Abstract
BackgroundKetamine 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.MethodsThe study used whole-cell patch-clamp to observe the effect of ketamine (30 μM–1000 μM) on glutamatergic neurotransmission in VPM slices.ResultsKetamine 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.ConclusionsIn VPM neurons, ketamine attenuates the glutamatergic neurotransmission mainly through postsynaptic mechanism and action potential may be involved in the process.
Highlights
Ketamine is a frequently used intravenous anesthetic, which can reversibly induce loss of consciousness (LOC)
Rath et al found that etomidate increases glutamatergic neurotransmission by inhibiting glutamate uptake in glial cells cultivated from the cortex of rats [7]
Effects of ketamine on miniature excitatory postsynaptic currents (mEPSCs) of neurons in ventral posteromedial nucleus (VPM) nucleus mEPSCs were recorded in the presence of TTX (0.5 μM) and bicuculline (BIC, 20 μM, Fig. 3a)
Summary
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 [1, 2]. Our previous studies suggest that thalamocortical system is involved in general anesthetics-induced loss of consciousness (LOC) [3,4,5,6]. The changes of glutamate transmission may play a critical role in general anesthetics-induced LOC. Our previous study found that etomidate decreases glutamatergic neurotransmission in thalamocortical neuronal network of rats [8].
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