What Do Changes in Brain Perfusion Induced by Etomidate Suggest about Epilepsy in Human Patients?
Figure 3
Theoretical mechanisms of etomidate effect on the epileptic activity. Astroc: astrocyte; pre-N: presinaptic neuron; post-N: postsinaptic neuron. (a) Reversal of Cl- potential. Here, represents GABA, represents a channel, represents NKCC1 (sodium-potassium chloride contransporter), represents KCC2 (potasium-chloride contransporter), represents a chloride anion, and represents etomidate. (b) Reduced re-uptake of glutamate by astrocytes through EAAT1 and 2 (Excitatory aminoacid transport) due to etomidate action through protein kinase A (PKA) pathways where represents glutamate, represents etomidate, represents EAAT 1 and 2, and represents a glutamate channel.
represents a channel, 
represents NKCC1 (sodium-potassium chloride contransporter), 
represents KCC2 (potasium-chloride contransporter), 
represents a chloride anion, and 
represents etomidate. (b) Reduced re-uptake of glutamate by astrocytes through EAAT1 and 2 (Excitatory aminoacid transport) due to etomidate action through protein kinase A (PKA) pathways where 
represents glutamate, 
represents etomidate, 
represents EAAT 1 and 2, and 
represents a glutamate channel.
