جستجوی مقالات مرتبط با کلیدواژه « قشر مغز » در نشریات گروه « پزشکی »

Ketamine is one of the most common drugs that weaken the central nervous system and alertness, and it is essential to know its side effects.

The purpose of this study is to investigate the effects of short-term and long-term anesthesia of ketamine on the histopathological changes of the cerebral cortex in rat infants.

This study was conducted on 15 female rats (3 groups of 5 including the control group, the long-term anesthesia group with ketamine, and the short-term and repeated anesthesia group (with ketamine). Then the histopathological changes of the cerebral cortex were analyzed by IHC immunohistochemistry method. SPSS software was used to compare the data.

The findings of our study showed that no changes were observed in the brain tissue and different layers in the samples of the control group, and the order and coherence of the brain tissue was reported to be completely clear and normal. There is no significant change in the short-term and long-term dose groups of ketamine, compared to the control group, and only the number of microglia cells was lower than the control group.

Ketamine reduces the number of microglia cells both in the short term and in the long term, and investigating the cause requires biochemical studies, free radicals and other effective factors that play a role in cell apoptosis. Although memory and learning were not examined in our study, the findings of our study did not show drastic changes in the tissue. However, a more detailed examination of the changes in the biochemical and behavioral changes of the mice needs a more detailed examination in subsequent studies to address all aspects of the effect of ketamine on the brain.

Functional magnetic resonance imaging (fMRI) has been widely used for pre-neurosurgical planning and may eventually become a routine pre- surgical imaging modality. The validity of fMRI for the clinical application depends on various factors such as proper task selection, correct statistical analysis, and threshold setting with appropriate patient cooperation. To compare the potential of five functional magnetic resonance imaging (fMRI) language paradigms in activating language areas in Persian-speaking volunteers in order to optimize these tasks for clinically useful protocol.

16 healthy right-handed Persian-speaking volunteers were studied. Each individual performed five tasks during the fMRI scan: word generation (WG), object naming (ON), word reading (WR), word production (WP), and reverse word reading (RWR). In the current study's first phase, each task's ability to activate classical language areas was assessed using group analysis. In addition, the lateralization index (LI) for each subject-task was calculated and compared. In the second phase, the optimized protocol was assessed on 40 patients with different types of brain mass lesions or hippocampal sclerosis to assess the role of appropriate patient selection for achieving a reliable fMRI result.

We found that WP, RWR, and WG robustly activated language-related areas in the dominant hemisphere. ON and WR failed to sufficiently delineate these activation areas. The highest activation intensities in the frontal lobe (including Broca's area) were seen with WP, whereas RWR showed the highest LI among all examined tasks. In the patient population, we found that accurate and reproducible fMRI strongly depends on the patient’s cooperation. In present study, we observed that a pre-test mock fMRI session held by a radiologist might help to predict which patients are more or less suitable candidates for fMRI.

Our results demonstrated that the Persian version of WG and newly presented WP and RWR tasks could be reliably used for the localization of language-related areas in Persian speakers. This type of language evaluation also can be used in the pre-surgical planning of neurosurgical procedures in the Persian population. We recommend the application of WP and RWR in routine clinical practice to avoid significant morbidities after brain lesion surgery.

Oxidative stress plays an essential role in the pathogenesis of seizures. In this study, we investigated the effect of ethyl acetate fraction of Tanacetum parthenium against oxidative brain damage in a pentylenetetrazole(PTZ)-induced seizure model in mice.

 In this experimental study, mice were divided into 6 groups: control, PTZ, and 4 other groups that, besides PTZ, received 25, 50, 100, and 200 mg/kg of the fraction. PTZ (100 mg/kg) and a fraction (30 min before PTZ) were administered intraperitoneally for 3 weeks. Delay in the onset of the minimal clonic seizure (MCS), generalized tonic-clonic seizure (GTCS), and the level of oxidative stress indexes in cortical and hippocampal tissues were measured.

 Pretreatment with fraction resulted in postponing the onset seizures in the Fraction+PTZ groups compared to the PTZ group (P<0.05, P<0.01, and P<0.001). In addition, all doses of ethyl acetate fraction decreased the concentration of malondialdehyde (MDA) and increased the level of tom thiol groups and the activity of superoxide dismutase and catalase enzymes in the brain tissues compared to the PTZ group. 

Ethyl acetate fraction of Tanacetum parthenium attenuated PTZ-stimulated seizures through improving brain tissue oxidative stress.

Neuropathy is the most common neurological complication of diabetes which affects the central nervous systems, especially the brain. The aim of this study was to investigate the effects of resistance training After Transplantation of stem cells on rate of TNF-α and NF-κB in cerebral Cortex of STZ-induced Diabetic Rats.

In this experimental study, 48 male wistar rats, 9 weeks old, weighing 220-240 g were randomly divided into six equal groups: control, sham, diabetes, diabetes + exercise,  diabetes + stem cells, diabetes + exercise + stem cells.The exercise groups, practiced treadmill resistance training for 6 weeks. In the stem cell receiver group, 1/5*106 number of stem cells were injected into diabetic rats. Diabetes was induced by injection of streptozotocin (60 mg/kg) intraperitoneally. All statistical analyzes were performed by SPSS 22 software.

