Abstract
1. Stimulation of the rostral-ventromedial pole of the cerebellar fastigial nucleus exerts powerful effects on systemic and cerebral circulation. 2. Excitation of fibers passing through the fastigial nucleus evokes sympathoactivation and increases in arterial pressure. 3. Increase in cerebral blood flow evoked by excitation of fibers passing through the FN is mediated by intrinsic brain mechanisms independently of metabolism. 4. Excitation of the fastigial nucleus neurons in contrast decreases arterial pressure and cerebral blood flow. The latter probably is secondary to the suppression of brain metabolism. 5. Excitation of the fastigial nucleus neurons significantly decreases damaging effects of focal and global ischemia on the brain. 6. The fastigial nucleus-evoked neuroprotection can be conditioned: 1-h stimulation protects the brain for up to 3 weeks. 7. Other brain structures such as subthalamic cerebrovasodilator area and dorsal periaqueductal gray matter also produce long-lasting brain salvage when stimulated. 8. More than one mechanism may account for neurogenic neuroprotection. 9. Early neuroprotection, which develops immediately after the stimulation, involves opening of potassium channels. 10. Delayed long-lasting neuroprotection may involve changes in genes expression resulting in suppression of inflammatory reaction and apoptotic cascade. 11. It is conceivable that intrinsic neuroprotective system exists within the brain, which renders the brain more tolerant to adverse stimuli when activated. 12. Knowledge of the mechanisms of neurogenic neuroprotection will allow developing new neuroprotective approaches.