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Morphine Withdrawal Increases Brain-Derived Neurotrophic Factor Precursor.

Alessia Bachis1, Lee A Campbell1,2, Kierra Jenkins1

  • 1Laboratory of Preclinical Neurobiology, Department of Neuroscience, Georgetown University Medical Center, 3970 Reservoir Rd NW, Washington, DC, 20057, USA.

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Morphine withdrawal significantly elevates pro-brain-derived neurotrophic factor (proBDNF) levels more than morphine treatment, potentially increasing neurotoxicity. Understanding these changes is crucial for mitigating opioid abuse effects.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pharmacology

Background:

  • Morphine increases brain-derived neurotrophic factor (BDNF) expression.
  • The impact of morphine withdrawal on BDNF and its precursor, proBDNF, is largely unknown.
  • ProBDNF can induce neuronal apoptosis, a critical factor in neurotoxicity.

Purpose of the Study:

  • To investigate changes in BDNF and proBDNF levels during chronic morphine treatment and withdrawal in rats.
  • To explore the underlying mechanisms, including the role of tissue plasminogen activator (tPA), in differential BDNF/proBDNF regulation.

Main Methods:

  • Rats received escalating doses of morphine, followed by 60 hours of spontaneous withdrawal.
  • BDNF, proBDNF, MMP-3, MMP-7, furin, and tPA levels were analyzed in the frontal cortex and striatum.
  • Cortical neurons were treated with morphine and a tPA inhibitor (PAI-1) to confirm tPA's role.

Main Results:

  • Both morphine treatment and withdrawal increased BDNF and proBDNF levels.
  • Withdrawal led to a more pronounced increase in proBDNF compared to morphine treatment.
  • Morphine elevated tPA levels, while withdrawal decreased them.
  • Inhibition of tPA reversed morphine's effect on proBDNF, indicating tPA's involvement in proBDNF processing.

Conclusions:

  • Morphine administration and withdrawal differentially regulate BDNF and proBDNF levels.
  • Morphine promotes extracellular proBDNF processing via tPA, increasing mature BDNF availability.
  • ProBDNF's potential negative impact on synaptic repair highlights the importance of preventing withdrawal to reduce opioid-induced neurotoxicity.