"Apoptotic" mechanisms in normal brain plasticity: caspase-3 and long-term potentiation.
The analysis of recent data indicates that a few enzymes that have been recognized as "apoptotic" so far may be involved in important cellular processes not related to cell death in the brain. For example, it can be demonstrated that caspase-3, an "apoptotic" enzyme that is active in neurons is necessary for normal neuroplasticity. Here we discuss the involvement of caspase-3 in long-term potentiation phenomenon. Proteins that are key players of molecular mechanisms of long-term potentiation induction and maintenance are also caspase-3 substrates. A concept on a new mechanism of synaptic plasticity modulation involving caspase-3 has been formulated postulating a specific role of caspase-3 in normal brain functioning.
Department of Functional Biochemistry of the Nervous System, Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, Moscow, Russia. nata_gul@yahoo.com
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D000818:Animals; D017209:Apoptosis; D001921:Brain / Q000201:enzymology / Q000502:physiology*; D002154:Calpain / Q000378:metabolism; D053148:Caspase 3; D020169:Caspases / Q000502:physiology*; D003598:Cytoskeletal Proteins / Q000378:metabolism; D017774:Long-Term Potentiation / Q000502:physiology*; D009474:Neurons / Q000201:enzymology*; D051381:Rats; D015398:Signal Transduction
D003598:Cytoskeletal Proteins; D002154:Calpain; C505410:Casp3 protein, rat; D053148:Caspase 3; D020169:Caspases