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The neuroprotective effect of memantine on methamphetamine-induced cognitive deficits

Jian-Dong Long1, Yao Liu2, Dong-Liang Jiao2

  • 1Key Laboratory of Receptor Research, Shanghai Institute of Materia Medica and Collaborative Innovation Center for Brain Science, Chinese Academy of Sciences, Shanghai 201203, China.

Behavioural Brain Research
|February 2, 2017
PubMed

Insights

Methamphetamine (METH) impairs long-term memory, but memantine (MEM) offers neuroprotection. Memantine reversed METH-induced cognitive deficits and reduced apoptosis in the prefrontal cortex.

Area of Science:

  • Neuroscience
  • Pharmacology

Background:

  • Methamphetamine (METH) exposure causes neurotoxicity and cognitive deficits.
  • Understanding the neuroprotective mechanisms against METH-induced impairments is crucial.

Purpose of the Study:

  • To investigate METH's effect on cognitive function.
  • To determine the neuroprotective potential of memantine (MEM) against METH-induced memory deficits.
  • To explore the underlying anti-apoptotic mechanisms.

Main Methods:

  • Mice were administered METH to induce cognitive impairment.
  • Memantine (MEM) was co-administered with METH to assess neuroprotection.
  • Protein levels of Bcl-2 and cleaved caspase-3 in the prefrontal cortex (PFC) were analyzed.

Main Results:

  • METH impaired long-term memory (24h) but not short-term memory (5min).
  • MEM pretreatment significantly improved METH-induced cognitive deficits.
  • METH decreased Bcl-2 and increased cleaved caspase-3 expression in the PFC, effects reversed by MEM.

Conclusions:

  • Memantine exhibits significant neuroprotective effects against METH-induced cognitive impairment.
  • The protective mechanism of memantine involves the modulation of apoptotic pathways in the prefrontal cortex.
  • These findings highlight memantine's potential therapeutic value for METH-related neurotoxicity.
Keywords:
ApoptosisCognitive deficitsMemantineMethamphetaminePrefrontal cortex

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