Neuroscience
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Numerous long-term studies have investigated the circadian clock system in mammals, which organizes physiological functions, including metabolism, digestion, and absorption of food, and energy expenditure. Food or nutrition can be a synchronizer for the circadian clock systems, as potent as the external light-dark signal can be. Recent studies have investigated different kinds of food, frequency of consumption, and time of consumption for optimizing body clock and ensuring healthy habits. In this review, we discuss recent studies investigating chronobiology and nutrition, and then summarize available information as "Chrono-nutrition" for the development of a new standardized research strategy.
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Randomized Controlled Trial
Plant-derived nanoparticle treatment with cocc 30c ameliorates attention and motor abilities in sleep-deprived rats.
Sleep is an essential physiological process that underlies crucial cognitive functions as well as emotional reactivity. Thus, sleep deprivation (SD) may exert various deleterious effects. In this study, we aimed to examine the adverse behavioral and hormonal effects of SD and a potential treatment with Plant-derived nanoparticle treatment - cocc 30c. ⋯ Likewise, SD led to increased levels of corticosterone and serotonin while decreasing testosterone and leptin. Interestingly, cocc 30c treatment has moderated these hormonal alterations. We conclude that the treatment with cocc 30c recovers both short-term behavioral and the long-term hormonal modulations following SD.
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The auditory system continuously monitors the environment for irregularities in an automatic, preattentive fashion. This is presumably accomplished by two mechanisms: a sensory mechanism detects a deviant sound on the basis of differential refractoriness of neural populations sensitive to the standard and deviant sounds, whereas the cognitive mechanism reveals deviance by comparing incoming auditory information with a template derived from previous input. ⋯ The sensory mechanism is supported by primary auditory areas in Heschl's gyrus whereas the cognitive mechanism is implemented in more anterior secondary auditory areas. Both mechanisms are equally engaged by simple sine-wave tones and speech-related phonemes indicating that streams of speech and non-speech stimuli are processed in a similar fashion.
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Phosphoinositide 3-kinase γ (PI3Kγ) is a shared downstream component of chemokine-mediated signaling pathways and regulates migration, proliferation and activation of inflammatory cells. PI3Kγ has been shown to play a crucial role in regulating inflammatory responses during the progression of several diseases. We investigated the potential function of PI3Kγ in mediating inflammatory reactions and the development of experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis (MS). ⋯ Consistently, we demonstrated that PI3Kγ deletion in knockout mice mitigates the clinical sign of EAE compared to PI3Kγ+/+ controls. PI3Kγ deletion increased the number of axons in the lumbar spinal cord, including descending 5-HT-positive serotonergic fiber tracts. Our results indicate that PI3Kγ contributes to development of autoimmune CNS inflammation and that PI3Kγ blockade may provide a great potential for treating patients with MS.
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Presynaptic functions of the mammalian central neurons are regulated by a network of protein interactions. Synaptic vesicle recycling in and neurotransmitter release from the presynaptic nerve terminals are altered when a glutamate-deleting mutation is present in the torsinA protein (ΔE-torsinA). This mutation is linked with a hereditary form of the movement disorder dystonia known as DYT1 dystonia. ⋯ These results were confirmed by fluorogram-based quantitation. Our findings indicate that neither the wild-type nor the ΔE-torsinA mutant protein is present at substantial levels in the presynaptic structures of cultured neurons. Thus, the effects of torsinA, in wild-type and mutant forms, appear to influence presynaptic function indirectly, without residing in presynaptic structures.