AIMS Neuroscience最新文献

Shapes can be displayed as parts but perceived as a whole through feedforward and feedback mechanisms in the visual system, though the exact spatiotemporal relationships for this process are still unclear. Our experiments examined the integration of letter fragments that were displayed as a rapid sequence. We examined the effects of timing and masking on integration, hypothesizing that increasing the timing interval between frames would impair recognition by disrupting contour linkage. We further used different mask types, a full-field pattern mask and a smaller strip mask, to examine the effects of global vs local masking on integration. We found that varying mask types and contrast produced a greater decline in recognition than was found when persistence or mask density was manipulated. The study supports prior work on letter recognition and provides greater insight into the spatiotemporal factors that contribute to the identification of shapes.

Background: Piper guineense and honey contain antioxidative, anti-inflammatory, and antimicrobial properties that can help restore neuronal and other cell damage. To investigate the neuromodulatory roles of p. guineense and honey against lead toxicity on the hippocampus and cerebellum, impairing social behaviors and motor activities.

Methodology: Thirty Wistar rats were separated into six groups of five rats each, marked with dye. Group A served as control; B was untreated lead; C was a medium dose of the extract (50 mg/kg) and honey (1000 mg/kg); D was a high dose of the extract (80 mg/kg) and honey (1500 mg/kg); E received extract (80 mg/kg), and F received honey (1500 mg/kg). All groups received 110 mg/kg of lead orally, except the control. Social interaction, antidepressant effects, and motor activities were studied using a sociability chamber (SC), Forced Swim Test (FST), and String methods. A blood sample was used to evaluate glutathione peroxidase (GPx) and glutathione oxide transaminase (GOT), while the lipid level was estimated using cerebellar homogenate. Neuronal damage, vacuolation, necrosis, cell degeneration, and alterations in both hippocampus and cerebellum marked untreated group, with decreased GPx and GOT activities followed by impaired motor activities, social behavior, memory, and motivation. Using SCT, group B spent significantly lesser time (47.60 ± 47.60) with stranger 1 compared to A (138.20 ± 34.05), while group C spent considerably more time with stranger 1 (86.80 ± 30.32) than group B at P ≥ 0.05. The treatment increased the enzyme level and restored histoarchitecture (Figures 1-12), improving motor activities, social behavior, memory, motivation, and social affiliation (Tables 3, 4, 2, and 6). The extract and honey may be helpful as neuromodulators in lead toxicity in a dose-dependent manner.

Background: Febrile seizures (FS) frequently manifest in children below 5 years of age. Although the exact etiology is still unknown, genetic predisposition, changes in neurotransmitter levels, and serum electrolyte imbalance are some of the known risk factors. This study examined the possible association between serum magnesium levels in children with FS compared to febrile children without seizures.

Methods: A retrospective case-control study was conducted from February 2019 to January 2021, recruiting 230 age and gender-matched cases and controls (115 each). Extracted data were analyzed using SPSS using an independent student's t-test, Chi-square test, and Pearson's correlation analysis.

Results: The mean serum magnesium levels were 0.93 ± 0.129 vs 0.97 ± 0.0961; p < 0.001, between cases and controls respectively. Similarly, hypomagnesemia (<0.85 mmol/L) was detected in 26.1% and 8.7% of the cases and controls, respectively; p < 0.001. A significant negative correlation was found between serum magnesium levels and the occurrence of febrile seizures; r = [-0.169], p < 0.05.

Conclusion: Serum magnesium was significantly low in febrile children with seizures compared to those without, and hypomagnesemia was associated with the occurrence of febrile seizures. These results portray hypomagnesemia as a possible risk factor for febrile seizure, and so should be validated in future large cohort studies so that guidelines are set for proper management of these children.

Vitamin D deficiency is prevalent in adults and is associated with cognitive impairment. However, the mechanism by which adult vitamin D (AVD) deficiency affects cognitive function remains unclear. We examined spatial memory impairment in AVD-deficient BALB/c mice and its underlying mechanism by measuring spine density, long term potentiation (LTP), nitric oxide (NO), neuronal nitric oxide synthase (nNOS), and endothelial NOS (eNOS) in the hippocampus. Adult male BALB/c mice were fed a control or vitamin D deficient diet for 20 weeks. Spatial memory performance was measured using an active place avoidance (APA) task, where AVD-deficient mice had reduced latency entering the shock zone compared to controls. We characterised hippocampal spine morphology in the CA1 and dentate gyrus (DG) and made electrophysiological recordings in the hippocampus of behaviourally naïve mice to measure LTP. We next measured NO, as well as glutathione, lipid peroxidation and oxidation of protein products and quantified hippocampal immunoreactivity for nNOS and eNOS. Spine morphology analysis revealed a significant reduction in the number of mushroom spines in the CA1 dendrites but not in the DG. There was no effect of diet on LTP. However, hippocampal NO levels were depleted whereas other oxidation markers were unaltered by AVD deficiency. We also showed a reduced nNOS, but not eNOS, immunoreactivity. Finally, vitamin D supplementation for 10 weeks to AVD-deficient mice restored nNOS immunoreactivity to that seen in in control mice. Our results suggest that lower levels of NO and reduced nNOS immunostaining contribute to hippocampal-dependent spatial learning deficits in AVD-deficient mice.

