Neuronal Survival After Dendrite Amputation: Investigation of Injury Current Blockage

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After dendrite transection, two primary injury current pathways may acount for cell death: (1) the lesion current at the site of injury and (2) the voltage sensitive calcium channels along the dendrite. Lesions were made with a laser microbeam in mouse spinal monolayer cell cultures. Polylysine was tried as a positively charged "molecular bandage" to block the lesion current. The calcium channel blockers, verapamil and nifedipine, were used to reduce the calcium channel current. Control toxicity curves were obtained for all three compounds. The results show that neither verapamil, nifedipine, nor polylysine (MW: 3,300) protect nerve cells after dendrite amputation … continued below

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vi, 105 leaves : ill.

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Shi, Ri Yi December 1988.

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  • Shi, Ri Yi

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After dendrite transection, two primary injury current pathways may acount for cell death: (1) the lesion current at the site of injury and (2) the voltage sensitive calcium channels along the dendrite. Lesions were made with a laser microbeam in mouse spinal monolayer cell cultures. Polylysine was tried as a positively charged "molecular bandage" to block the lesion current. The calcium channel blockers, verapamil and nifedipine, were used to reduce the calcium channel current. Control toxicity curves were obtained for all three compounds. The results show that neither verapamil, nifedipine, nor polylysine (MW: 3,300) protect nerve cells after dendrite amputation 100 ptm from the soma. The data also indicate that these compounds do not slow the process of cell death after such physical trauma.

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vi, 105 leaves : ill.

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  • December 1988

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  • March 9, 2015, 8:15 a.m.

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  • April 13, 2020, 1:40 p.m.

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Shi, Ri Yi. Neuronal Survival After Dendrite Amputation: Investigation of Injury Current Blockage, thesis, December 1988; Denton, Texas. (https://digital.library.unt.edu/ark:/67531/metadc501278/: accessed August 15, 2024), University of North Texas Libraries, UNT Digital Library, https://digital.library.unt.edu; .

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