Alireza Azizzadeh Delshad; Marjan Heshmati; Taki Tiraihi
Volume 3, Issue 2 , March 2008, , Pages 67-74
Abstract
Background and Objective: As apoptotic cell death is extremely involved in physiological development and many pathological situations such as cancer and neurodegenerative diseases, the understanding of its molecular machinery can be useful in designing new therapeutic strategies. The present ...
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Background and Objective: As apoptotic cell death is extremely involved in physiological development and many pathological situations such as cancer and neurodegenerative diseases, the understanding of its molecular machinery can be useful in designing new therapeutic strategies. The present study investigated the temporal expression of the proapoptotic protein Bax in adult spinal motoneurons. Materials and Methods: Following unilateral mid-thigh sciatic transection in adult rats, the incidence and nature of spinal motoneuron loss were evaluated by means of light microscopic cell count and electron microscopy 1 day, 1 week, 1 month and 3 months post-operatively. In all groups the temporal expression of Bax was immunohistochemically determined and the findings were compared with the results of the cell count. Results: Following axotomy the related motoneurons underwent chromatolytic changes which increased up to one month and diminished in the 3-month group. One day following axotomy the number of motoneurons did not show any significant reduction, but thereafter a progressive cell loss occurred, which was most prominent after three months. Electron microscopic study confirmed the ultrastructural apoptotic nature of cell death. Bax immunohistochemistry indicated an increasing immunoreactivity up to one month post-axotomy, but in 3-month group it was clearly diminished. Conclusion: Following transection of a peripheral nerve in adult animals, related motoneurons undergo chromatolytic changes which in some neurons may proceed to apoptotic cell death. Although the proapoptotic protein Bax has long been believed as the main apoptotic factor, other Bax-independent pathways may also participate in the axotomy-induced neuronal apoptosis which must not be ignored.
Alireza Azizzadeh Delshad; Taki Tiraihi
Volume 2, Issue 3 , June 2007, , Pages 83-88
Abstract
Background and Objective: Evaluation of degenerative changes of motoneurons and their related synapses can be useful in understanding the mechanisms of neurodegenerative diseases and their potential treatment. The present electron microscopic and immunohistochemical study investigates the axotomy-induced ...
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Background and Objective: Evaluation of degenerative changes of motoneurons and their related synapses can be useful in understanding the mechanisms of neurodegenerative diseases and their potential treatment. The present electron microscopic and immunohistochemical study investigates the axotomy-induced changes of adult spinal motoneurons up to 3 months following sciatic nerve transection. Materials and Methods: Following unilateral mid-thigh sciatic transection in adult rats, the synaptophysin expression and ultrastructure of synapses in ventral horn of related spinal cord segments were studied 1 day, 1 week, 1 month, and 3 months postoperatively. In all groups the unaxotomized side of spinal cord was considered as control. The pattern of synaptophysin immunolabeling was classified into intact, partial, diffused, and negative types. Results: In 1 week and 1 month groups, the intact pattern decreased and the other 3 patterns increased, whereas 3 months postoperatively the patterns changed vice versa, i.e. intact pattern increased and the other 3 decreased. Electron microscopic studies indicated consistent ultrastructural changes such as synaptic vesicle displacement, synaptic membrane irregularity and synaptic stripping, which were most prominent after 1 month and declined in 3 month group. Conclusion: The present data indicate that following axon injury in adult motoneurons, synapses undergo obvious changes in ultrastructure and synaptophysin distribution, which increase up to 1 month postoperatively, and if the cell survives the insult the changes will attenuate and return to normal conditions thereafter.
