Effect of thalamic nucleus reuniens on spindle waves in the medial prefrontal cortex during non-rapid eye movement sleep

To determine the effect of thalamic nucleus reuniens（RE） on sleep spindles and neuronal activity in the medial prefrontal cortex（mPFC） during non-rapid eye movement（NREM） sleep.

Thirteen wild-type C57BL/6 male mice（8～12 weeks old, weighing 22～28 g） were randomly divided into an experimental group（n=7） and a control group（n=6）. Optogenetic inhibition combined with multi-channel recording technology was used to specifically inhibit RE projections to mPFC during NREM sleep with yellow light for 20 s, in a 5-min interval between 2 times of light stimuli. The types and distribution of neurons were identified based on the waveform width and firing frequency of neurons. The changes in spindle activity in the mPFC following inhibition, as well as in firing of interneurons and pyramidal neurons were analyzed.

Morphological data confirmed that neural fibers originating from the RE densely projected to the mPFC, primarily distributed in the deep layers. In the experimental group, light stimulation significantly affected the spindle activity in the mPFC when compared with the period before light stimulation,mainly manifested as a decrease in spindle rate, central frequency, and peak-to-peak amplitude（P＜0. 05）.However, no impacts on spindle duration, number of cycles, symmetry, and power were observed. Meanwhile,there were no significant changes in the spindle activity of the control group. The proportion of interneurons in the mPFC area was 21. 9%, while pyramidal neurons accounted for 78. 1%. The firing rates of interneurons in the experimental group decreased significantly during light stimulation（P＜0. 05）, whereas there was no significant change in the firing rates of pyramidal neurons. In addition, the firing activities of both interneurons and pyramidal neurons in the control group remained unaffected.

During NREM sleep, RE inputs may participate in the generation of sleep spindles network oscillations in the mPFC by activating interneurons.