Mitochondria at the neuronal presynapse in health and disease

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Abstract

Synapses enable neurons to communicate with each other and are therefore a prerequisite for normal brain function. Presynaptically, this communication requires energy and generates large fluctuations in calcium concentrations. Mitochondria are optimized for supplying energy and buffering calcium, and they are actively recruited to presynapses. However, not all presynapses contain mitochondria; thus, how might synapses with and without mitochondria differ? Mitochondria are also increasingly recognized to serve additional functions at the presynapse. Here, we discuss the importance of presynaptic mitochondria in maintaining neuronal homeostasis and how dysfunctional presynaptic mitochondria might contribute to the development of disease.

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The effects of temperature, pH, and magnesium on the diffusion coefficient of ATP in solutions of physiological ionic strength.

Jeff Locke, Anita M. Hubley, T Moerland (1996)

Intracellular diffusive transport of adenosine triphosphate (ATP) is critical to cellular metabolism. Physical models predict that diffusion coefficients (D) of small molecules are functions of temperature and viscosity of the diffusive environment. Therefore, changes in body temperature, commonly experienced by poikilotherms, are expected to result in changes in the rate of intracellular ATP transport. However, it has been postulated that changes in the electrical charge of ATP may influence the interaction between ATP and the cytosol and that the temperature sensitivity of DATP may deviate from the predicted relationship. To investigate the effects of changes in electrical charge on the temperature sensitivity of DATP, we measured DATP under various conditions of temperature, pH, and pMg2+. Changes in pH and pMg2+ were used to alter the net charge of ATP, and DATP was measured in solutions of physiological ionic strength. Results showed a positive correlation between DATP and temperature; DATP = 1.75 +/- 0.09, 3.68 +/- 0.14, and 4.64 +/- 0.13 (mean +/- S.E.M.) x 10(-6) cm2/s at 5 degrees C, 25 degrees C, and 40 degrees C, respectively. Changes in pH and pMg2+ did not significantly influence DATP, and the change in DATP with respect to temperature was similar to that predicted on the basis of changes in temperature and viscosity of the aqueous medium.

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Amyloid beta-peptide effects on synaptosomes from apolipoprotein E-deficient mice.

J Keller, C Lauderback, D A Butterfield … (2000)

Apolipoprotein E (apoE) is present in the brain and may contribute to neurophysiologic or neuropathologic events, depending on environmental and genetic influences. Recent studies indicate a role for apoE in synaptic plasticity and maintenance of synaptic membrane symmetry, suggesting that apoE may be involved in regulating synaptic homeostasis. In the present study, cerebrocortical synaptosomes were prepared from transgenic mice lacking apoE (apoE KO) to analyze the possible contribution of apoE toward maintaining homeostasis in synaptosomes. Synaptosomal preparations from apoE KO and wild-type mice exhibited similar basal levels of reactive oxygen species, mitochondrial function, and caspase activity; however, following application of amyloid beta-peptide [Abeta(1-40)], apoE KO synaptosomes displayed increased levels of oxidative stress, mitochondrial dysfunction, and caspase activation compared with synaptosomes from wild-type mice. Synaptosomal membranes from apoE KO mice were more fluid than wild-type synaptosomes and contained higher levels of thiobarbituric acid-reactive substances, consistent with elevated levels of lipid peroxidation occurring in the synapses of apoE KO mice. Together, these data are consistent with a role for apoE in maintaining homeostasis by attenuating oxidative stress, caspase activation, and mitochondrial homeostasis in synapses.

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Author and article information

Journal

Title: Nature Reviews Neuroscience

Abbreviated Title: Nat Rev Neurosci

Publisher: Springer Science and Business Media LLC

ISSN (Print): 1471-003X

ISSN (Electronic): 1471-0048

Publication date Created: February 2018

Publication date (Electronic): January 19 2018

Publication date (Print): February 2018

Volume: 19

Issue: 2

Pages: 63-80

Article

DOI: 10.1038/nrn.2017.170

PubMed ID: 29348666

SO-VID: 8f944114-4216-43ab-9e9a-edc03b3c53d7

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http://www.springer.com/tdm

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