Acta neurobiologiae experimentalis最新文献

Language disorders can occur as a consequence of stroke or neurodegenerative disorders, among other causes. Post‑stroke aphasia (PSA) and primary progressive aphasia (PPA) are syndromes that, despite having common features, differ in the brain mechanisms that cause their symptoms. These differences in the underlying functional neuroanatomical changes may influence the way they are addressed by different non‑invasive brain stimulation techniques and, in particular, by repetitive transcranial magnetic stimulation (rTMS). The aim of this systematic review is to evaluate the efficacy of rTMS in the treatment of PSA and PPA, as well as the differences in the approach to these disorders using rTMS. To this end, a total of 36 articles were found in the Web of Science, Scopus, and PubMed. The results obtained suggest that whereas in PSA, the selection of the stimulation paradigm is based on bi‑hemispheric functional reorganisation models with a tendency towards the application of inhibitory rTMS in the contralateral right hemisphere, in PPA, the application of excitatory rTMS in functionally compromised areas seems to show promising changes. It is concluded that rTMS is a potential treatment in the therapy of both disorders, although differences in the underlying brain mechanisms differentiate the rTMS approach in each case.

Studies have shown that vitamin D plays a crucial role in brain development, brain metabolism and neuroprotection. There is little evidence for the neuroprotective effect of 1, 25‑dihydroxyvitamin D3 (1,25‑(OH)2D3) on various brain injury models. The aim of this study was to investigate the neuroprotection effect of 1,25‑(OH)2D3 against hyperoxia‑induced brain injury in premature rats. Sprague‑Dawley rats were exposed to 95% oxygen or room air for 24 h and treated with 1,25‑(OH)2D3 or normal saline for 14 consecutive days. The histopathological changes of optic chiasma tissue were observed by hematoxylin‑eosin staining. Immunohistochemistry, qRT‑PCR, and western blot were performed to detect the expression of integrin‑β1 and yes‑associated protein (YAP) in the organization of the optic chiasm. Histopathological sections of optic chiasma showed visible optic nerve swelling, expanded nerve fiber space, uneven staining, obvious oligodendrocyte proliferation and disordered cell arrangement accompanied by inflammatory cell infiltration and exudation after 7 days and 14 days of hyperoxia exposure. The hyperoxia group treated with 1,25‑(OH)2D3 were showed improvement of brain injury with reduced inflammatory exudation, uniform nerve fiber staining and less obvious oligodendrocyte proliferation. Immunohistochemical staining, qRT‑PCR and western blot indicated that 1,25‑(OH)2D3 treatment upregulated the expression of integrin‑β1 and YAP in the hyperoxia group on day 7. However, the expression of YAP was significantly increased compared with control group and treatment with 1,25‑(OH)2D3 reduced the expression of YAP in the hyperoxic group on day 14. 1,25‑(OH)2D3 may regulate the expression of integrin‑β1 and YAP to alleviate hyperoxia‑induced brain injury in premature rats.

The aim of this study is to evaluate the dose‑dependent effect of bee venom (BV) on behavioral functions in rats and the physiological role of leptin in the prefrontal cortex, hippocampus, and amygdala tissues. Adult Sprague‑Dawley male rats were used in the experiments. The rats were divided into three groups of control, 0.1 mg/kg BV, and 0.5 mg/kg BV. The rats were injected with BV subcutaneously for 15 consecutive days. The open field test (OFT), the elevated plus maze test (EPM), and the forced swimming test (FST) were performed as behavioral assessments. Animals were sacrificed, and brain regions were removed. Leptin levels were measured in various brain regions by ELISA. In the OFT, the total distance and speed for the 0.1 mg/kg BV group increased compared to controls and the 0.5 mg/kg BV group. In the EPM, the 0.1 mg/kg BV group remained in the open arm for a significantly longer period of time compared to the other groups. In the FST, the 0.5 mg/kg BV group was more mobile than the other groups. Leptin levels in the prefrontal cortex were significantly higher in the 0.1 mg/kg BV group compared to the control and 0.5 mg/kg groups. There were no significant differences between groups in hippocampus and amygdala leptin levels. The results of the study show that BV has a positive effect on behavioral parameters. BV may have a positive effect on anxiety‑ and depression‑like behaviors by increasing leptin levels in the prefrontal cortex.

