The amount of NREM sleep was comparable between the control and VMCalb1-ablated mice (Fig. 3A, B). However, the sleep spindles were significantly reduced in the frontal cortex, but they were not changed in the parietal cortex after VMCalb1 ablation (Fig. 3C, D), suggesting that VMCalb1 neurons are necessary for regulating normal sleep spindles in the frontal cortex.Fig. 3. (A, B) 24-hr amount and episode duration of NREM sleep after ablation of VMCalb1 neurons. (C, D) Sleep spindles on the frontal and parietal EEG after ablation of VMCalb1 neurons. Treatment *p<0.0001, Repeated measures two-way ANOVA. Data are presented as mean ± SEM.Increased startle response in the VMCalb1-ablated miceSensorimotor gating, the ability of a sensory event to suppress a motor response, is impaired in patients with schizophrenia and schizophrenia-like mouse models 3,4). I examined prepulse inhibition (PPI) in mice, a behavioral assay for studying impaired sensorimotor gating in schizophrenia. As a result, the PPI reactivity remained similar in both the control and VMCalb1-ablated mice (Fig. 4A). Furthermore, the startle response was also unchanged without or with pre-pulse (Fig. 4B, C). These results indicate that neither PPI nor startle response was significantly affected after VMCalb1 ablation. However, it is noted that the variation of acoustic startle was higher in the VMCalb1-ablated mice, suggesting the circuits involved in generating the startle response may become unstable after ablation of VMCalb1 neurons.Fig. 4. (A) The PPI reactivity after ablation of VMCalb1 neurons. (B, C) Startle response without or with pre-pulse after ablation of VMCalb1 neurons.― 259 ―
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