Neuronal damage and

Tomassini N, Renaud F, Roy S, Loh HH (2004) Morphine inhibits Fc-mediated phagocytosis through mu and delta opioid receptors. J Neuroimmunol 147 131-133 Trillo-Pazos G, Kandanearatchi A, Eyeson J, King D, Vyakamam A, Everall IP (2004) Infection of stationary human brain aggregates with HIV-1 SF162 and IIIB results in transient neuronal damage and neurotoxicity. Neuropathol Appl Neurobiol 30 136-147... 

Deficiency of this coenzyme can lead to many manifestations. Clinical signs include retarded growth, acrodynia, alopecia, skeletal changes and anemia, while changes in neurotransmitters, such as dopamine, serotonin, norepinephrine (noradrenaline), tryptamine, tyramine, histamine, y-aminobutyric acid, and taurine, affect the brain function and can lead to seizures and convulsions. An overdose of vitamin Bg leads to neuronal damage and sensory and motor effects [417],... 

Synthetic drugs of comparable selectivity and affinity to the 1,4-dihydropyridines do not yet exist for the other channel types, T, N, P/Q, and R these remain characterized by complex polypeptide toxins of the aga- and conotoxin classes. Neuronal pharmacology, including that of the central nervous system (CNS), is dominated by the N, P/Q, and R channels. This underscores the normally weak effect of L-channel antagonists on CNS function. Drugs that act at the N, P, and R channels with comparable selectivity and affinity to the 1,4-dihydropyridines may be expected to offer major potential for a variety of CNS disorders, including neuronal damage and death from ischemic insults. 

Al-Omar, F.A. et al., Immediate and delayed treatments with curcumin prevent forebrain ischemia-induced neuronal damage and oxidative insult in rat hippocampus, Neu-mchem. Res., 31, 611, 2006. 

Various studies have been conducted on excitatory amino acids and their receptors to explain the neuronal cell death (necrosis) after cerebral ischemia. The mechanism of ischemia-induced neuronal damage and the efficacies of antagonists were reviewed by Hara et al. (1994). Recendy, using caspase-1 knockout or transgenic mice (Friedlander et al., 1997) and Bcl-2 transgenic mice (Martinou et al., 1994), it was shown that the neuronal cell death induced by cerebral ischemia includes apoptosis. 

The brain uses a substantial proportion of body oxygen and there is a generous blood supply to the brain from the carotid and vertebral arteries. Interruption of brain blood flow for more than a very short time causes neuronal damage and ultimately cell death. Cerebral blood flow is normally controlled by autoregulation. 

The exact role that lOP plays in combinadon wdth these other factors and the latter s significance in the inidadon and progression of subsequent glaucomatous neuronal damage and cell death requires further studies. 

Bilobalide. Bilobalide (BB) is one of the major active compounds extracted from Ginkgo biloba leaves. BB protects against learning and memory impairments induced by AP25-35, attenuates the neuronal damage and apoptosis in frontal cortex and hippocampus, and inhibits TNF-a and A(f w expression [266],... 

Ziconotide is neuroprotective in rat models of ischemic neuronal damage and after intrathecal administration, antinociception is observed in rats with limited toxicity. The neuroprotective effects observed in rat models are thought to be due to a reduction in body temperature. Analgesic effects are observed in cancer and AIDS patients whose pain was not relieved after opioid administration and in neuropathic conditions. Intrathecal administration of ziconotide prevents mechanical and cold allodynia and heat hyperalgesia " in neuropathic rats. The use of N-type VSCC inhibitors in both ischemic brain injury and pain treatment is complicated by their important role in the synapse. Adverse effects are observed in patients but they are managed through dose reduction or symptomatic treatment, although serious supraspinal and systemic adverse effects have been seen. ... 

Ferger, D. and Krieglstein, J., Determination of intracellular Ca concentration can be a useful tool to predict neuronal damage and neuroprotection properties of drugs, Brain Res., 932, 87, 1996. 

The second action that prevents neuron damage and which could be considered, at least conceptually, as feedback control is oxygen consumption rate. Even though the brain normally operates at a constant consumption rate, recent experimental results (8) indicate that the rate decreases when the tissue oxygen tension drops. 

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