A gastrin-releasing peptide receptor antagonist blocks d-amphetamine-induced hyperlocomotion and increases hippocampal NGF and BDNF levels in rats Academic Article uri icon

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  • The gastrin-releasing peptide receptor (GRPR) has emerged as a novel molecular target in neurological and psychiatric disorders, and previous animal studies suggest that GRPR antagonists might display cognitive-enhancing and antipsychotic properties. Hyperlocomotion produced by administration of D-amphetamine (D-AMPH) to rats has been put forward as a model of the manic phase of bipolar disorder (BD). In the present study, we examined the effects of a single systemic administration of the GRPR antagonist [D-Tpi(6), Leu(13) psi(CH(2)NH)-Leu(14)] bombesin (6-14) (RC-3095) on hyperlocomotion induced by a single systemic injection of D-AMPH in male rats. We also evaluated the levels of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in the hippocampus of rats treated with D-AMPH and RC-3095. Administration of RC-3095 at any of the doses used blocked D-AMPH-induced hyperlocomotion. Specific doses of RC-3095 increased the levels of NGF and BDNF in the dorsal hippocampus. Administration of D-AMPH did not affect NGF or BDNF levels by itself, but blocked the RC-3095 effects. The results suggest that GRPR antagonists might display anti-manic activity.


  • Kauer-Sant’Anna, Márcia
  • Andreazza, Ana Cristina
  • Valvassori, Samira S
  • Martins, Márcio Rodrigo
  • Barbosa, Luciana M
  • Schwartsmann, Gilberto
  • Roesler, Rafael
  • Quevedo, João
  • Kapczinski, Flavio

publication date

  • July 2007