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Article type: Research Article
Authors: Kohmura, Eiji | Yuguchi, Takamichi | Yamada, Kazuo | Sakaguchi, Tateo | Hayakawa, Toru
Affiliations: Department of Neurosurgery, Osaka University Medical School, 2-2 Yamadaoka, Suitashi, Osaka 565, Japan
Note: [] Correspondence: E. Kohmura, Department of Neurosurgery, Osaka Rosai Hospital, 1179-3 Nagasonecho, Sakaishi, Osaka 591, Japan. Fax: (81)(722) 55 3349. Present address: Department of Neurosurgery, Osaka Rosai Hospital 1179-3 Nagasonecho, Sakaishi, Osaka 591, Japan
Abstract: Retrograde degeneration of thalamic neurons after cortical ablation has long been recognized. Neuronal loss following axotomy eliminates the possibility of regeneration and might prevent the recovery from axonal injury in patients with brain trauma. We investigated whether CS23, a stable recombinant variant of human basic fibroblast growth factor (bFGF), could protect neurons from retrograde degeneration. Four weeks after ablation of the somatosensory cortex in young female rats, there was extensive neuronal degeneration and loss in the lateral ventro-posterior nucleus (VPL) of the ipsilateral thalamus. When Gelfoam soaked in bFGF(CS23) (1 μg/0.l ml) was applied topically at the time of surgery, this neuronal degeneration in the VPL was markedly reduced and macroscopic atrophy of the lateral and medial ventroposterior nucleus (VPL + VPM) was significantly reduced. In contrast, application of bFGF at three days after surgery failed to prevent retrograde degeneration. These resuts indicate that bFGF can prevent thalamic atrophy after ablation of the somatosensory cortex and that administration of bFGF is only effective in the very early period after brain injury.
Keywords: Fibroblast growth factor, Injury, Neuron, Thalamic degeneration
DOI: 10.3233/RNN-1994-6407
Journal: Restorative Neurology and Neuroscience, vol. 6, no. 4, pp. 309-316, 1994
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