Abstract
The transition from wakefulness to a nonrapid eye movement (NREM) sleep state at the onset of sleep involves a transition from low-voltage, high-frequency irregular electroencephalography (EEG) waveforms to large-amplitude, low-frequency EEG waveforms accompanying synchronized oscillatory activity in the thalamocortical circuit. The thalamocortical circuit consists of reciprocal connections between the thalamus and cortex. The cortex sends strong excitatory feedback to the thalamus, however the function of which is unclear. In this study, we investigated the role of the thalamic metabotropic glutamate receptor 1 (mGluR1)-phospholipase C β4 (PLCβ4) pathway in sleep control in PLCβ4-deficient (PLCβ4−/−) mice. The thalamic mGluR1-PLCβ4 pathway contains synapses that receive corticothalamic inputs. In PLCβ4−/− mice, the transition from wakefulness to the NREM sleep state was stimulated, and the NREM sleep state was stabilized, which resulted in increased NREM sleep. The power density of delta (δ) waves increased in parallel with the increased NREM sleep. These sleep phenotypes in PLCβ4−/− mice were consistent in TC-restricted PLCβ4 knockdown mice. Moreover, in vitro intrathalamic oscillations were greatly enhanced in the PLCβ4−/− slices. The results of our study showed that thalamic mGluR1-PLCβ4 pathway was critical in controlling sleep architecture.Electronic supplementary materialThe online version of this article (doi:10.1186/s13041-016-0276-5) contains supplementary material, which is available to authorized users.
Highlights
Sleep-wake control has been attributed to many brain regions, including the brain stem [1,2,3], hypothalamus [4], basal forebrain [5], basal ganglia [6], and thalamus [7]
Increased non-rapid eye movement (NREM) sleep in phospholipase C β4 (PLCβ4)−/− mice First, we examined the patterns of the natural sleep-wake cycles in PLCβ4+/+ and PLCβ4−/− mice
(26.9 ± 4.9; Fig. 3l), more frequent occurrence of the NREM sleep. These results suggested that a transition from the NREM to the rapid eye movement (REM) sleep state was less likely to occur during both the dark and light phases in PLCβ4−/− mice. These results indicated that PLCβ4−/− mice could not maintain the awake state during the dark phase and that their vigilance states were more frequently directed towards NREM sleep, which resulted in an increase in the amount of total NREM sleep
Summary
Sleep-wake control has been attributed to many brain regions, including the brain stem [1,2,3], hypothalamus [4], basal forebrain [5], basal ganglia [6], and thalamus [7]. Sleep is composed of the non-rapid eye movement (NREM) and rapid eye movement (REM) sleep states, which are categorized by characteristic brain rhythms in electroencephalography (EEG) recordings and distinctive eye movements [7, 8]. The NREM sleep state is characterized by large-amplitude, low-frequency EEG waveforms, and the REM sleep state is marked by distinctive regular theta (θ) waves [7]. The EEG waveform components that are observed during NREM sleep are further subdivided according to frequency into very slow waves (
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