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Neurotrophin-3 modulates noradrenergic neuron function and opiate withdrawal

  1. Author:
    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.

  2. Author Address

    Whitehead Inst, 9 Cambridge Ctr, Cambridge, MA 02142 USA. Whitehead Inst, Cambridge, MA 02142 USA. Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA. Yale Univ, Dept Psychiat, New Haven, CT 06520 USA. Univ Washington, Dept Physiol & Biophys, Seattle, WA 98195 USA. NCI, Frederick, MD 21701 USA. MIT, Dept Biol, Cambridge, MA USA. Boston Univ, Dept Neurol, Boston, MA 02215 USA. Jaenisch R Whitehead Inst, 9 Cambridge Ctr, Cambridge, MA 02142 USA.
    1. Year: 2001
  2. Journal: Molecular Psychiatry
    1. 6
    2. 5
    3. Pages: 593-604
  4. Type of Article: Article
  1. Abstract:

    Somatic 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 noncatecholaminergic neurons may modulate opiate withdrawal and noradrenergic signalling.

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