Biogenetic and morphofunctional heterogeneity of mitochondria: the case of synaptic mitochondria

被引:38
作者
Fedorovich, Sergei V. [1 ]
Waseem, Tatyana V. [2 ]
Puchkova, Ludmila V. [3 ,4 ,5 ]
机构
[1] Inst Biophys & Cell Engn, Akad Skaya St 27, Minsk 220072, BELARUS
[2] Univ Oxford, Dept Pharmacol, Oxford OX1 3QT, England
[3] Peter Great St Petersburg Polytech Univ, Polytech Skaya Str 29, St Petersburg 195251, Russia
[4] ITMO Univ, Kronverksky Ave 49, St Petersburg 197101, Russia
[5] Inst Expt Med, Pavlova Str 12, St Petersburg 197376, Russia
关键词
calcium; mtDNA; neuron; presynaptic endings; ROS; synapse; NONSYNAPTIC MITOCHONDRIA; ALZHEIMERS-DISEASE; WILSONS-DISEASE; NERVE-ENDINGS; NITRIC-OXIDE; RAT-BRAIN; CALCIUM; COPPER; DNA; METABOLISM;
D O I
10.1515/revneuro-2016-0077
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The mitochondria of different cells are different in their morphological and biochemical properties. These organelles generate free radicals during activity, leading inevitably to mitochondrial DNA damage. It is not clear how this problem is addressed in long-lived cells, such as neurons. We propose the hypothesis that mitochondria within the same cell also differ in lifespan and ability to divide. According to our suggestion, cells have a pool of 'stem' mitochondria with low metabolic activity and a pool of 'differentiated' mitochondria with significantly shorter lifespans and high metabolic activity. We consider synaptic mitochondria as a possible example of 'differentiated' mitochondria. They are significantly smaller than mitochondria from the cell body, and they are different in key enzyme activity levels, proteome, and lipidome. Synaptic mitochondria are more sensitive to different damaging factors. It has been established that neurons have a sorting mechanism that sends mitochondria with high membrane potential to presynaptic endings. This review describes the properties of synaptic mitochondria and their role in the regulation of synaptic transmission.
引用
收藏
页码:363 / 373
页数:11
相关论文
共 138 条
[1]  
AITKEN PG, 1989, NEUROTOXICOLOGY, V10, P239
[2]   Different responses of astrocytes and neurons to nitric oxide:: The role of glycolytically generated ATP in astrocyte protection [J].
Almeida, A ;
Almeida, J ;
Bolaños, JP ;
Moncada, S .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2001, 98 (26) :15294-15299
[3]  
ARORA KK, 1988, J BIOL CHEM, V263, P17422
[4]   Mitophagy of damaged mitochondria occurs locally in distal neuronal axons and requires PINK1 and Parkin [J].
Ashrafi, Ghazaleh ;
Schlehe, Julia S. ;
LaVoie, Matthew J. ;
Schwarz, Thomas L. .
JOURNAL OF CELL BIOLOGY, 2014, 206 (05) :655-670
[5]   Neuroenergetics and the kinetic design of excitatory synapses [J].
Attwell, D ;
Gibb, A .
NATURE REVIEWS NEUROSCIENCE, 2005, 6 (11) :841-849
[6]   An energy budget for signaling in the grey matter of the brain [J].
Attwell, D ;
Laughlin, SB .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 2001, 21 (10) :1133-1145
[7]   Partial mitochondrial inhibition causes striatal dopamine release suppression and medium spiny neuron depolarization via H2O2 elevation, not ATP depletion [J].
Bao, L ;
Avshalumov, MV ;
Rice, ME .
JOURNAL OF NEUROSCIENCE, 2005, 25 (43) :10029-10040
[8]   Mitochondrial bioenergetics and structural network organization [J].
Benard, Giovanni ;
Bellance, Nadege ;
James, Dominic ;
Parrone, Philippe ;
Fernandez, Helder ;
Letellier, Thierry ;
Rossignol, Rodrigue .
JOURNAL OF CELL SCIENCE, 2007, 120 (05) :838-848
[9]  
Billups B, 2002, J NEUROSCI, V22, P5840
[10]   Glycolysis: a bioenergetic or a survival pathway? [J].
Bolanos, Juan P. ;
Almeida, Angeles ;
Moncada, Salvador .
TRENDS IN BIOCHEMICAL SCIENCES, 2010, 35 (03) :145-149