Journal
JOURNAL OF NEUROSCIENCE
Volume 35, Issue 4, Pages 1481-1492Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.4883-13.2015
Keywords
anesthesia; GABAA receptor; glutamate; low-voltage-activated; T-channels; thalamus
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Funding
- NICHD NIH HHS [HD-044517, R01 HD044517] Funding Source: Medline
- NIGMS NIH HHS [R01 GM102525, GM-102525] Funding Source: Medline
- NINDS NIH HHS [NS-067439, R01 NS067439] Funding Source: Medline
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Prevailing literature supports the idea thatcommongeneral 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.
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