Skip to main content
. Author manuscript; available in PMC: 2013 Oct 19.
Published in final edited form as: Epilepsia. 2011 Jan 4;52(3):551–561. doi: 10.1111/j.1528-1167.2010.02920.x

Figure 6. Hypothetical mechanism of PAF in experimental epilepsy.

Figure 6

Hyperexcitability state facilitates evoked or spontaneous seizures that release platelet-activating factor (PAF). PAF induces molecular signaling, c-jun N-terminal kinase (JNK) and cyclooxygenase (COX)-2 activation through its receptor. This signaling cascade promotes neuronal damage and neuronal hyperexcitability, which contributes to epileptiform activity. LAU-0901, a PAF antagonist, attenuates PAF receptor signaling and therefore limits seizure susceptibility and hippocampal hyperexcitability.