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Conditioned aversive memory associated with morphine withdrawal increases brain-derived neurotrophic factor in

Elena Martínez-Laorden1, Javier Navarro-Zaragoza1, María-Victoria Milanés1

  • 1Department of Pharmacology, Faculty of Medicine, University of Murcia, Murcia, Spain.

Addiction Biology
|July 9, 2019
PubMed

Insights

Conditioned morphine withdrawal increases brain-derived neurotrophic factor (BDNF) and hypothalamic-pituitary-adrenocortical (HPA) axis activity, crucial for forming aversive memories. Blocking CRF1 receptors disrupts this process, highlighting the HPA axis and BDNF connection.

Area of Science:

  • Neuroscience
  • Neurobiology
  • Pharmacology

Background:

  • Morphine increases brain-derived neurotrophic factor (BDNF) expression.
  • The impact of conditioned naloxone-precipitated morphine withdrawal on BDNF and proBDNF is largely unknown.
  • Corticotropin-releasing factor (CRF)/CRF1 receptor signaling's role in withdrawal-induced neuroplasticity requires further investigation.

Purpose of the Study:

  • To investigate the role of CRF/CRF1 receptor signaling in BDNF expression and hypothalamic-pituitary-adrenocortical (HPA) axis activity during conditioned morphine withdrawal.
  • To examine the involvement of BDNF and proBDNF in the acquisition and extinction of aversive memories associated with morphine withdrawal.
  • To elucidate the connection between the HPA axis and BDNF in the formation and extinction of aversive memories.

Main Methods:

  • Utilized the conditioned place aversion (CPA) paradigm in male mice dependent on morphine.
  • Administered naloxone to precipitate withdrawal and assessed BDNF and proBDNF expression in the dentate gyrus (DG) and basolateral amygdala (BLA).
  • Measured corticosterone plasma levels and evaluated the effects of CRF1 receptor blockade (CP-154,526) on CPA acquisition, extinction, and associated neurobiological changes.

Main Results:

  • Conditioned naloxone-induced morphine withdrawal increased BDNF expression in the DG and BLA, paralleled by elevated corticosterone plasma levels.
  • These findings indicate that BDNF expression and HPA axis activation are critical for aversive memory acquisition.
  • CPA extinction led to decreased corticosterone levels and BDNF expression, underscoring BDNF's role in maintaining aversive memory. CRF1 receptor antagonist treatment before conditioning impaired aversive memory acquisition and associated neurobiological changes.

Conclusions:

  • The study reveals a significant connection between the HPA axis and BDNF in the formation and extinction of aversive memories.
  • CRF1 receptor signaling plays a crucial role in mediating the neurobiological adaptations during conditioned morphine withdrawal.
  • BDNF expression and HPA axis activity are key components in the neurocircuitry underlying drug withdrawal-associated learning and memory.
Keywords:
aversive memory acquisition and extinctionbrain-derived neurotrophic factor (BDNF)conditioned place aversion (CPA)corticotropin-releasing factor (CRF) 1 receptorhypothalamic-pituitary-adrenocortical (HPA) axis

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