An adaptive neural network with asymmetric connections is introduced. This network is related to the Hopfield network with graded neurons and uses a recurrent generalization of the 6 rule of Rumelhart, Hinton, and Williams to modify adaptively the synaptic weights. The new network bears a resemblance to the master/slave network of Lapedes and Farber, but it is architecturally simpler.
Mitochondrial fission and fusion are linked to synaptic activity in healthy neurons and are implicated in the regulation of apoptotic cell death in many cell types. We developed fluorescence microscopy and computational strategies to directly measure mitochondrial fission and fusion frequencies and their effects on mitochondrial morphology in cultured neurons. We found that the rate of fission exceeds the rate of fusion in healthy neuronal processes, and, therefore, the fission/fusion ratio alone is insufficient to explain mitochondrial morphology at steady state. This imbalance between fission and fusion is compensated by growth of mitochondrial organelles. Bcl-xL increases the rates of both fusion and fission, but more important for explaining the longer organelle morphology induced by Bcl-xL is its ability to increase mitochondrial biomass. Deficits in these Bcl-xL–dependent mechanisms may be critical in neuronal dysfunction during the earliest phases of neurodegeneration, long before commitment to cell death.
To promote cell survival, the antiapoptotic factor Bcl-xL both
inhibits Bax-induced mitochondrial outer membrane permeabilization and
stabilizes mitochondrial inner membrane ion flux and thus overall mitochondrial
energetic capacity.
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