Stimulation of the Fastigial Nucleus Enhances EEG Recovery and Reduces Tissue Damage after Focal Cerebral Ischemia

Abstract

Stimulation of the cerebellar fastigial nucleus (FN) increases CBF but not metabolism and reduces the tissue damage resulting from focal cerebral ischemia. This effect may result from enhancing CBF in the ischemic tissue without increasing local metabolic demands. To test this hypothesis, we studied whether the reduction in tissue damage is restricted to the neocortex, a region in which the CBF increase is independent of metabolism, and whether stimulation of the dorsal medullary reticular formation (DMRF), a treatment that increases both cerebral metabolism and CBF, also protects the brain from ischemia. In halothane-anesthetized Sprague–Dawley rats, the middle cerebral artery (MCA) was occluded either proximally or distally to the lenticulostriate branches. The FN or DMRF were then stimulated for 1 h (50–100 μA; 50 Hz; 1 s on/1 s off). Twenty-four hours later, the infarct volume was determined. FN stimulation substantially reduced the size of the infarct, an effect that was greater with distal (− 69 ± 8%; n = 6; p < 0.001; mean ± SD) than with proximal (−38 ± 8%; n = 8; p < 0.001) MCA occlusion. The reduction occurred only in neocortex (−43 ± 9%; p < 0.001) and not in striatum (− 16 ± 21%; p > 0.05). Stimulation of the FN also enhanced recovery of EEG amplitude in the ischemic cortex (+ 48%; p < 0.003). DMRF stimulation (n = 7) did not affect the stroke size or EEG recovery ( p > 0.05). Thus, stimulation of the FN, but not the DMRF, attenuates the damage resulting from focal ischemia. The finding that the protection is limited to the neocortex and that the amount of tissue salvaged is greater after distal occlusions suggests that the FN, unlike the DMRF, may rescue tissue from infarction by enhancing collateral flow without increasing local energy requirements. Activation of selected neural networks may modulate the expression of the damage resulting from focal cerebral ischemia.