Neuroscience
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Postoperative cognitive dysfunction (POCD) is characterized by impaired cognitive function, such as decreased learning and memory after anesthesia and surgery. This study aimed to explore the effect of luteoloside, a flavonoid extracted from natural herbs, on sevoflurane-induced cognitive dysfunction. Aged Sprague-Dawley male rats (20 months old) were treated with luteoloside for 7 days prior to sevoflurane exposure. ⋯ Notably, silencing Opa1 blocked the protective effect of luteoloside on hippocampal neurons and mitochondrial function. In summary, luteoloside prevented sevoflurane-induced cognitive dysfunction in aged rats, which may be achieved by regulating mitochondrial dynamics. Our study reveals the potential of luteoloside in preventing POCD in aged patients.
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In this study, the relationships between lifestyle behaviors within the scope of neuroplasticity and neurogenesis approach and depression, anxiety and neuropsychological test scores were examined. As this study aimed to reveal the relationships between events or variables, it was designed using the "descriptive cross-sectional study" method, one of descriptive and relational research methods, was used. The data were collected from 117 students by the researchers using the Öktem Verbal Memory Test, WCST, Digit Span Test, Beck Depression Inventory, Beck Anxiety Scale and Lifestyle Behaviors Survey. ⋯ Moreover, those with good levels of sleep quality, social interaction and nutrition had significantly lower depression scores. Both depression and anxiety scores of those who did sport/exercise, which was among the lifestyle behaviors, were found to be significantly lower. Lastly, the correlations between the neuropsychological test scores and the depression and anxiety scores were examined, and a significant positive correlation was found between both depression and anxiety scores and the "failure to maintain set" scores.
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Targeting reconsolidation with propranolol, a blocker of β-adrenergic receptors (β-ARs), emerged as a potential treatment for maladaptive memories such as those involved in posttraumatic stress disorder (PTSD). Reconsolidation targeting treatments for PTSD are becoming a common practice in the clinic and it is important to unveil any side effects upon 'non-targeted' memories. While previous studies have focused on propranolol's effects on the reconsolidation of emotional/distressful memories, the present study asked whether propranolol is involved in the reconsolidation of recognition memories - by assessing its effects on distinct memory components and the role of the dorsal hippocampus. ⋯ Propranolol infusions consistently impaired the addition of novel information to the previously consolidated memory trace regardless of dose, and the retention of familiar objects was not affected. Higher doses of propranolol also hindered memory of a familiar object that was not presented during the reactivation session, but was previously placed at the same location where novel information was presented during reactivation. The present results shed light on the role of β-ARs on the reconsolidation of different memory components and argue for the need for further studies examining possible recognition memory deficits following propranolol treatment.
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We accurately sense locations of objects touching various points on the body and, if they are irritants, make accurate rapid movements to remove them. Such movements require accurate proprioception of orientation and motion of the reaching limb and of the target. However, it is unknown whether acuity of these sensations is similar for different points on the body. ⋯ Mean errors for reaches to touch points on the left lower limb were least accurate (p < 0.05), with mean errors averaging 1.5-3.1 cm relative to movements made with vision. We conclude that there is high proprioceptive acuity for locations of points on axial structures and the left upper limb including the digits, which contrasts with previous reports of greatly distorted proprioceptive maps of the face/head and hand. Apparently low proprioceptive acuity for points on the leg may be task sensitive as many lower limb motor tasks can be performed accurately without vision.
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Kainic acid (KA), an analogue of the excitatory neurotransmitter glutamate, when administered systemically can trigger seizures and neuronal loss in a manner that mirrors the neuropathology of human mesial temporal lobe epilepsy (mTLE), which affects ∼50 million people globally. Evidence suggests that changes in astrocytes which precede neuronal damage play an important role in the degeneration of neurons and/or development of seizures in TLE pathogenesis. Additionally, a role for microtubule associated tau protein, involved in various neurodegenerative diseases including Alzheimer's disease, has also been suggested in the development of seizure and/or neurodegeneration in TLE pathogenesis. ⋯ Concurrently, the total (Tau1 and Tau5) and phospho-tau (AT270 and PHF1) levels are transiently enhanced following KA administration. Furthermore, the level/expression of cleaved-tau, which is apparent in a subset of GFAP-, S100B- and A2-positive astrocytes, are increased in KA-treated rats. These results, taken together, suggest a differential role for various astrocytic subpopulations and tau protein in the development of seizure and/or loss of neurons in KA model of TLE and possibly in human mTLE pathogenesis.