The autonomic nervous system regulates internal organs and peripheral circulation, which enables the maintenance of homeostasis in vertebrate species. One of the brain regions involved in autonomic and endocrine homeostasis regulation is the paraventricular nucleus of the hypothalamus (PVN). The PVN is a unique site at which multiple input signals can be assessed and integrated. The regulation of the autonomic system by the PVN and, especially, the sympathetic flow, depends upon the integration of inhibitory and excitatory neurotransmitter action. The excitatory neurotransmitters such as glutamate and angiotensin II, and inhibitory neurotransmitters such as γ‑aminobutyric acid and nitric oxide, play a key role in the physiological function of the PVN. Moreover, arginine-vasopressin (AVP) and oxytocin (OXT) are important in the regulation of sympathetic system activity. The PVN is also crucial for maintaining cardiovascular regulation, with its integrity being pivotal for blood pressure regulation. Studies have shown that pre‑autonomic sympathetic PVN neurons increase blood pressure and the dysfunction of these neurons is directly related to elevated sympathetic nervous system activity under hypertension. Etiology of hypertension in patients is not fully known. Thus, understanding the role of PVN in the generation of hypertension may help to treat this cardiovascular disease. This review focuses on the PVN's inhibitory and excitatory neurotransmitter interactions that regulate sympathetic system activity in physiological conditions and hypertension.

Reports suggest that a high‑cholesterol diet may induce neuroinflammation, oxidative stress, and neurodegeneration in brain tissue. Brain‑derived neurotrophic factor (BDNF) might play a role in protecting against changes induced by high cholesterol. We aimed to assess behavioral correlates and biochemical alterations in the motor and sensory cortices following a high‑cholesterol diet under normal and reduced BDNF concentrations. C57Bl/6 strain, wild‑type (WT) and BDNF heterozygous (+/‑) mice were used to reveal the effects of endogenous BDNF concentrations. We compared diet and genotype effects using four experimental groups: WT and BDNF heterozygous (+/‑) groups of mice were each fed a normal or high‑cholesterol diet for 16 weeks. The cylinder test and wire hanging test were performed to evaluate neuromuscular deficits and cortical sensory‑motor functions, respectively. In addition, neuroinflammation was assessed by tumor necrosis factor alpha and interleukin 6 levels measured in the somatosensory and motor areas. Additionally, MDA levels and SOD and CAT activity were evaluated as oxidative stress parameters. Results showed that a high‑cholesterol diet significantly impaired behavioral performance in the BDNF (+/‑) group. Diet did not change the levels of neuroinflammatory markers in any of the groups. However, MDA levels, an indicator of lipid peroxidation, were significantly higher in the high‑cholesterol‑fed BDNF (+/‑) mice. The results suggest that BDNF levels might be a critical factor in determining the extent of neuronal damage induced in the neocortex by a high‑cholesterol diet.

Dopamine (DA) depletion in the dorsal striatum underlies symptoms of basal ganglia pathologies, including Parkinson's disease (PD). Various drug compounds are used to enhance DA levels for therapeutic purposes. Understanding neural signaling and movement patterns associated with over‑ and under‑stimulation of the DA system is essential. This study investigated striatal local field potential (LFP) oscillation and locomotor activity following treatments with morphine, a DA release enhancer, and haloperidol (HAL), a DA D2 receptor (D2R) antagonist in mice. After intracranial electrodes were placed into the dorsal striatum of male Swiss albino ICR mice, intraperitoneal injections of morphine or HAL were administered. LFP signals and spontaneous motor activity were recorded simultaneously. The results showed that morphine significantly increased locomotor speed, both low (30.3-44.9 Hz) and high (60.5-95.7 Hz) LFP gamma powers and delta (1-4 Hz)‑gamma (30.3-95.7 Hz) phase‑amplitude coupling. In contrast, HAL treatments were found to significantly decrease these parameters. Moreover, regression analyses also revealed significant positive correlations between locomotor speed and high gamma powers. Taken together, these results demonstrate opposite LFP oscillations in the dorsal striatum with low and high gamma activities, and delta‑gamma couplings in response to a DA release enhancer and D2R antagonist by morphine and HAL, respectively. These parameters reflect fluctuation of neuronal activity in the dorsal striatum that might be useful for pathological research and drug discovery for PD.

