Neuroscience
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A periodic sound with a fixed inter-stimulus interval elicits an auditory steady-state response (ASSR). An abrupt change in a continuous sound is known to affect the brain's ongoing neural oscillatory activity, but the underlying mechanism has not been fully clarified. We investigated whether and how an abrupt change in sound intensity affects the ASSR. ⋯ The two-dipole model obtained for the 40-Hz ASSR in the control condition was applied to all of the stimulus conditions for each subject, and then the time-frequency analysis was conducted. We observed that both the amplitude and the inter-trial phase coherence of the 40-Hz ASSR transiently decreased and returned to the steady state after the change onset, i.e., the desynchronization of 40-Hz ASSR. The degree of desynchronization depended on the magnitude of the change regardless of whether the sound intensity increased or decreased, which might be a novel neurophysiological index of cerebral response driven by a change in the sensory environment.
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Chronic pain is prevalent among aging adults. Epidemiologic evidence has demonstrated that individuals with chronic pain have accelerated memory decline and increased probability of dementia. ⋯ We validate this with multiple independent data sets and identify cortical microglia as a likely mechanism by which chronic pain can increase dementia risk. Our analyses support the molecular hypothesis for the role of chronic pain in cognitive decline and identifies several potential therapeutic targets.
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Deficits in social communication and language development are a hallmark of autism spectrum disorder currently with no effective approaches to reduce the negative impact. Interventional studies using animal models have been very limited in demonstrating improved vocal communication. Autism has been proposed to involve metabolic dysregulation. ⋯ Composition of call categories and transitioning between individual call subtypes were more effectively altered to more closely align with the control group in juvenile BTBR mice. Together, our data provide further support to the hypothesis that metabolism-based dietary intervention could modify disease expression, including core symptoms, in autism. Future studies should tease apart the molecular mechanisms of KD's effects on vocalization.
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The neuroinflammatory response promotes secondary brain injury after traumatic brain injury (TBI). Triggering receptor expressed on myeloid cells 1 (TREM1) is a key regulator of inflammation. However, the role of TREM1 in TBI is poorly studied. ⋯ Moreover, after TREM1 was inhibited, the secretion of the proinflammatory factors TNF-α and IL-1β was significantly reduced, while the secretion of the anti-inflammatory factors IL-4 and IL-10 was significantly increased. Additionally, inhibition of TREM1 by LP17 significantly reduced neuronal apoptosis and ameliorated nerve dysfunction in TBI model rats. In conclusion, our findings suggest that TREM1 enhances neuroinflammation and promotes neuronal apoptosis after TBI, and these effects may be partly mediated via the ERK/cPLA2 signalling pathway.
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Transparency of C. elegans enables microscopic in vivo imaging of cellular processes, but immobilization is required due to high locomotor activity. Here, anesthetic-like effects of dissociate anesthetic ketamine in adult C. elegans are presented using video recordings and infrared-based automated activity tracking. Ketamine caused a reversible blockade of locomotion at a similar concentration (20-50 mM) at which conventionally used immobilizing agent sodium azide (NaN3) produces paralysis. ⋯ However, a marked chemosensation deficiency was noted immediately after 20 mM ketamine exposure. Short-term ketamine treatment did not show signs of SKN-1 (skinhead-1) activation, a marker of the stress response associated with NaN3. In sum, our results show ketamine's potential as a non-toxic nematode immobilizing agent and rationalize C. elegans as a model organism to understand its pharmacology.