Cerebral metabolic responses to clomipramine are greatly reduced following pretreatment with the specific serotonin neurotoxin para-chloroamphetamine (PCA). A 2-Deoxyglucose study in rats

Ulderico Freo, Pietro Pietrini, Gilberto Pizzolato, Maura Furey, Antonio Merico, Susanna Ruggero, Mauro Dam, Leontino Battistin

Research output: Contribution to journalArticle

Abstract

To determine if reported reductions of regional cerebral metabolic rates for glucose (rCMRglc) induced by the tryciclic antidepressant clomipramine (CMI) (10 mg/kg) are due to a presynaptic action on serotonin (5-HT) terminals, 3-month-old Fischer-344 rats were given parachloroamphetamine (PCA), a serotonin neurotoxin. rCMRglc was measured 3 weeks later in 55 brain regions after the administration of saline or CMI using the quantitative autoradiographic [14C]2-deoxyglucose procedure. PCA alone increased rCMRglc in the visual cortex. CMI alone reduced rCMRglc in 18 (33%) of the studied regions, including telencephalic, diencephalic, limbic, and brain stem areas. In PCA-lesioned rats, metabolic responses to CMI (10 mg/kg) were greatly reduced, and significant rCMRglc decreases were observed only in 4 (7%) of the brain areas, including the hippocampus and raphe nuclei. Abolition by PCA of the metabolic responses to CMI confirms that CMI, at the dose studied, reduces rCMRglc via a presynaptic mechanism, likely the 5-HT reuptake sites.

Original languageEnglish
Pages (from-to)215-222
Number of pages8
JournalNeuropsychopharmacology
Volume13
Issue number3
DOIs
Publication statusPublished - 1995

Keywords

  • Amphetamine
  • Antidepressants
  • Clomipramine
  • Deoxyglucose
  • Rat
  • Serotonin

ASJC Scopus subject areas

  • Psychiatry and Mental health
  • Pharmacology

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