term><term>Histidine decarboxylase</term><term>Important role</term><term>Limbic system</term><term>Mammalian brain</term><term>Medicales elsevier</term><term>Neuron</term><term>Nucleus accumbens</term><term>Pharmacol</term><term>Pharmacol biochem behav</term><term>Presynaptic histamine</term><term>Receptor</term><term>Receptor agonist</term><term>Receptor antagonist</term><term>Stress vulnerability</term><term>Striatum</term><term>Turnover</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Summary: As a neurotransmitter or neuromodulator, brain histamine has a variety of physiological roles in brain functions. Acute stress increases the histamine turnovers in the diencephalon, nucleus accumbens and striatum. Histamine regulates anterior pituitary hormones. Anxiolytic drugs also decrease brain histamine turnover. Histamine H1 receptor antagonists and H3 receptor agonists decrease the anxiety state. These findings show that acute stresses increase brain histamine turnover, especially in the diencephalon, which would be partly related to the pathology of anxiety. Moreover, chronic restraint stress continued to increase the histamine turnovers in the nucleus accumbens and striatum, not in the diencephalon. Chronic administration of psychostimulants also increase the striatal histamine release. Histamine agonists prevent psychostimulant-induced behavior and the development of behavioral sensitization. These results indicate that chronic stress continues to increase the histamine turnovers in the nucleus accumbens and striatum, which would have a role of preventing stress vulnerability. Moreover, histamine H3 receptor antagonists have antidepressive effects. Therefore, no increase of histamine turnover in the diencephalon is related to the pathology of depressive state.</div></front></TEI><affiliations><list><country><li>Japon</li></country></list><tree><country name="Japon"><noRegion><name sortKey="Ito, C" sort="Ito, C" uniqKey="Ito C" first="C." last="Ito">C. Ito</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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