Ketamine attenuates the glutamatergic neurotransmission in the ventral posteromedial nucleus slices of rats.

Background: Ketamine is a frequently used intravenous anesthetic, which can reversibly induce loss of consciousness (LOC). Previous studies have demonstrated that thalamocortical system is critical for information transmission and integration in the brain. The ventral posteromedial nucleus (VPM) is a critical component of thalamocortical system. Glutamate is an important excitatory neurotransmitter in the brain and may be involved in ketamine-induced LOC. Methods: The study used whole-cell patch-clamp to observe the effect of ketamine (30 µM-1000 µM) on glutamatergic neurotransmission in VPM slices. Results: Ketamine significantly decreased the amplitude of glutamatergic spontaneous excitatory postsynaptic currents (sEPSCs), but only higher concentration of ketamine (300 µM and 1000 µM) suppressed the frequency of sEPSCs. Ketamine (100 µM-1000 µM) also decreased the amplitude of glutamatergic miniature excitatory postsynaptic currents (mEPSCs), without altering the frequency. Conclusions: In VPM neurons, ketamine attenuates the glutamatergic neurotransmission mainly through postsynaptic mechanism and action potential may be involved in the process. [ABSTRACT FROM AUTHOR]