Neuroscience
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The vast majority of stroke cases are classified as ischemic stroke, but effective pharmacotherapy strategies to treat brain infarction are still limited. Glutamate, which is a primary mediator of excitotoxicity, contributes to neuronal damage in numerous pathologies, including ischemia. The aim of this study was to investigate the effect of the hydrogen sulfide donor AP39 on excitotoxicity. ⋯ The results showed a significant longitudinal decrease in extracellular glutamate concentrations in the motor cortex and hippocampus in MCAO + AP39 rats compared to MCAO rats. Moreover, the administration of AP39 increased the content of the GLT-1 transporter and reduced the content of VGLUT1 in the ischemic core. Upregulation of the GLT-1 transporter responsible for glutamate reuptake from the synaptic cleft, and downregulation of VGLUT1, which regulates glutamate transport to synaptic vesicles, indicate that these are important mechanisms by which AP39 reduces extracellular glutamate concentrations and, consequently, excitotoxicity after ischemia.
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The use of mu-opioid receptor (MOP-r) agonists such as oxycodone together with cocaine is prevalent, and deaths attributed to using these combinations have increased. ⋯ These studies demonstrated that this functional genetic variation in Oprm1 affected dual opioid and cocaine SA and altered specific gene expression in the striatum.
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Virgin and pups-naïve female and male adult mice display two opposite responses when they are exposed to pups for the first time. While females generally take care of the pups, males attack them. Since the nucleus accumbens (NA), and its dopaminergic modulation, is critical in integrating information and processing reward and aversion, we investigated if NMDA- and 6-OHDA-induced lesions, damaging mostly NA output and dopaminergic inputs respectively, affected female maternal behavior (MB) or male infanticidal behavior (IB) in mice. ⋯ The current study shows that an intact NA is not necessary for the expression of MB and IB. However, dopaminergic inputs to NA play different role in MB and IB. While damaging dopaminergic terminals into the NA did not affect IB, it clearly delayed the more flexible and rewarding expression of parental behavior.
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With the deepening of population aging, the treatment of cognitive impairment and dementia is facing increasing challenges. Vascular dementia (VaD) is a cognitive dysfunction caused by brain blood flow damage and one of the most common causes of dementia after Alzheimer's disease. White matter damage in patients with chronic ischemic dementia often occurs before cognitive impairment, and its pathological changes include leukoaraiosis, myelin destruction and oligodendrocyte death. ⋯ The current proposed mechanisms include calcium overload, oxidative stress, nitrative stress and inflammatory damage, which can lead to hypoxia-ischemia and demyelination. Oligodendrocytes are the only myelinating cells in the central nervous system and closely associated with VaD. In this review article, we intend to further discuss the role of oligodendrocytes in white matter and myelin injury in VaD and the development of anti-myelin injury target drugs.
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Randomized Controlled Trial
A causal role of right TPJ in prosocial learning: a tDCS study.
Prosocial behavior is a common and important aspect of everyday social life. To behave prosocially, we need to learn the consequences of our actions for other people, known as prosocial learning. Previous studies have identified the right temporoparietal junction (rTPJ) as the critical neurological substrate for prosocial behavior. ⋯ Participants were able to learn to obtain rewards for themselves or others, and learning performance in the self-learning condition was better than that in the prosocial-learning condition. However, anodal tDCS over the rTPJ significantly improved learning performance in the prosocial-learning condition. These results indicate that the rTPJ plays a causal role in prosocial learning.