ObjectiveThe research goal: to study the diagnostic value of T2-flair sequence of magnetic resonance imaging (MRI) in hippocampal sclerosis. MethodsThe clinical data of 135 patients with epilepsy caused by hippocampal sclerosis in the Epilepsy Center of Tianshui Third People's Hospital from March 2019 to December 2020 were analyzed retrospectively, studying the correlation between the changes of hippocampal sclerosis signal and the frequency of epileptic seizures in MRI T2-flair sequence multi axial scanning. ResultsThere were 109 cases of simple hippocampal sclerosis and 26 cases of hippocampal sclerosis with other lesions, including 8 cases of cavernous hemangioma, 9 cases of traumatic or infectious malacia, 2 cases of focal cortical dysplasia, 1 case of cerebral fissure malformation, 1 case of giant gyrus and 5 cases of perinatal brain injury. MRI features of hippocampal sclerosis were as follows: ① hippocampal volume increased slightly, structure blurred, and T2-flair showed slightly increased hippocampal signal in 15 cases, accounting for 11.11%; ② The hippocampal formation was fuzzy, T2-flair was punctate hyperintense, and the volume did not change in 17 cases (12.59%); ③ Hippocampal pyknosis into small lumps, T2-flair sequence showed high signal in 103 cases, accounting for 76.30%. Statistics showed that there was a correlation between hippocampal sclerosis signal and seizure frequency (χ2=94.94, P<0.05). The higher the hippocampal sclerosis signal, the more the seizure frequency. ConclusionMRI T2-flair sequence multi axial scanning can improve the diagnostic accuracy of hippocampal sclerosis. As the change of hippocampal sclerosis signal becomes more obvious, the trend of seizure frequency increases.
ObjectiveTo investigate the effect of dexamethasone on mammalian target of rapamycin (mTOR) expression of astrocytes in hippocampus of rats with sepsis associated encephalopathy (SAE). MethodsTotally, 90 cases of 30-day-old male Wistar rats were randomly divided into sham-operation group (n=10) and cecal ligation and puncture (CLP) group (n=80). Models of rats with sepsis were established by CLP. At 12 hours after CLP, if rats appeared lower neurobehavioral scores, abnormal electroencephalogram (EEG) and somatosensory evoked potential (SEP), they were diagnosed with SAE. And then, they were randomly divided into non-treated group and dexamethasone group. Rats in the dexamethasone group were injected with dexamethasone (1 mg/kg) via tail vein every other day for a total of 3 times. The same dose of saline was used in the non-treated group. The neurobehavioral score was measured, SEP and EEG were examined in the age of 40 days, and then the rats were killed and the hippocampus was taken. Expressions of mTOR protein were measured by Western blot. The glial fibrillary acidic protein (GFAP) and mTOR were detected by immunofluorescence assay, and the number of positive cells was calculated by image analysis system software. ResultsSix of 80 CLP rats died in 12 hours after operation, and 28 of 74 rats were diagnosed as SAE because they appeared lower neurobehavioral scores, abnormal EEG and SEP at 12 hours after CLP. The incidence of SAE was 37.84% (28/74). In the age of 40 days, compared with non-treated group, neurobehavioral score of rats in the dexamethasone group was low, the amount of alpha waves in EEG reduced, delta waves increased, the amplitude of P1 waves in SEP was decreased, and the latencies of P1 and N1 waves were prolonged (P＜0.05). GFAP immunofluorescence staining showed astrocytic body and processes were small in the sham operation group. However, astrocytes in the non-treated group had large body and hypertrophic processes, and compared with the sham operation group, the number of these cells increased significantly (P＜0.05). Astrocytic body and processes were small in the dexamethasone group compared with the non-treated group, and the number of cells also decreased (P＜0.05). The mTOR positive astrocytes in the non-treated group were more than those in the sham operation group (P＜0.05). But mTOR positive astrocytes in the dexamethasone group were fewer than those in the non-treated group (P＜0.05). ConclusionsAstrocytes are activated in the hippocampus of rats with SAE. They show features of reactive hyperplasia, and the expression of mTOR is up-regulated, while dexamethasone can inhibit effects on these.
