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Article: Neurotrophin-3 modulates noradrenergic neuron function and opiate withdrawal

TitleNeurotrophin-3 modulates noradrenergic neuron function and opiate withdrawal
Authors
Akbarian, S.Bates, B.Liu, R. J.Skirboll, S. L.Pejchal, T.Coppola, V.Sun, L. D.Fan, G.Kucera, J.Wilson, M. A.Tessarollo, L.Kosofsky, B. E.Taylor, J. R.Bothwell, M.Nestler, E. J.Aghajanian, G. K.Jaenisch, R.
KeywordsAddiction
Cre recombinase
Locus coeruleus
Medulla
Morphine
Norepinephrine
Pons
Issue Date2001
Citation
Molecular Psychiatry, 2001, v. 6, n. 5, p. 593-604 How to Cite?
DOI: http://dx.doi.org/10.1038/sj.mp.4000897
AbstractSomatic symptoms and aversion of opiate withdrawal, regulated by noradrenergic signaling, were attenuated in mice with a CNS-wide conditional ablation of neurotrophin-3. This occurred in conjunction with altered cAMP-mediated excitation and reduced upregulation of tyrosine hydroxylase in A6 (locus coeruleus) without loss of neurons. Transgene-derived NT-3 expressed by noradrenergic neurons of conditional mutants restored opiate withdrawal symptoms. Endogenous NT-3 expression, strikingly absent in noradrenergic neurons of postnatal and adult brain, is present in afferent sources of the dorsal medulla and is upregulated after chronic morphine exposure in noradrenergic projection areas of the ventral forebrain. NT-3 expressed by non-catecholaminergic neurons may modulate opiate withdrawal and noradrenergic signalling.
Persistent Identifierhttp://hdl.handle.net/10722/365664
ISSN
1359-4184
2023 Impact Factor: 9.6
2023 SCImago Journal Rankings: 3.895

 

DC FieldValueLanguage
dc.contributor.authorAkbarian, S.-
dc.contributor.authorBates, B.-
dc.contributor.authorLiu, R. J.-
dc.contributor.authorSkirboll, S. L.-
dc.contributor.authorPejchal, T.-
dc.contributor.authorCoppola, V.-
dc.contributor.authorSun, L. D.-
dc.contributor.authorFan, G.-
dc.contributor.authorKucera, J.-
dc.contributor.authorWilson, M. A.-
dc.contributor.authorTessarollo, L.-
dc.contributor.authorKosofsky, B. E.-
dc.contributor.authorTaylor, J. R.-
dc.contributor.authorBothwell, M.-
dc.contributor.authorNestler, E. J.-
dc.contributor.authorAghajanian, G. K.-
dc.contributor.authorJaenisch, R.-
dc.date.accessioned2025-11-05T09:46:41Z-
dc.date.available2025-11-05T09:46:41Z-
dc.date.issued2001-
dc.identifier.citationMolecular Psychiatry, 2001, v. 6, n. 5, p. 593-604-
dc.identifier.issn1359-4184-
dc.identifier.urihttp://hdl.handle.net/10722/365664-
dc.description.abstractSomatic symptoms and aversion of opiate withdrawal, regulated by noradrenergic signaling, were attenuated in mice with a CNS-wide conditional ablation of neurotrophin-3. This occurred in conjunction with altered cAMP-mediated excitation and reduced upregulation of tyrosine hydroxylase in A6 (locus coeruleus) without loss of neurons. Transgene-derived NT-3 expressed by noradrenergic neurons of conditional mutants restored opiate withdrawal symptoms. Endogenous NT-3 expression, strikingly absent in noradrenergic neurons of postnatal and adult brain, is present in afferent sources of the dorsal medulla and is upregulated after chronic morphine exposure in noradrenergic projection areas of the ventral forebrain. NT-3 expressed by non-catecholaminergic neurons may modulate opiate withdrawal and noradrenergic signalling.-
dc.languageeng-
dc.relation.ispartofMolecular Psychiatry-
dc.subjectAddiction-
dc.subjectCre recombinase-
dc.subjectLocus coeruleus-
dc.subjectMedulla-
dc.subjectMorphine-
dc.subjectNorepinephrine-
dc.subjectPons-
dc.titleNeurotrophin-3 modulates noradrenergic neuron function and opiate withdrawal-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1038/sj.mp.4000897-
dc.identifier.pmid11526474-
dc.identifier.scopuseid_2-s2.0-17944374357-
dc.identifier.volume6-
dc.identifier.issue5-
dc.identifier.spage593-
dc.identifier.epage604-

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