Biochemical Mechanisms Underlying Primary Degeneration of Axons

摘要: Every student of neurobiology is familiar with the specialized functional architecture “typical” mammalian neuron its isolated somal synthesis center that responsible for maintaining entire volume elongated axon. Less well appreciated are extraordinary liabilities this unusual cellular arrangement imparts to long axons in abnormal metabolic states. First, there a relatively huge surface area entry toxic agents. Second, maintenance and restoration damaged axoplasmic components depend large extent on rate-limited axonal transport system shuttles materials from remote source supply neuronal soma. Third, available energy supplies axon must be divided among bidirectional transport, impulse propagation, other energy-dependent functions. Taken together, these special features offer basis explore why degeneration encountered so many neurological conditions diverse etiology. Cardinal primary axonopathies peripheral nerve spinal cord, expressed clinically as polyneuropathy or spinocerebellar degeneration, associated nutritional deficiency, specific intoxication, inherited abnormalities. Our purpose here identify common axonopathies, consider what little known their underlying biochemical mechanisms, provide cogent framework future research elucidate molecular degeneration.