Do Sang-Hwan, Ham Byung-Moon, Zuo Zhiyi
Department of Anesthesiology, University of Virginia Health System, 1 Hospital Drive, PO Box 800710, Charlottesville, VA, USA.
Neurosci Lett. 2003 Jun 5;343(2):113-6. doi: 10.1016/s0304-3940(03)00358-6.
We investigated the effects of propofol on one type of glutamate transporter, excitatory amino acid transporter 3 (EAAT3) and the role of protein kinase C (PKC) in mediating these effects. Rat EAAT3 was expressed in Xenopus oocytes. L-glutamate (30 microM)-induced membrane currents were measured. Propofol increased glutamate-induced inward currents significantly at two tested concentrations (30 and 100 microM) but not at other concentrations. Propofol (30 microM) significantly increased V(max), but not K(m) of EAAT3 for glutamate. The combination of phorbol-12-myrisate-13-acetate (PMA, a PKC activator) and propofol did not increase the responses further compared with PMA or propofol alone. Three PKC inhibitors (staurosporine, calphostin C, and chelerythrine) did not affect basal EAAT3 activity but significantly inhibited the propofol-enhanced EAAT3 activity. Our results suggest that propofol enhances EAAT3 activity at clinically relevant concentrations and PKC may mediate these effects.