Parkinson's disease (PD) is a neurodegenerative disease, however, besides the motor symptoms, such as rest tremor, hypokinesia, postural instability and rigidity, PD patients have also non-motor symptoms, namely neuropsychiatric disorders. Apart from the required motor symptoms, psychopathological symptoms are very common and include mood disorders, anxiety disorders, hallucinations, psychosis, cognitive deterioration and dementia. The underlying pathophysiological process in PD is mainly due to the loss of dopaminergic neural cells and thereby causes the shortage of nigrostriatal dopamine content in them. In addition, it may involve other neurotransmitter systems such as the noradrenergic, serotonergic, cholinergic and noradrenergic systems as well. Depression can result from any unhealthy conditions making the diagnosis a challenging task. The manifestation of depression associated with or without PD is inadequate. The co-occurrence of depression and PD often leads to the conceptual discussion on whether depressive symptoms appear before or after PD develops. This paper will discuss the conceptual mechanism of PD and depression. Keep in mind both conditions belong to two separate entities but share some similar aspects in their pathophysiology.

Exposure to vanadium has been known to lead to a progressive neurodegenerative disorder like Parkinson's disease. Naringin is a known flavonoid glycoside that is mostly seen in the flesh of grapefruit and orange and is believed to have protective effects for the treatment of neurodegenerative disorders. This study sought to investigate the role of Naringin in the treatment of vanadium-induced neurotoxicity. Vanadium (10 mg/kg BW) was injected intraperitoneally to induce motor dysfunction, followed by treatment with Naringin (30 mg/kg BW) intraperitoneally for 14 days. Oxidative stress imbalance was monitored by checking Glutathione Peroxidase (GPX) and Catalase levels. Histological and immunohistochemical alterations were observed using RBFOX3 polyclonal antibody to determine neuronal cell distribution and NLRP3 inflammasome antibody as a marker of inflammation. Exposure to vanadium induces neurotoxicity by significantly increasing the Catalase and Glutathione Peroxidase (GPX) levels. Vanadium administration also led to increased inflammatory cells and a significant reduction of the viable neuronal cells in the SNc and CPu. Treatment with Naringin showed a neuroprotective role by dependently restoring the Catalase and Glutathione Peroxidase (GPX) levels, inflammasome activation, and neuronal damage in the SNc and CPu. Naringin demonstrated anti-oxidative, and anti-inflammatory responses by inhibiting oxidative stress, and inflammation and exerts neuroprotective effects by inhibiting apoptosis following vanadium-induced neurotoxicity in adult Wistar rats.

Background: Previous studies have shown controversial results regarding the pro- or anticonvulsant effects of tramadol. Additionally, the underlying mechanism of seizure induction or alleviation by tramadol has not been fully understood. In the current study, the effects of tramadol on pentylenetetrazole (PTZ)-induced seizure and the possible involvement of the N-methyl-D-aspartate (NMDA) pathway were assessed in mice.

Methods: Male Naval Medical Research Institute (NMRI) mice were treated with intravenous infusion of PTZ in order to induce clonic seizures and determine seizure threshold. Tramadol was injected intraperitoneally (0.1-150 mg/kg) 30 minutes prior to elicitation of seizures. The possible effects of intraperitoneal injections of NMDA receptor antagonists, ketamine (0.5 mg/kg) and MK-801 (0.5 mg/kg) on the anticonvulsant property of tramadol were investigated subsequently.

Results: Tramadol (1-100 mg/kg) increased PTZ-induced seizure threshold in a dose-dependent, time-independent manner, with optimal anticonvulsant effect at a dose of 100 mg/kg. Acute administration of either ketamine (0.5 mg/kg) or MK-801 (0.5 mg/kg) potentiated the anticonvulsant effect of a subeffective dose of tramadol (0.3 mg/kg).

Conclusion: These results suggest a possible role of the NMDA pathway in the anticonvulsant effect of tramadol.

Objectives: Neuro-inflammation occurs as a sequence of brain injury and is associated with production of cytokines. Cytokines can modulate the function and survival of neurons, microglia and astrocytes. The objective of this study is to examine the effect of TNF on the neurons, microglia and astrocytes in normal brain and stab wound brain injury.

Methods: Normal BALB/c male mice (N) without any injury were subdivided into NA and NB groups. Another set mouse was subjected to stab wound brain injury (I) and were subdivided into IA and IB. NA and IA groups received intraperitoneal injections of TNF (1 µg/kg body weight/day) for nine days, whereas NB and IB groups received intraperitoneal injections of PBS. Animals were killed on 1^st, 2^nd, 3^rd, 7^th, and 9^th day. Frozen brain sections through the injury site in IA and IB or corresponding region in NA and NB groups were stained for neurodegeneration, immunostained for astrocytes, microglia and neurons. Western blotting for GFAP and ELISA for BDNF were done from the tissues collected from all groups.

Results: The number of degenerating neurons significantly decreased in TNF treated groups. There was a significant increase in the number of astrocytes and microglia in TNF treated groups compared to PBS treated groups. In addition, it was found that TNF stimulated the expression of GFAP and BDNF in NA and IA groups.

Conclusions: TNF induces astrogliosis and microgliosis in normal and injured brain and promotes the survival of cortical neurons in stab wound brain injury, may be by upregulating the BDNF level.