Neuroscience
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Serotonin (5-HT) is a key regulator of mood and sexual behaviors. 5-HT reuptake inhibitors have been used as antidepressants. Really interesting new gene (RING) finger proteins have been associated with 5-HT regulation but their role remains largely unknown. Some RING finger proteins are involved in the serotonergic system, therefore, we speculate that the gene expression of RING finger protein38 (rnf38) is regulated by the serotonergic system. ⋯ On the other hand, rnf38 gene was significantly high (P<0.05) in the telencephalon and the hypothalamus. This shows that 5-HT synthesis and transport in the hindbrain is suppressed by CIT, which induces rnf38 gene expression in the forebrain where 5-HT neurons project. Thus, the expression of rnf38 is negatively regulated by the serotonergic system.
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Using ERP adaptation paradigms, studies have shown that the N170 adaptation effect is a stable phenomenon for both faces and words. However, the N170 adaptation effect for repeated identity remains unclear, so we have addressed this with two experiments. In Experiment 1, we investigated the face-related N170 repeated adaptation effect in a short interstimulus interval (ISI) and found that the N170 response elicited by faces was smaller when preceded by a same face adaptor than by another face adaptor. ⋯ For the first time, the results indicated that the N170 response elicited by words was larger with a different word as an adaptor relative to the same word as an adaptor. Our results demonstrate that the face-related N170 response is sensitive to visual face features and extend the characteristics of N170 with the sensitivity to repeated items to other familiar objects of expertise (i.e. words). The results also suggest that there are some common characteristics between faces and words in the early perceptual processing.
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Icariin (ICA), a flavonoid extracted from the traditional Chinese herb Herba Epimedii that can freely cross the blood-brain barrier, inhibits neuroinflammation and attenuates oxidative stress damage. Our previous studies demonstrated that icariin exerts an antidepressant-like activity in a social defeat mouse model. However, it is unknown whether icariin is beneficial for the treatment of depression via its modulation of oxidative stress and neuroinflammation. ⋯ Interestingly, icariin negatively regulated the activation of the nod-like receptor protein 3 (NLRP3) inflammasome/caspase-1/IL-1β axis in the hippocampus of CMS rats. These results confirm that icariin exerts antidepressant-like effects, which may be mediated, at least in part, by enhanced antioxidant status and anti-inflammatory effects on the brain tissue via the inhibition of NF-κB signaling activation and the NLRP3-inflammasome/caspase-1/IL-1β axis. Our findings provide new information to understand the antidepressant action of icariin, which is targeted to the NLRP3-inflammasom in brain.
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Multiple sclerosis (MS) is thought to result from a combination of genetics and environmental factors. Several lines of evidence indicate that significant prevalence of anxiety and depression-related disorders in MS patients can influence the progression of the disease. Although we and others have already reported the consequences of prenatal maternal immune activation on anxiety and depression, less is known about the interplay between maternal inflammation, MS and gender. ⋯ Interestingly, the severity of the disease was associated with increased anxiety/depressive-like behaviors and elevated corticosterone or TNF-α levels in both sexes. Overall, these data suggest that maternal immune activation with Poly I:C during mid-pregnancy increases anxiety- and depressive-like behaviors, and the clinical symptoms of EAE in a sex-dependent manner in non-EAE or EAE-induced offspring. Finally, the progression of EAE in offspring seems to be linked to maternal immune activation-induced dysregulation in neuro-immune-endocrine system.
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Parkinson's disease (PD) is characterized by selective loss of dopaminergic neurons in the substantia nigra (SN). Epidemiological evidence has suggested a link between type 2 diabetes and PD, although the mechanisms remain largely unknown. We applied LC-MS/MS-based pattern analysis to investigate altered proteomes in the SN of db/db mice (db-SN) and high-fat diet mice (HFD-SN), revealing that the level of mitochondrial proteins has changed in the SN of diabetic mice compared to that of control mice. ⋯ Interestingly, these alterations were reversed by the administration of metformin, one of most frequently prescribed anti-hyperglycemic agents. The slight loss of dopaminergic neurons was found in chronic HFD-SN that was restored by metformin. Taken together, our data suggest that the dysregulation of Parkin-PARIS-PGC-1α pathway by metabolic malregulation may contribute to the pathogenesis of PD and metformin might exert a neuroprotective effect on PD via the restoration of parkin.