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Chapter Molecular Pathophysiology of Stroke aminobutyric acid receptor. Propagation of the action po- progressively less effective; however, such agents are effective tential induced by depolarization of the neuronal cell body up to 2 hours after the onset of middle cerebral artery occlu- requires voltage-dependent sodium channels. In the clinical trials, most patients were release of glutamate itself depends on P- and Q-type voltage- enrolled 6 to 12 hours after the onset of ischemia, long after dependent calcium channels. Glutamate release into the the time that these drugs were effectively administered in synaptic cleft can bind to the NMDA receptor and open animal studies.

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Drugs that prevent prolonged opening of P- and Q-type calcium chan- nel antagonists are also neuroprotective in animal models of stroke In contrast to their very limited effects in primary neuronal tissue culture models, non-NMDA antag- onists are very effective in both global and focal ischemia models in rodents. Indeed, such agents have a longer time window of efficacy than do NMDA antagonists when ad- ministered after the onset of ischemia 53, Likewise, voltage-dependent calcium channel antagonists are not ef- fective in vitro; however, the voltage-dependent calcium channel antagonist nimodipine is effective in reducing in- farction volume in temporary focal ischemia in rats Blockade of excitotoxicity via all these pharmacologic strategies has proved effective in temporary focal ischemia models in rodents, the model that most closely resembles human stroke.

Unfortunately, results with these agents in human trials have to date been very disappointing, for sev- eral possible reasons. First, drugs that affect neurotransmis- sion in the brain have many undesirable side effects, which in turn have led to reductions to doses that may have been ineffective. Side effects include effects on respiration and cardiac rhythm. In addition, agents that directly antagonize the NMDA receptor may injure a circumspect population of neurons in the cingulate and retrosplenial cortex in ro- dents 56, and may induce hallucinations and psychosis in humans Another obvious reason for the lack of efficacy in these drugs in clinical trials is the time interval between the onset of ischemia and the administration of drug.

When given after the onset of ischemia, they are mechanisms that control programmed cell death. Caspase 9 then cleaves and activates other cas- 69, Activation of these receptors triggers activation of pases, including caspase 3. The cleaved bid then translocates from the cyto- executing programmed cell death. They were first identified plasm to the mitochondria, where it initiates cytochrome c by their homology with CED3, the key gene that irreversibly egress Other mechanisms by which the initiation of commits neurons in C.

These and other mechanisms may role as the final committed step in programmed cell death. The result is cleavage of DNA between histosomes, a hallmark of programmed cell death Evidence indicates that many of the mechanisms that initi- The mRNA of the Fas ligand is the cytosol is controlled by several mechanisms. Expression of the Fas the bcl-2 family play an important role in controlling cyto- ligand and associated proteins and infarction volumes was chrome c egress.

Anti-apoptotic bcl-2 family members, such smaller in LPR mice that expressed a dysfunctional Fas li- as bcl-2 itself and bcl-x-long, inhibit the egress of cyto- gand than in wild-type controls Pro-apoptotic members of the bcl-2 fam- also up-regulated after cerebral ischemia in rat brain Expression of the TNF receptor balance between the pro-apoptotic and anti-apoptotic bcl-2 is also increased after cerebral ischemia TNF-binding family proteins in the mitochondrial membrane determines protein, a protein that binds and inhibits TNF-, reduced whether permeability of the membrane will increase to allow infarction volume after middle cerebral artery occlusion in egress of cytochrome c into the cytoplasm.

However, ischemic injury was exacerbated in circumstances, cytochrome c exits the mitochondria via the TNF- -receptor null mice, which suggests that TNF signal- mitochondrial permeability transition pore. This pore can ing pathways may instead have beneficial effects in ischemic open in response to prolonged depolarization, produced by injury under some circumstances Caspase 8, which is such stimuli as an increase in intracellular calcium Changes in bax may also interact with this pore The M-termi- 65, and some evidence indicates that bax induces egress nal kinases of c-Jun are activated after ischemia and phos- of cytochrome c from the mitochondria independently of phorylate c-Jun The increased expression of ERK after the mitochondrial permeability transition pore Initia- focal ischemia and inhibitor of NEK-1, another kinase in tion of the mitochondrial apoptosis is also controlled by the ERK pathway, protect the brain against focal cerebral expression and translocation of other numerous bcl-2 family ischemia 83, For example, translocation of bax from the cyto- event in cerebral ischemia reperfusion injury and may trig- sol to the mitochondria initiates programmed cell death ger expression of p53 85, Bad is phosphorylated before being translocated to the after cerebral ischemia In rodent models of ischemia, anti-apoptotic mem- in apoptosis, egress of cytochrome c from the mitochondria, bers of the bcl-2 family, including bcl-2 and bcl-x long, are is controlled by bcl-2 family proteins.

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