Reactive Structural Dynamics of Synaptic Mitochondria in Ischemic Delayed Neuronal Death

:  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 d...

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Veröffentlicht in:Annals of the New York Academy of Sciences 2006-12, Vol.1090 (1), p.26-34
Hauptverfasser: BERTONI-FREDDARI, CARLO, FATTORETTI, PATRIZIA, CASOLI, TIZIANA, DI STEFANO, GIUSEPPINA, SOLAZZI, MORENO, PERNA, ELISA, DE ANGELIS, CLARA
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container_title Annals of the New York Academy of Sciences
container_volume 1090
creator BERTONI-FREDDARI, CARLO
FATTORETTI, PATRIZIA
CASOLI, TIZIANA
DI STEFANO, GIUSEPPINA
SOLAZZI, MORENO
PERNA, ELISA
DE ANGELIS, CLARA
description :  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.
doi_str_mv 10.1196/annals.1378.003
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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. 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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. 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subjects Animals
Brain Ischemia - pathology
CA1 neurons
Cell Death
experimental ischemia-delayed cell death
Female
mitochondrial structural dynamics
morphometry
Neurons - pathology
Rats
Rats, Inbred WKY
Synapses
synaptic mitochondria
title Reactive Structural Dynamics of Synaptic Mitochondria in Ischemic Delayed Neuronal Death
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