Propofol is widely used for the induction and maintenance of anesthesia, which causes a rapid loss of consciousness. However, the mechanisms underlying the hypnosis effect of propofol are still not fully understood. The thalamic reticular nucleus (TRN) is crucial for regulating wakefulness, sleep rhythm generation, and sleep stability, while the role of TRN in the process of propofol-induced anesthesia is still unknown. Here, we investigated the function of the anterior TRN in propofol general anesthesia. Our results demonstrated that the neural activity of anterior TRN is suppressed during propofol anesthesia, whereas it is robustly activated from anesthesia by recording the calcium signals using fiber photometry technology. The results showed that the activation of anterior TRN neurons by chemogenetic and optogenetic methods shortens the emergency time without changing the induction time. Conversely, chemogenetic or optogenetic inhibition of the TRN neurons leads to a delay in the recovery time. Our study showed that anterior TRN is crucial for behavioral arousal without affecting the induction time of propofol anesthesia.
IntroductionProcedural pain in neonates is associated with impaired neurodevelopment. Whether hearing development is impaired, however, remains unknown. This study examined potential cause-and-effect relationship between neonatal pain and subsequent hearing loss in mice.MethodsMale C57BL/6J mouse pups received an intra-plantar injection of complete Freund’s adjuvant on postnatal day 7 or repetitive needle prick stimuli from postnatal days 0–7. Mechanical and thermal pain thresholds were tested between postnatal days 14 and 49. The auditory brainstem response test was used to determine hearing thresholds. The inner ear structures and dendritic morphology in auditory cortex were assessed using immunofluorescence and Golgi-staining. The effects of oxycodone, tropomyosin receptor kinase B agonists and antagonists were tested.ResultsNeonatal pain resulted in impaired hearing in adulthood of both pain models No damage or synapse loss was found in the cochlea but increased dendritic spine density and reduced brain-derived neurotrophic factor level were found in auditory cortex in neonatal pain group. Oxycodone attenuated hearing loss and the associated changes in dendritic spine density and brain-derived neurotrophic factor changes in auditory cortex. A tropomyosin receptor kinase B agonist reversed neonatal pain-induced hearing impairment and decreased caspase 3 expression in auditory cortex. Administration of tropomyosin receptor kinase B antagonist in naïve mouse pups impaired hearing development suppressed phosphorylated-AKT, and increased caspase 3 expression.ConclusionChronic pain during the neonatal period resulted in impaired hearing in adulthood in mice, possibly via the brain-derived neurotrophic factor signaling pathway and dendritic spine pruning deficiency in auditory cortex.
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