This study investigated the effects of sub‑chronic administration of lead (Pb) acetate on thiobarbituric acid reactive substances (TBA‑RS), total sulfhydryl content, protein carbonyl content, antioxidant enzymes (superoxide dismutase [SOD], catalase [CAT], glutathione peroxidase [GSH‑Px]), acetylcholinesterase (AChE), and Na+K+‑ATPase in the cerebral structures of rats. Male Wistar rats aged 60 days were treated with saline (control group) or Pb (treatment group), at various doses, by gavage, once a day for 35 days. The animals were sacrificed twelve hours after the last administration, and the cerebellum, hippocampus and cerebral cortex were removed. The results showed that Pb did not alter the evaluated oxidative stress parameters. Furthermore, Pb (64 and/or 128 mg/kg) altered SOD in the cerebellum, cerebral cortex and hippocampus. Pb (128 mg/kg) altered CAT in the cerebellum and cerebral cortex and GSH‑Px in the cerebral cortex. Also, Pb (64 mg/kg and 128 mg/kg) altered GSH‑Px in the cerebellum. Moreover, Pb (128 mg/kg) increased AChE in the hippocampus and decreased Na+K+‑ATPase in the cerebellum and hippocampus. In conclusion, sub‑chronic exposure to Pb (occupational and environmental intoxication) altered antioxidant enzymes, AChE, and Na+K+‑ATPase, contributing to cerebral dysfunction.

Neurodegeneration is characterized by loss of neurons causing changes that lead individuals to debilitating conditions; the most common of this condition is the Alzheimer's disease. It has been related that enriched environment (EE) induces experience‑dependent plasticity mechanisms, improving the performance of the animals in learning and memory tests. This study evaluated the effects of EE on histological parameters of the cerebellum in rats that received intracerebroventricular streptozotocin. In the standard environment, streptozotocin (STZ) promoted a significant increase between the gaps in the Purkinje layer of approximately 20%. On the other hand, in an enriched environment, the control result (EE) was similar to the result under streptozotocin effect (STZEE). In the standard environment (SE) group a 26% significant reduction in Purkinje cell density was observed under STZ presence. By analyzing the results of the density of Purkinje cells under the effect of streptozotocin in a standard environment (STZSE) against the density of the layer of Purkinje cells also under the effect of streptozotocin in an enriched environment (STZEE), a significant reduction of approximately 76% in density was observed of Purkinje cells in standard environment (STZSE), the mean number of Purkinje cells in enriched environments was not reduced, despite of STZ. According to the results, treatment with STZ and exposure to EE did not change the cerebellum general morphology/cytoarchitecture, hence was no significant difference in the layers thickness. These facts demonstrate that the enriched environment appears to protect the Purkinje cells layer of cerebellum from possible degeneration.

Aminopyridines constitute a drug family with the ability to enhance synaptic transmission. In particular, 4‑aminopyridine (4‑AP) has been used as a model of generalized seizures. 4‑AP is a K+ channel blocker, but its mechanism of action has not yet been fully described; some evidence has shown that it acts on the K+ channel types Kv1.1, Kv1.2, Kv1.4 and Kv4, which are localized in the axonic terminals of pyramidal neurons and interneurons. When 4‑AP blocks the K+ channels it triggers depolarization and prolongs the action potential in the neuron, which causes nonspecific neurotransmitter release. Among these neurotransmitters, glutamate is the principal excitatory neurotransmitter released in the hippocampus. Once glutamate is released, it reaches its ionotropic and metabotropic receptors continuing the neuronal depolarization chain and propagation of hyperexcitability. This brief review is focused on the use of 4‑AP as an effective seizure model for testing antiseizure drugs in relevant in vitro and in vivo studies.

We aim to investigate the role and biological mechanisms of the weekend warrior (WW) exercise model on depression‑induced rats in comparison to the continuous exercise (CE) model. Sedentary, WW, and CE rats were subjected to chronic mild stress (CMS) procedure. CMS and exercise protocols continued for six weeks. Anhedonia was evaluated by sucrose preference, depressive behavior by Porsolt, cognitive functions by object recognition and passive avoidance, and anxiety levels by open field and elevated plus maze. After behavioral assessments, brain tissue myeloperoxidase (MPO) activity, malondialdehyde (MDA) levels, superoxide dismutase and catalase activities and GSH content, tumor necrosis factor‑α (TNF‑α), interleukin‑6 (IL‑6), IL‑1β, cortisol and brain‑derived neurotrophic factor levels and histological damage was assessed. CMS‑induced depression‑like outcomes with increases in anhedonia and decreases in cognitive measures that are rescued with both exercise models. The increased immobilization time in the Porsolt test was decreased with only WW. Exercise also normalized the suppression of antioxidant capacity and MPO increase induced by CMS in both exercise models. MDA levels also declined with both exercise models. Anxiety‑like behavior, cortisol levels, and histological damage scores were exacerbated with depression and improved by both exercise models. TNF‑α levels were depleted with both exercise models, and IL‑6 only with WW. WW was as protective as CE in CMS‑induced depression‑like cognitive and behavioral changes via suppressing inflammatory processes and improving antioxidant capacity.