State‐dependent modulation of sensory systems has been studied in many organisms and is possibly mediated through neuromodulators such as monoamine neurotransmitters. Among these, dopamine is involved in many aspects of animal behaviour, including movement control, attention, motivation and cognition. However, the precise neural mechanism underlying dopaminergic modulation of behaviour induced by sensory stimuli remains poorly understood. Here, we used Drosophila melanogaster to show that dopamine can modulate the optomotor response to moving visual stimuli including noise. The optomotor response is the head‐turning response to moving objects, which is observed in most sight‐reliant animals including mammals and insects. First, the effects of the dopamine system on the optomotor response were investigated in mutant flies deficient in dopamine receptors D1R1 or D1R2, which are involved in the modulation of sleep‐arousal in flies. We examined the optomotor response in D1R1 knockout (D1R1 KO) and D1R2 knockout (D1R2 KO) flies and found that it was not affected in D1R1 KO flies; however, it was significantly reduced in D1R2 KO flies compared with the wild type. Using cell‐type‐specific expression of an RNA interference construct of D1R2, we identified the fan‐shaped body, a part of the central complex, responsible for dopamine‐mediated modulation of the optomotor response. In particular, pontine cells in the fan‐shaped body seemed important in the modulation of the optomotor response, and their neural activity was required for the optomotor response. These results suggest a novel role of the central complex in the modulation of a behaviour based on the processing of sensory stimulations.
Purpose Various biofeedback stimulation techniques of managing sleep bruxism (SB) have recently emerged; however, the effect of successive application of vibratory feedback stimulation has not been clarified. This study elucidated the effect of vibration feedback stimulation via an oral appliance (OA) on SB when vibration feedback was applied for 4 weeks. Methods This was a prospective, single-arm, open-label, intervention study. Ten participants diagnosed with "definite" SB wore a specially designed OA for 45 nights in a home-setting. A force-based SB detection system, including a pressuresensitive piezoelectric film placed internally in the OA, triggered a vibrator attached to the OA. Vibratory stimulation was withheld during the first 2-week adaptation period (1st-15th nights), applied during the 4-week stimulation period (16th-43rd nights), and again withheld during the post-stimulation period (44th and 45th nights). The number and duration of SB episodes/hour of sleep were calculated based on masseter electromyographic activity recorded with in-home portable polysomnography and compared between the 15th and 45th nights (without stimulation) and the 17th and 43rd nights (with stimulation).
ResultsThe number and duration of SB episodes significantly decreased after vibratory stimulation (15th vs. 17th nights: p = 0.012 and p = 0.012, respectively), then significantly increased upon cessation of vibratory stimulation after the stimulation period (43rd vs. 45th nights: p = 0.023 and p = 0.023, respectively). Conclusion Contingent vibratory stimulation through an OA may suppress SB-related masticatory muscle activity continuously for 4 weeks and may be an effective alternative for the management of SB. Trial registration https:// jrct. niph. go. jp/; trial registration number: jRCTs032190225
Purpose: To test the validity of a force-based detection system (ISFD: intra-splint force detector) to record sleep bruxism (SB) in comparison to portable polysomnography (PSG). Methods: Simultaneous portable PSG recordings with a masseter electromyography (EMG) channel and ISFD with a deformation-sensitive piezoelectric film were performed on six participants with definite SB. First, simulated bruxism behaviors (static clenching, grinding, tapping, and rhythmic clenching) were recorded using both EMG and ISFD. Using these data, interval and duration criteria for ISFD data conditioning were established. Then, portable PSG recordings were conducted with the ISFD during sleep. Using the above criteria, ISFD events were compared with EMG-based SB episodes (the gold standard), and the sensitivity and positive predictive value of ISFD events were calculated. Spearman's correlation coefficients between true-positive ISFD events and SB episodes were then calculated. Results: Among the tested conditioning criteria, a 3-s interval combined with a 1-s duration was selected. The median sensitivity and positive predictive value for the ISFD were 0.861 and 0.585, respectively. The duration of true-positive ISFD events was correlated with that of EMG-based SB episodes (rho = 0.658, P < 0.01). Conclusion: ISFD has validity for SB detection and could be an alternative to single-channel EMG-based recordings.
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