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Increased CRF signalling in a ventral tegmental area-interpeduncular nucleus-medial habenula circuit induces anxiety during nicotine withdrawal

Academic Article
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Overview

authors

  • Zhao-Shea, R.
  • DeGroot, S. R.
  • Liu, L.
  • Vallaster, M.
  • Pang, X.
  • Su, Q.
  • Gao, G.
  • Rando, O. J.
  • Martin, G. E.
  • George, Olivier
  • Gardner, P. D.
  • Tapper, A. R.

publication date

  • 2015

journal

  • Nature Communications  Journal

abstract

  • Increased anxiety is a prominent withdrawal symptom in abstinent smokers, yet the neuroanatomical and molecular bases underlying it are unclear. Here we show that withdrawal-induced anxiety increases activity of neurons in the interpeduncular intermediate (IPI), a subregion of the interpeduncular nucleus (IPN). IPI activation during nicotine withdrawal was mediated by increased corticotropin releasing factor (CRF) receptor-1 expression and signalling, which modulated glutamatergic input from the medial habenula (MHb). Pharmacological blockade of IPN CRF1 receptors or optogenetic silencing of MHb input reduced IPI activation and alleviated withdrawal-induced anxiety; whereas IPN CRF infusion in mice increased anxiety. We identified a mesointerpeduncular circuit, consisting of ventral tegmental area (VTA) dopaminergic neurons projecting to the IPN, as a potential source of CRF. Knockdown of CRF synthesis in the VTA prevented IPI activation and anxiety during nicotine withdrawal. These data indicate that increased CRF receptor signalling within a VTA-IPN-MHb circuit triggers anxiety during nicotine withdrawal.

subject areas

  • Animals
  • Anxiety
  • Corticotropin-Releasing Hormone
  • Habenula
  • Interpeduncular Nucleus
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Nerve Net
  • Nicotine
  • Receptors, Corticotropin-Releasing Hormone
  • Signal Transduction
  • Substance Withdrawal Syndrome
  • Ventral Tegmental Area
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Identity

PubMed Central ID

  • PMC4405813

International Standard Serial Number (ISSN)

  • 2041-1723

Digital Object Identifier (DOI)

  • 10.1038/ncomms7770

PubMed ID

  • 25898242
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Additional Document Info

start page

  • 6770

volume

  • 6

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