The transmission and interaction of neural information between the hippocampus and the prefrontal cortex play an important role in learning and memory. However, the specific effects of learning memory-related tasks on the connectivity characteristics between these two brain regions remain inadequately understood. This study employed in vivo microelectrode recording to obtain local field potentials (LFPs) from the ventral hippocampus (vHPC) and medial prefrontal cortex (mPFC) in eight rats during the performance of a T-maze task, assessed both before and after task learning. Additionally, dynamic causal modeling (DCM) was utilized to analyze alterations in causal connectivity between the vHPC and the mPFC during memory task execution pre- and post-learning. Results indicated the presence of forward connections from vHPC to mPFC and backward connections from mPFC to vHPC during the T-maze task. Moreover, the forward connection between these brain regions was slightly enhanced after task learning, whereas the backward connection was diminished. These changes in connectivity corresponded with the observed trends when the rats correctly performed the T-maze task. In conclusion, this study may facilitate future investigations into the underlying mechanisms of learning and memory from the perspective of connectivity characteristics between distinct brain regions.
Epilepsy is a heterogeneous disease with a very complex etiological mechanism, characterized by recurrent and unpredictable abnormal neuronal discharge. Epilepsy patients mainly rely on oral antiseizure medication (ASMs) the for treatment and control of disease progression. However, about 30% patients are resistance to ASMs, leading to the inability to alleviate and cure seizures, which gradually evolve into refractory epilepsy. The most common type of intractable epilepsy is temporal lobe epilepsy. Therefore, in-depth exploration of the causes and molecular mechanisms of seizures is the key to find new methods for treating refractory epilepsy. Mitochondria are important organelles within cells, providing abundant energy to neurons and continuously driving their activity. Neurons rely on mitochondria for complex neurotransmitter transmission, synaptic plasticity processes, and the establishment of membrane excitability. The process by which the autophagy system degrades and metabolizes damaged mitochondria through lysosomes is called mitophagy. Mitophagy is a specific autophagic pathway that maintains cellular structure and function. Mitochondrial dysfunction can produce harmful reactive oxygen species, damage cell proteins and DNA, or trigger programmed cell death. Mitophagy helps maintain mitochondrial quality control and quantity regulation in various cell types, and is closely related to the occurrence and development of epilepsy. The imbalance of mitophagy regulation is one of the causes of abnormal neuronal discharge and epileptic seizures. Understanding its related mechanisms is crucial for the treatment and control of the progression of epilepsy in patients.
ObjectiveTo explore the clinical features and surgical treatment effects of the temporal lobe epilepsy with hippocampal sclerosis.MethodsForty two patients diagnosed as temporal lobe epilepsy with hippocampal sclerosis and underwent protemporal lobectomy in Wuhan Brain Hospital from Jan. 2012 to Dec. 2018 were collected, which included 30 males and 12 females, with the age between 9 to 60 years. Their disease duration ranged from 3 to 10 years. The clinical manifestations showed complex partial seizure in 18 cases, partial-secondary –generalized seizure in 4 cases, and generalized tonic-clonic seizure in 20 cases. Based on their results of clinical manifestations, combined with MRI and VEEG results, all the patients underwent anterior temporal lobectomy (including the most parts of the hippocampus and amydala).ResultsThe postoperative pathology confirmed the diagnosis of hippocampal sclerosis. The follow-up of more than 1 year showed seizure-free in 38 cases, and significant improvement in 4 cases.ConclusionsTo the patients of temporal lobe epilepsy with hippocampal sclerosis, anterior temporal lobectomy should be performed (including the most parts of the hippocampus and amydala) if the VEEG monitoring results show that there are epileptic discharges in the ipsilateral temporal lobe. And the postoperative curative result is satisfactory.
Febrile seizures (FS) are one of the most common neurological disorders in pediatrics, commonly seen in children from three months to five years of age. Most children with FS have a good prognosis, but some febrile convulsions progress to refractory epilepsy (RE). Epilepsy is a common chronic neurological disorder , and refractory epilepsy accounts for approximately one-third of epilepsies. The etiology of refractory epilepsy is currently complex and diverse, and its mechanisms are not fully understood. There are many pathophysiological changes that occur after febrile convulsions, such as inflammatory responses, changes in the blood-brain barrier, and oxidative stress, which can subsequently potentially lead to refractory epilepsy, and inflammation is always in tandem with all physiological changes as the main response. This article focuses on the pathogenesis of refractory epilepsy resulting from post-febrile convulsions.
