Neuroscience
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Neuroinflammation can be directly linked to the imbalance in the Kynurenine-tryptophan Pathway (KP) metabolism. Under inflammatory circumstances, the KP is activated, resulting in a rise in the KP metabolite L-kynurenine (KYN) in the peripheral and central nervous systems (CNS). Increased amounts of KYN in the brain may lead to neurotoxic KYN metabolites, mostly due to breakdown by Kynurenine-3-monooxygenase (KMO). ⋯ The neurobehavioural assessment involving elevated plus-maze, sucrose preference test, line crossing, and actophotometer revealed that the test drug is capable of decreasing LPS-induced anxiety, depression, and anhedonia at both low and high doses respectively. The histopathological analysis indicated that the neurodegeneration is attenuated at high doses of Tetrahydrocoptisine. A test drug demonstrated potency in inhibiting Kynurenine monooxygenase (KMO) expression in the brain, leading to reduced levels of nitric oxide and lipid peroxidation compared to a control group.
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Diabetes mellitus is recognized as an important cause of cognitive dysfunction. Ferroptosis plays a key role in diabetic cognitive dysfunction (DCD). Dihydromyricetin (DHM) has promising neuronal protective effects, but it is unclear the mechanism. ⋯ Meanwhile, JNK agonist Anisomycin could attenuate these effects of DHM. Taken together, our data suggest that DHM can ameliorate HG-induced neurotoxicity in HT22 cells by inhibiting ferroptosis via the JNK-inflammatory signaling pathway. Hence, DHM may represent a novel and promising therapeutic intervention for DCD.
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Increasing evidence indicates that neuropeptide FF (NPFF) produces analgesic effects and augments opioid-induced analgesia at the spinal level. However, our recent research demonstrated that NPFF exerted complex opioid-modulating effects in an inflammatory pain model after intrathecal (i.t.) injection. Consistent with previous findings, we found that i.t. ⋯ Moreover, these modulating effects of spinal NPFFR2 were selectively targeting mu-opioid receptor, had no effect on delta- and kappa-opioid receptor agonist-induced analgesia. Finally, the opioid-modulating effects of NPFF were further verified using in vitro calcium imaging assay, demonstrating that pretreated with NPFF in primary-cultured spinal neurons significantly attenuated the inhibitory effects of morphine on high-K+-induced neuronal excitability. Taken together, our results suggested that NPFF exhibited dual modulating effects on morphine-induced analgesia after i.t. administration, which provides a possible mechanism to explain the complex opioid-modulating effects of endogenous NPFF systems.
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Face recognition is an important aspect of human non-verbal communication. Event-related potentials or magnetic fields, such as the N170/M170 component, are considered essential neural markers of face processing. Compared to upright human faces, inverted human faces and upright but not inverted animal faces cause longer latencies and larger amplitudes of these components. ⋯ Additionally, face orientation differentially modulated the anterior region of the fusiform gyrus (FG) in both face categories. These results suggest that spatiotemporal dynamics differ in face orientation regardless of category and that the FG contributes little or nothing to the M170 modulation recorded in the scalp sensor. Furthermore, we demonstrated that inverted human and animal faces are processed via different mechanisms.
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Sciatic nerve crush in neonatal rats leads to an extensive death of motor and sensory neurons, serving as a platform to develop new neuroprotective approaches. The endocannabinoid system plays important neuromodulatory roles and has been involved in neurodevelopment and neuroprotection. The present work investigated the role of the cannabinoid receptors CB1 and CB2 in the neuroprotective response after neonatal axotomy. ⋯ Interestingly, Cnr1 (CB1) and Bdnf gene transcripts were downregulated in the spinal cords of the antagonist-treated groups. Despite no intergroup difference regarding neuronal survival in the DRG, the simultaneous blockade of CB1 and CB2 receptors led to an increased expression of both Cnr1 and Cnr2, combined with Gdnf upregulation. The results indicate that the selective antagonism of cannabinoid receptors facilitates neuroprotection and decreases glial reactivity, suggesting new potential treatment approaches.