Reactive structural dynamics of synaptic mitochondria in ischemic delayed neuronal death

Carlo Bertoni-Freddari, Patrizia Fattoretti, Tiziana Casoli, Giuseppina Di Stefano, Moreno Solazzi, Elisa Perna, Clara De Angelis

Research output: Chapter in Book/Report/Conference proceedingConference contribution


The effect of transient global ischemia on the ultrastructural features of synaptic mitochondria at the distal dendrites of CA1 hippocampal neurons was investigated in 3-month-old rats. Sham surgery was performed on age-matched controls. The number of mitochondria/μm3 of neurophils (Nv: numeric density), the mitochondrial average size (average volume: V), and longer diameter (Fmax) as well as the overall fraction of neurophils occupied by mitochondria (volume density: Vv) were measured by computer-assisted morphometry. In ischemic rats, a 10% nonsignificant decrease of Nv was found, V increased nonsignificantly by 11%, and Fmax increased nonsignificantly by 5% versus controls. As a final outcome of these balanced changes, Vv remained unchanged between the two experimental groups investigated. In ischemic animals, the percentage distribution of V showed that the population of CA1 synaptic mitochondria was composed by an increased fraction of oversized organelles, while the Fmax distribution revealed that this enlargement was due to an increased percentage of elongated organelles. Thus, the observed increase in size should not be considered as a swelling phenomenon; on the contrary, it may represent a physiological and well-documented step in mitochondrial biogenesis. The above parameters are currently supposed to provide information on the adaptive structural reorganization of mitochondrial morphology under different environmental stimulations. Conceivably, these findings document a positive reactive response to ischemia of the mitochondrial structural dynamics at CA1 synaptic terminals and suggest consideration of these organelles as reliable targets in the development of neuroprotective therapeutic interventions to treat vascular brain diseases, for example, stroke.

Original languageEnglish
Title of host publicationAnnals of the New York Academy of Sciences
Number of pages9
Publication statusPublished - Dec 2006

Publication series

NameAnnals of the New York Academy of Sciences
ISSN (Print)00778923
ISSN (Electronic)17496632


  • CA1 neurons
  • Experimental ischemia-delayed cell death
  • Mitochondrial structural dynamics
  • Morphometry
  • Synaptic mitochondria

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)


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