Alzheimer’s disease (AD) is a chronic central neurodegenerative disease. The pathological features of AD are the extracellular deposition of senile plaques formed by amyloid-β oligomers (AβOs) and the intracellular accumulation of neurofibrillary tangles formed by hyperphosphorylated tau protein. In this paper, an in vitro pathological model of AD based on neuronal network chip and its real-time dynamic analysis were presented. The hippocampal neuronal network was cultured on the microelectrode array (MEA) chip and induced by AβOs as an AD model in vitro to simultaneously record two firing patterns from the interneurons and pyramidal neurons. The spatial firing patterns mapping and cross-correlation between channels were performed to validate the degeneration of neuronal network connectivity. This biosensor enabled the detection of the AβOs toxicity responses, and the identification of connectivity and interactions between neuronal networks, which can be a novel technique in the research of AD pathological model in vitro.
ObjectiveTo observe the dynamic changes of neuroglobin (NGB) expression in hippocampus after status epilepticus(SE) in rats, and to explore the role of NGB in epileptic seizures.Methods40 healthy male Sprague Dawley rats were randomly divided into two group according to random number table method:control group (n=5) and epilepsy model group(n=35).Epilepsy model group according to observation time was divided into:0h, 1h, 3h, 12h, 24h, 10d and 30d.Intraperitoneal injection Lithium-pilocarpine (20 mg/kg~127 mg/kg, Li-PC) to establish the rat model of SE.Observe the behavioral changes in rats with epilepsy.Nissl staining was used to detect the neuronal damage in hippocampus. Streptavidin-biotin-peroxidase complex immunohistochemical method was used to detect the expression level of NGB in hippocampus;ResultsAfter SE, the neurons in hippocampus were severely damaged with the progress of epileptic seizures, the number of surviving neurons in CA1, CA3 regions showed a near linear decline.Among them, the number of surviving neurons in (12h, 24h, 10d, 30d)CA1, (0h, 12h, 24h, 10d, 30d)CA3 and(12h, 24h, 10d, 30d) DG area were significantly lower than that of the control group (P < 0.05).The expression level of NGB in CA1, CA3 and DG region of hippocampus were increased after SE, and both of CA1 and DG were reached peak in 24h after SE, but was still higher than the control group.And the CA3 area showed a continue rising trend.Among them, CA1(24h, 10d, 30d), CA3(24h, 10d, 30d) and DG(12h, 24h, 10d, 30d) were higher than that of control group significantly (P < 0.05).In addition, it was found that there was a positive correlation between the number of surviving neurons in CA3 area and the expression level of NGB (R=0.306, P=0.011).ConclusionUp-regulation of NGB expression in hippocampus after status epilepticus, and was positively correlated with the number of neurons in the CA3 area, suggesting that up regulation of NGB expression may be a compensatory protective mechanism of ischemic injury induced by seizures, and participate in the protection of epilepsy related neuronal damage.
It has been found that in biological studies, the simple linear superposition mathematical model cannot be used to express the feature mapping relationship from multiple activated grid cells' grid fields to a single place cell's place field output in the hippocampus of the cerebral cortex of rodents. To solve this problem, people introduced the Gauss distribution activation function into the area. We in this paper use the localization properties of the function to deal with the linear superposition output of grid cells' input and the connection weights between grid cells and place cells, which filters out the low activation rate place fields. We then obtained a single place cell field which is consistent with biological studies. Compared to the existing competitive learning algorithm place cell model, independent component analysis method place cell model, Bayesian positon reconstruction method place cell model, our experimental results showed that the model on the neurophysiological basis can not only express the feature mapping relationship between multiple activated grid cells grid fields and a single place cell's place field output in the hippocampus of the cerebral cortex of rodents, but also make the algorithm simpler, the required grid cells input less and the accuracy rate of the output of a single place field higher.