The role of cytosolic free calcium in the regulation of pyruvate dehydrogenase in synaptosomes

1994 ◽  
Vol 19 (1) ◽  
pp. 89-95 ◽  
Author(s):  
H. M. Huang ◽  
L. Toral-Barza ◽  
K. F. R. Sheu ◽  
G. E. Gibson
1992 ◽  
Vol 3 (2) ◽  
pp. 235-248 ◽  
Author(s):  
A Martínez-Serrano ◽  
J Satrústegui

By the use of digitonin permeabilized presynaptic nerve terminals (synaptosomes), we have found that intrasynaptic mitochondria, when studied "in situ," i.e., surrounded by their cytosolic environment, are able to buffer calcium in a range of calcium concentrations close to those usually present in the cytosol of resting synaptosomes. Adenine nucleotides and polyamines, which are usually lost during isolation of mitochondria, greatly improve the calcium-sequestering activity of mitochondria in permeabilized synaptosomes. The hypothesis that the mitochondria contributes to calcium homeostasis at low resting cytosolic free calcium concentration ([Ca2+]i) in synaptosomes has been tested; it has been found that in fact this is the case. Intrasynaptic mitochondria actively accumulates calcium at [Ca2+]i around 10(-7) M, and this activity is necessary for the regulation of [Ca2+]i. When compared with other membrane-limited calcium pools, it was found that depending on external concentration the calcium pool mobilized from mitochondria is similar or even greater than the IP3- or caffeine-sensitive calcium pools. In summary, the results presented argue in favor of a more prominent role of mitochondria in regulating [Ca2+]i in presynaptic nerve terminals, a role that should be reconsidered for other cellular types in light of the present evidence.


1994 ◽  
Vol 5 (3) ◽  
pp. 331-341 ◽  
Author(s):  
Rui Malho ◽  
Nick D. Read ◽  
M. Salome Pais ◽  
Anthony J. Trewavas

1998 ◽  
Vol 78 (4) ◽  
pp. 949-967 ◽  
Author(s):  
ELIZABETH J. PETTIT ◽  
FREDRIC S. FAY†

Pettit, Elizabeth J., and Frederic S. Fay. Cytosolic Free Calcium and the Cytoskeleton in the Control of Leukocyte Chemotaxis. Physiol. Rev. 78: 949–967, 1998. — In response to a chemotactic gradient, leukocytes extravasate and chemotax toward the site of pathogen invasion. Although fundamental in the control of many leukocyte functions, the role of cytosolic free Ca2+in chemotaxis is unclear and has been the subject of debate. Before becoming motile, the cell assumes a polarized morphology, as a result of modulation of the cytoskeleton by G protein and kinase activation. This morphology may be reinforced during chemotaxis by the intracellular redistribution of Ca2+stores, cytoskeletal constituents, and chemoattractant receptors. Restricted subcellular distributions of signaling molecules, such as Ca2+, Ca2+/calmodulin, diacylglycerol, and protein kinase C, may also play a role in some types of leukocyte. Chemotaxis is an essential function of most cells at some stage during their development, and a deeper understanding of the molecular signaling and structural components involved will enable rational design of therapeutic strategies in a wide variety of diseases.


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