Ischemic Preconditioning and Clinical Scenarios

Srinivasan V. Narayanan; Kunjan R. Dave; Miguel A. Perez-Pinzon


Curr Opin Neurol. 2013;26(1):1-7. 

In This Article

Synaptic Targets of Ischemic Preconditioning and Functional Recovery

Excitotoxicity was identified as one of the first steps in the pathology of cerebral ischemia.[21] IPC was found to ameliorate excitotoxicity by inhibiting glutamate release,[22,23] increasing inhibitory neurotransmitter gamma-aminobutyric acid (GABA) release,[22] and enhancing GABA presynaptic and postsynaptic activities, thus making neurons more resistant to the excitotoxic insult.[24–26] These findings suggest that IPC promotes synaptic modifications that may preserve synaptic function and functional recovery following cerebral ischemia. This hypothesis is further supported by the findings that show IPC improves spatial memory, a well established memory system in humans and in animal models. In animals, spatial memory allows them to acquire and retain information about a surrounding environment. This type of memory resides in the hippocampus and entorhinal cortex.[27] In rats, spatial memory, evaluated by the Morris water maze, was shown to be impaired following asphyxial cardiac arrest.[28] However, IPC ameliorated spatial memory deficits after global cerebral ischemia,[29] suggesting that IPC targets synaptic terminals in order to improve functional recovery.