Visual evoked potentials and brainstem auditory evoked potentials in experimental hydrocephalus.
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Biomedical subjects
G Biessels
Publications and source records attributed to G Biessels.
The calcium hypothesis of brain aging and neurodegenerative disorders: significance in diabetic neuropathy.
In this paper we discuss the possible role of disturbed neuronal calcium homeostasis in brain aging and diabetic neuropathy. Disturbances in the homeostasis of cytosolic calcium concentration have been implicated in the pathogenesis of various acute and chronic neurodegenerative disorders and in brain aging. Obviously, these disorders do not all share the same pathogenetic mechanisms. However, a number of the pathogenetic mechanisms involved have in common that they may ultimately cause loss of calcium homeostasis, leading to neuronal damage. By identifying the possible role of calcium, treatment strategies can be developed that may be effective in a variety of neurodegenerative disorders, despite differences in their pathogenesis. Our aim is to explore some of the similarities that exist between a number of processes that have been implicated in the pathogenesis of brain aging and diabetic neuropathy, including ischemia, oxidative stress and non-enzymatic protein glycosylation. Each of these factors might impair neuronal calcium homeostasis, and ultimately lead to neurodegenerative changes. By discussing the putative role of these specific factors in two apparently dissimilar disorders, such as brain aging and diabetic neuropathy, we obviously do not intend to suggest that their pathogenesis is one and the same. Instead, by examining the relative role of these factors in two different types of neurodegenerative disorders we would like to emphasize the importance of disturbances in cellular calcium homeostasis as a final common pathway in neuronal damage resulting from various noxious events.
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Beneficial effect of the Ca2+ antagonist, nimodipine, on existing diabetic neuropathy in the BB/Wor rat.
1. Neuropathy is a frequently diagnosed complication of diabetes mellitus. Effective pharmacotherapy is not available. 2. The spontaneously diabetic BB/Wor rats develop secondary complications like neuropathy as do human diabetic patients. 3. BB/Wor rats treated with insulin via a subcutaneous implant show a significant impairment of sensory and motor nerve conduction velocity 6 weeks after the onset of diabetes mellitus. 4. Intraperitoneal treatment of diabetic BB/Wor rats with the Ca2+ antagonist, nimodipine (20 mg kg-1), from week 6 onwards every 48 h for a period of 6 weeks resulted in a significant increase of sensory and motor nerve conduction velocity. 5. Twelve weeks after the onset of diabetes mellitus BB/Wor rats show a 40% impairment of sciatic nerve blood flow as compared to the non-diabetic age-matched controls. Treatment with nimodipine (20 mg kg-1) from week 6 onwards significantly increased the sciatic nerve blood flow as compared to placebo-treated diabetic BB/Wor rats. 6. The adrenergic responsiveness of the vasa nervorum of the sciatic nerve to tyramine and phenylephrine was investigated as a parameter for autonomic neuropathy. 7. The fact that nimodipine treatment restored the reduced response to tyramine independently of the reduced postsynaptic phenylephrine responsiveness indicates that nimodipine improves adrenergic responsiveness mainly at the presynaptic level.
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