Methamphetamine self-administration attenuates hippocampal serotonergic deficits: Role of brain-derived neurotrophic factor

Lisa M. McFadden, Paula L. Vieira-Brock, Glen R. Hanson, Annette E. Fleckenstein

Research output: Contribution to journalArticlepeer-review

19 Scopus citations


Preclinical studies suggest that prior treatment with escalating doses of methamphetamine (METH) attenuates the persistent deficits in hippocampal serotonin (5-hydroxytryptamine; 5HT) transporter (SERT) function resulting from a subsequent 'binge' METH exposure. Previous work also demonstrates that brain-derived neurotrophic factor (BDNF) exposure increases SERT function. The current study investigated changes in hippocampal BDNF protein and SERT function in rats exposed to saline or METH self-administration prior to a binge exposure to METH or saline. Results revealed that METH self-administration increased hippocampal mature BDNF (mBDNF) immunoreactivity compared to saline-treated rats as assessed 24 h after the start of the last session. Further, mBDNF immunoreactivity was increased and SERT function was not altered in rats that self-administered METH prior to the binge METH exposure as assessed 24 h after the binge exposure. These results suggest that prior exposure to contingent METH increases hippocampal mBDNF, and this may contribute to attenuated deficits in SERT function.

Original languageEnglish (US)
Pages (from-to)1315-1320
Number of pages6
JournalInternational Journal of Neuropsychopharmacology
Issue number8
StatePublished - Aug 20 2014
Externally publishedYes


  • Brain-derived neurotrophic factor
  • hippocampus
  • methamphetamine
  • self-administration
  • serotonin transporter

ASJC Scopus subject areas

  • Pharmacology
  • Psychiatry and Mental health
  • Pharmacology (medical)


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