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Functional nerve growth factor and trkA autocrine/paracrine circuits in adult rat cortex are revealed by episodic ethanol exposure and withdrawal.

Functional nerve growth factor and trkA autocrine/paracrine circuits in adult rat cortex are revealed by episodic ethanol exposure and withdrawal. Research Abstract Details 

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  • Functional nerve growth factor and trkA autocrine/paracrine circuits in adult rat cortex are revealed by episodic ethanol exposure and withdrawal. Abstract Text:

    marla b brunsMarla B Bruns,michael w millerMichael W Miller,

    The hypothesis tested is that cortical neurotrophins communicate through an inducible autocrine/paracrine mechanism. As ethanol (Et) can induce cortical nerve growth factor (NGF) expression, adult rats were challenged with Et on three consecutive days per week for 6 weeks. The focus of the study was layer V, the chief repository of receptor-expressing neuronal cell bodies. Brains were collected immediately after the sixth Et exposure or 72 h later [i.e., following withdrawal (WD)]. Double-label in situ hybridization-immunohistochemistry studies showed that many neuronal somata co-expressed NGF mRNA with NGF, trkA, or phosphorylated trk (p-trk), essential components of an inducible autocrine system. The frequencies of co-labeling were affected by neither Et nor WD. On the contrary, Et increased the number of NGF mRNA-expressing neurons and the amount of NGF mRNA expressed per cell. Et also increased total cortical concentration of NGF protein, the number of layer V neurons expressing trkA transcript, the amount of trkA mRNA expressed per neuron, and trkA phosphorylation. Following WD, the frequency of NGF-mRNA-expressing cells increased, although transcript and protein content fell. WD induced an increase in trkA mRNA and protein expression, however, p-trk expression was unaffected. Thus, Et treatment reveals that layer V has inducible autocrine/paracrine and anterograde neurotrophin systems. WD unveils the dynamism and recruitability of these systems.

    Functional nerve growth factor and trkA autocrine/paracrine circuits in adult rat cortex are revealed by episodic ethanol exposure and withdrawal. Publishing Authors By Initials

    mb brunsMB Bruns,mw millerMW Miller,

    For similar disorders of environmental origin: substance-related disorders: substance withdrawal syndrome research abstracts see: disorders of environmental origin: substance-related disorders: substance withdrawal syndrome research

    PUBMED ID PMID:

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    Functional nerve growth factor and trkA autocrine/paracrine circuits in adult rat cortex are revealed by episodic ethanol exposure and withdrawal. Journal Published:

    PUBLICATION TYPE: Research Support, N.I.H., Extr

    Journal: Journal of neurochemistry

    VOLUME: 100

    Page Numbers: 1155-68

    Journal Abbreviation: J. Neurochem.

    ISSN: 0022-3042

    DAY: 3

    MONTH: Mar

    YEAR: 2007

    Functional nerve growth factor and trkA autocrine/paracrine circuits in adult rat cortex are revealed by episodic ethanol exposure and withdrawal. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 2985190

    Functional nerve growth factor and trkA autocrine/paracrine circuits in adult rat cortex are revealed by episodic ethanol exposure and withdrawal. Keywords Mesh Terms:

    KEYWORDS: Substance Withdrawal Syndrome

    MESH TERMS: metabolism

    Chemical & Substance for Abstract: Functional nerve growth factor and trkA autocrine/paracrine circuits in adult rat cortex are revealed by episodic ethanol exposure and withdrawal. Information

    Substance Name: Receptor, trkA

    Registry Number: EC 2.7.1.112

    Grant and Affiliation Information for Functional nerve growth factor and trkA autocrine/paracrine circuits in adult rat cortex are revealed by episodic ethanol exposure and withdrawal.

    AFFILIATION: Department of Neuroscience and Physiology, State University of New York-Upstate Medical University, Syracuse, New York 13210, USA.

    Country: England

    England Research PublicationEngland Research Publication

    AGENCY: United States NIAAA

    GRANT: AA15245

    ACRONYM: AA

    MEDLINETA: J Neurochem

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

    Number Hits: 0

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