When cells are injured, activation of phosphodiesterases and aberrant expression Cross-Heart Kirtan Kriya Meditation of cell cycle proteins can induce cell programmed death. In vitro studies of phosphodiesterase inhibitors PDEIs Cross-Heart Kirtan Kriya Meditation indicate that vinpocetine protected rat neuronal cells 55-77% from destruction by four neurotoxic mechanisms, hypoxia/hypoglycemia, veratridine, staurosporine, or glutamate. PDEIs also suppressed upregulation of cyclin D1 and proapoptotic caspase-3 activity Chen, Williams, Liao, Yao, Tortella et al., 2007. One of the mechanisms for seizure control by antiepileptic drugs is reduction in cerebral presynaptic voltage-sensitive Na+ channel permeability and, consequently, reduction in glutamate excitatory neurotransmitter release.
In a study of hippocampal nerve endings preloaded with labeled glutamate, vinpocetine inhibited the veratridine Na+ channel opener release of glutamate at lower concentrations than carbamazepine Tegretol, phenytoin Dilontin, lamotrigine Lamictal, and topiramate Topomax Sitges, Chiu, Guarneros, & Nekrassov, 2007. Vinpocetine inhibits the molecular cascade precipitated by increases in intracellular calcium. Neuroprotective effects include inhibition of calcium/calmodulin-dependent cyclic GMP-phosphodiesterase 1; enhancement of intracellular cyclic guanidine monophosphate GMP levels in vascular smooth muscle; reduction in resistance of cerebral blood vessels; and increased blood flow.
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