Yaghoob Farbood1,2, Alireza Sarkaki1,2, Leila Khalaj3, Fariba Khodagholi4,5, Mohammad Badavi1,2, Ghorbangol Ashabi1,2. 1. Department of Physiology, Faculty of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. 2. Ahvaz Physiology Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. 3. Medical School, Alborz University of Medical Sciences, Alborz, Iran. 4. Neuroscience Research Center, ShahidBeheshti University of Medical Sciences, Tehran, Iran. 5. Neurobiology Research Center, ShahidBeheshti University of Medical Sciences, Tehran, Iran.
Abstract
OBJECTIVE: I/R and its subsequent reactive hyperemia results in different adverse effects such as brain edema and BBB disruption. AMPK activation has been perceived as one of the target factors for I/R treatment. We investigated the effect of Met (an AMPK activator) on some physiological parameters including vascular responses, hyperemia, BBB disruption, and electrophysiological activity following tGCI. METHODS: Rats were pretreated with Met for two weeks and CC was administered half an hour before tGCI. Brain vascular responses, hyperemia, BBB disruption, and electrophysiological activity were evaluated following the ischemia. RESULTS: Met attenuated BBB disruption and reactive hyperemia in tGCI rats compared with the untreated I/R rats (p < 0.001). Met administration along with CC in the ischemic rats reversed the beneficial effects of Met on BBB disruption and reactive hyperemia (p < 0.001). Electrophysiological records indicated that Met increased spike rates in the ischemic rats comparing with I/R rats (p < 0.001), whereas, CC administration blocked the beneficial effects of Met on the neuronal discharges (p < 0.05). CONCLUSION: We established a regulatory role for AMPK in vascular and electrophysiological responses to tGCI. Studies are ongoing to determine if activation of AMPK in the reperfusion period would offer similar protection.
OBJECTIVE: I/R and its subsequent reactive hyperemia results in different adverse effects such as brain edema and BBB disruption. AMPK activation has been perceived as one of the target factors for I/R treatment. We investigated the effect of Met (an AMPK activator) on some physiological parameters including vascular responses, hyperemia, BBB disruption, and electrophysiological activity following tGCI. METHODS:Rats were pretreated with Met for two weeks and CC was administered half an hour before tGCI. Brain vascular responses, hyperemia, BBB disruption, and electrophysiological activity were evaluated following the ischemia. RESULTS: Met attenuated BBB disruption and reactive hyperemia in tGCI rats compared with the untreated I/R rats (p < 0.001). Met administration along with CC in the ischemicrats reversed the beneficial effects of Met on BBB disruption and reactive hyperemia (p < 0.001). Electrophysiological records indicated that Met increased spike rates in the ischemicrats comparing with I/R rats (p < 0.001), whereas, CC administration blocked the beneficial effects of Met on the neuronal discharges (p < 0.05). CONCLUSION: We established a regulatory role for AMPK in vascular and electrophysiological responses to tGCI. Studies are ongoing to determine if activation of AMPK in the reperfusion period would offer similar protection.