Data showed that the TNF-α (p>0.01) and NF-κB (p<0.001) levels was significant difference between the six groups. It was observed that in the exercise + stem cells group, TNF-α level was significantly lower than that of the diabetes group (p=0.05). There was a statistically significant decrease in NF-κB level in exercise and exercise + stem cells groups compared to the diabetes group (p<0.001).

Injection of adipose-derived stem cells along with exercise training can be a protective and therapeutic strategy to reduce cortical inflammatory markers and the effects of diabetes on the central nervous system.

Organophosphorus (OP) compounds are highly toxic and are widely used as an insecticide in agriculture and domestic consumptions. Acetylcholinesterase (AChE) inhibition is the primary mechanism of acute in vivo toxicity of organophosphorus compounds. In the present study we evaluated inhibition and recovery of the plasma, cerebral cortex and hippocampus AChE activity and their correlations following systemic administration of three doses of paraoxon in three different time points in rat. Eighty four male Wistar rats (200-270 g) were used in this study and divided into groups of seven. Animals were given a single intraperitoneal injection of corn oil (vehicle group) or one of the doses of paraoxon (0.1, 0.3, or 0.7 mg/kg) and AChE activity in the plasma, cerebral cortex, and hippocampus was measured at 30 min, 4 h, and 18 h after exposure using the modified method of Ellman. Plasma and brain AChE activity was inhibited in a dose dependent manner by paraoxon. After 18 h, plasma AChE activity was recovered 32, and 42 percent (p<0.001) in animals exposed to 0.3, and 0.7 mg/kg paraoxon, respectively. 18 h after 0.7 mg/kg paraoxon, AChE activity was significantly recovered (p<0.001) in both brain areas (about 20%). Plasma AChE activity correlated significantly with both cerebral cortex and hippocampus AChE activity in rats treated with paraoxon (0.3 and 0.7 mg/kg). In both brain areas, paraoxon (only 0.7 mg/kg) inhibited AChE activity to induce seizure activity after 30 min. Inhibition of the plasma AChE activity can use as a marker of exposure only in severe toxicities with OP compounds.

Paraoxon (the neurotoxic metabolite of organophosphorus (OP) insecticide, parathion) exerts acute toxicity by inhibition of acetylcholinesterase (AChE), leading to the accumulation of acetylcholine in cholinergic synapses and hence overstimulation of the cholinergic system. Since, reports on changes in the level of γ- amino butyric acid (GABA) during OP-induced convulsion have been controversial, in present study we used cortical and hippocampal synaptosomes from rats after paraoxon poisoning to detect changes in GABA uptake. Male Wistar rats (200-270 g) were used in this study. Animals were given a single intraperitoneal injection of corn oil (vehicle group) or one of doses of paraoxon (0.1, 0.3, or 0.7 mg/kg) and [3H]GABA uptake by cerebral cortex and hippocampal synaptosomes was measured at 30 min, 4 h, and 18 h after the exposure (n= 7 rats/group). Type of transporter involved in the uptake was also determined using β-alnine, and L-diaminobutyric acid (L-DABA), a glial and a neuronal GABA uptake inhibitor, respectively. GABA uptake was significantly (p<0.001) reduced by both cerebral cortex (18-32%) and hippocampal (16-21%) synaptosomes compared with their respective control groups at all three time points after administering 0.7 of paraoxon (convulsive dose). β-alnine had no inhibitory effect on the uptake, whereas L-DABA abolished most of the transporter mediated GABA uptake. Since GABA uptake did not change in other two paraoxon treated groups, it may be indicating that decrement of GABA uptake is convulsion-related. The decrease in GABA uptake, presumably due to a change in the function of GABA transporters, may represent a compensatory response modulating neuronal overexcitation. Most of synaptosomal GABA uptake was blocked by L-DABA, indicating that the uptake was primarily by a neuronal GABA transporter (GAT), GAT-1.

Many factors can have a neuroprotective role after brain damage. The neuroprotective Effect of melatonin as a highly potent antioxidant and a free radical scavenger is well known. The purpose of this study was to investigate the effect of such melatonin on mice sensorimotorcortex after cold injury.

In order to test such this objective, melatonin was injected intraperitoneally in 1,5,50 and 100 mg/kg to the mice (prepared by cortical cold injury induced brain lesion at the parietal lobe) within three intervals (0.5 h before injury, 12 h and 48 h after injury). Brains were removed 72 hours after injury. Appropriate brain sections were stained with cresyl fast violet for histological assessment of cerebral cortex structures by using light microscope (LM).

After cell count of alive cells in the cerebral cortex the results showed that the cold injury caused significantly reduction in living cells. Melatonin administration in the experimental groups increased such living cells in compare to model group. Alive cells in cerebral cortex of animals which received melatonin at lower doses (1 and 5 mg/kg) were lower than the control group, melatonin at optimum dose (50 mg/kg) did not show any significant change in the number of alive cells in comparing with the control group (P>0/05). The highest dose (100mg/kg) was toxic.

Melatonin with optimum dose can reduce cerebral cortex damage due to cold injury in mouse model and overcome cell damages fallowing injury.