Neuroscience
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Memory impairment is one of the neuropsychological effects of hypobaric hypoxia (HH), which can be associated with programmed cell death, such as apoptosis and ferroptosis. Emerging evidence indicates crosstalk between apoptosis and ferroptosis, while the crosstalk between HH-induced apoptosis and ferroptosis in the hippocampus has not been clarified. Here, microarray profiles were extracted to analyze the differentially expressed genes with and without HH exposure, and keratin 18 (Krt18) was found to be a potential gene related to both apoptosis and ferroptosis. ⋯ Combined with the real-time q-PCR analysis, the mRNA expression of Krt18 decreased significantly after HH exposure for 1 day and 3 days, and Mapk10 (JNK3) was upregulated at the corresponding time points. After exposure for 7 days, Krt18 and JNK3 showed no significant change. In conclusion, Krt18 may regulate apoptosis and ferroptosis simultaneously, possibly via the JNK signaling pathway, which might provide a potential central target for apoptosis and ferroptosis in hippocampal injury after HH exposure.
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The contactin-associated protein-like 2 (CNTNAP2) gene encodes for the CASPR2 protein, which plays an essential role in neurodevelopment. Mutations in CNTNAP2 are associated with neurodevelopmental disorders, including autism spectrum disorder and schizophrenia. Rats with a loss of function mutation in the Cntnap2 gene show increased acoustic startle response (ASR) and decreased prepulse inhibition (PPI). ⋯ Female Cntnap2-/- rats showed considerably increased PnC firing rates compared with female wildtypes, whereas the difference between the genotypes was modest in male rats. In contrast, for both females and males we found meager differences between the genotypes for PPTg firing rates and inhibition of PnC firing rates, indicating that altered firing rates of these brainstem structures are not responsible for decreased PPI in Cntnap2-/- rats. We conclude that the auditory processing changes seen in Cntnap2-/- rats are associated with, but cannot be fully explained by, differences in PnC firing rates, and that a loss of function mutation in the Cntnap2 gene has differential effects depending on sex.
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Alzheimer's disease (AD) is a chronic neurological disorder with high morbidity. Exercise is one of the effective ways to ameliorate AD. In this study, we assessed the effects of exercise on cognition and inflammation and studied the role of miR-148a-3p in AD. ⋯ MiR-148a-3p silencing reversed these abovementioned tendencies. Patients with AD exhibited a low level of miR-148a-3p, which was increased after exercise. Therefore, exercise might improve the cognitive function and memory of mice with AD by upregulating miR-148a-3p.
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Locomotor movements in mammals are generated by neural networks, situated in the spinal cord, known as central pattern generators (CPGs). Recently, significant strides have been made in the genetic identification of interneuronal components of the locomotor CPG and their specific function. Despite this progress, a population of interneurons that is required for locomotor rhythmogenesis has yet to be identified, and it has been suggested that subsets of interneurons belonging to several genetically-defined populations may be involved. ⋯ Focal application of 5-hydroxytryptamine creatine sulfate complex (5-HT) and N-methyl-D-aspartate (NMDA) to the central canal of the rostral lumbar segments of newborn male and female mouse spinal cords quickly generates a robust pattern of fictive locomotion, while inhibition or ablation of neurons in this region disrupts the locomotor rhythm in both rostral and caudal lumbar segments. When applied to the central canal at caudal lumbar levels a higher volume of 5-HT and NMDA are required to elicit fictive locomotion, while inhibition of neurons surrounding the central canal at caudal levels again interrupts rhythmic activity at local segmental levels with minimal effects rostrally. The results of this study indicate that interneurons in the most medial laminae of the neonatal mouse spinal cord are both necessary and sufficient for the generation of locomotor activity, and suggests that this is the region where the rhythm generating core of the locomotor CPG resides.