RT Journal Article
SR Electronic
T1 Hyperexcitability of Rat Thalamocortical Networks after Exposure to General Anesthesia during Brain Development
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 1481
OP 1492
DO 10.1523/JNEUROSCI.4883-13.2015
VO 35
IS 4
A1 DiGruccio, Michael R.
A1 Joksimovic, Srdjan
A1 Joksovic, Pavle M.
A1 Lunardi, Nadia
A1 Salajegheh, Reza
A1 Jevtovic-Todorovic, Vesna
A1 Beenhakker, Mark P.
A1 Goodkin, Howard P.
A1 Todorovic, Slobodan M.
YR 2015
UL http://www.jneurosci.org/content/35/4/1481.abstract
AB Prevailing literature supports the idea that common general anesthetics (GAs) cause long-term cognitive changes and neurodegeneration in the developing mammalian brain, especially in the thalamus. However, the possible role of GAs in modifying ion channels that control neuronal excitability has not been taken into consideration. Here we show that rats exposed to GAs at postnatal day 7 display a lasting reduction in inhibitory synaptic transmission, an increase in excitatory synaptic transmission, and concomitant increase in the amplitude of T-type calcium currents (T-currents) in neurons of the nucleus reticularis thalami (nRT). Collectively, this plasticity of ionic currents leads to increased action potential firing in vitro and increased strength of pharmacologically induced spike and wave discharges in vivo. Selective blockade of T-currents reversed neuronal hyperexcitability in vitro and in vivo. We conclude that drugs that regulate thalamic excitability may improve the safety of GAs used during early brain development.