The research on fastigial nucleus could be traced back to 19th century. However the great achievements on cerebrum overshadowed the importance of cerebellum and its nucleus. In recent 30 years, with the finding of brain protection effect of fastigial nucleus stimulation, much attention has been given to this field. Now its widely accepted that electrical stimulation of fastigial nucleus has brain protection effect and concrete mechanisms can be concluded as: improving the electrical instability around the infarct zone, reducing peri-infarction depolarizing wave and cortical spreading depression; suppressing microvessels inflammatory reaction; inhibiting cell apoptosis; reducing the neurons damage and facilitates neovascularization and so on. These new discoveries was reviewed and further expectation on this field was put forward by the authors.

Objective:To evaluate the effect of dexmedetomidine pretreatment on the autophagy of hippocampal neurons in the developing rats under sevoflurane anesthesia.Methods:Thirty-six clean-grade healthy Sprague-Dawley rats of either sex, aged 7 days, weighing 12-15 g, were divided into 3 groups ( n=12 each) using a random number table method: control group (group C), sevoflurane group (group S), and sevoflurane plus dexmedetomidine group (group S+ D). On 7-9 days after birth, and the animals were exposed to 3% sevoflurane (oxygen concentration inhaled 29%, oxygen flow 2 L/min, 2 h/day) after intraperitoneal injection of 25 μg/kg dexmedetomidine every day in group S+ D, the animals were exposed to sevoflurane after intraperitoneal injection of the equal volume of normal saline in group S, and the animals were exposed to gas mixture after intraperitoneal injection of the equal volume of normal saline in group C. The Morris water maze test was carried out at 20 days after birth, and the place navigation test and spatial probe test were performed.After the end of Morris water maze test, the anesthetized rats were sacrificed, and the hippocampus was obtained for determination of the expression of microtubule-associated protein light chain 3(LC3), BECN1 and P62 by Western blot. Results:Compared with group C, the escape latency was significantly prolonged, the frequency of crossing the original platform was decreased, the expression of LC3 and BECN1 was up-regulated, and the expression of P62 was down-regulated in group S and group S+ D ( P<0.05). Compared with group S, the escape latency was significantly shortened, the frequency of crossing the original platform was increased, the expression of LC3 and BECN1 was down-regulated, and the expression of P62 was up-regulated in group S+ D ( P<0.05). Conclusions:The mechanism by which dexmedetomidine pretreatment improves sevoflurane-induced cognitive dysfunction is related to reduction of excessive autophagy in hippocampal neurons of developing rats.