Pre‐conditioning to global cerebral ischemia changes hippocampal acetylcholinesterase in the rat

Abstract

This study shows the effect of transient global cerebral ischemia (ISC) on hippocampal acetylcholinesterase (AChE) activity. Naive adult Wistar rats received either a brief (2 min) or a long (10 min) ischemic episode by the four‐vessel occlusion method. Pre‐conditioned rats received double ischemia: a 10 min episode inflicted 24 h after a 2 min event, a condition known to confer cytoprotection to CA1 pyramidal cells of hippocampus. 2 min of ischemia caused an increase in acetylcholinesterase activity both immediately and 30 min after the episode, however enzyme activity was significantly decreased after 24 h of reperfusion. 10 min of ischemia caused an increase in activity both 60 min and 24 h after ischemia. Conversely, pre‐conditioned rats displayed lower activity both immediately and 60 min after ischemia. Our results suggest that: a) neuronal death, that follows 10 min of ischemia, is associated to a late increase in acetylcholinesterase activity; b) pre‐conditioning is related to diminished acetylcholinesterase activity. This is in agreement with previous evidence that acetylcholinesterase inhibition and maintenance of acetylcholine levels are beneficial for cell surviving after cerebral ischemia.

Correlations Between Cholinesterase Activity and Cognitive Scores in Post-Ischemic Rats and Patients with Vascular Dementia

“…However, in contrast to our data, a significant decreased AChE activity was found in the hippocampus and the frontal cortex after ischemia in the SHspR brains (Ogawa et al 1996). Furthermore, it was reported that a brief or long ischemia by the four-vessel occlusion caused an increase in AChE activity, whereas the pre-conditioned rats displayed lower AChE activity after ischemia, suggesting that neuronal death is associated to an increase in AChE activity and pre-conditioning could diminish AChE activity (Schetinger et al 1999). …”

Preventive Effect of Chotosan, a Kampo Medicine, on Transient Ischemia-Induced Learning Deficit Is Mediated by Stimulation of Muscarinic M1 But Not Nicotinic Receptor

“…20,21) Moreover, many studies have demonstrated that ischemia causes a reduction of memory and judgment that is associated with the cholinergic dysfunction in affected brain areas 22) and that ischemic insults decreases in ACh level in the affected regions of the brain. [23][24][25] Thus, in animals subjected to transient ischemia, an impairment of spatial cognitive performance in a water maze task is likely attributed to dysfunction of the central cholinergic system due to disturbance of energy metabolism and hypoxia in the ischemic brain. Consistent with previous reports from this 3,11) and other laboratories, 26,27) we found that transient ischemia caused a significant reduction of the ACh level in the hippocampus and that pretreatment with a cholinesterase inhibitor tacrine produced a protective effect not only on learning deficits but also on the reduction of the hippocampal ACh level in T2VO mice.…”

Biological Effects of Tetrahydroxystilbene Glucoside: An Active Component of a Rhizome Extracted from Polygonum multiflorum

“…Neuronal death that follows 10 min of ischemia is associated with a late increase in AChE activity [ 93 ]. Microtubule-associated protein-2 (MAP-2) is depleted in the early hours after an in vivo ischemia insult in a rat hippocampal slice [ 94 ].…”