Nucleus accumbens shell electrical lesion attenuates seizures and gliosis in chronic temporal lobe epilepsy rats.

Objective: Temporal lobe epilepsy (TLE) is the most prevalent form of epilepsy. Prior research has indicated the involvement of the nucleus accumbens shell (NAcSh) in the process of epileptogenesis, thereby implying its potential as a therapeutic target for TLE. In the present study, we investigated the antiepileptic effect of the NAcSh electrical lesion.

Nucleus accumbens shell modulates seizure propagation in a mouse temporal lobe epilepsy model.

Temporal lobe epilepsy (TLE) is the most common form of epilepsy with focal seizures which in some conditions can develop into secondarily generalized tonic-clonic seizures by the propagation of epileptic activities in the temporal lobe to other brain areas. The nucleus accumbens (NAc) has been suggested as a treatment target for TLE as accumulating evidence indicates that the NAc, especially its shell, participates in the process of epileptic seizures of patients and animal models with TLE. The majority of neurons in the NAc are GABAergic medium spiny neurons (MSNs) expressing dopamine receptor D1 (D1R) or dopamine receptor D2 (D2R).

TRESK channel contributes to depolarization-induced shunting inhibition and modulates epileptic seizures.

Glutamatergic and GABAergic synaptic transmission controls excitation and inhibition of postsynaptic neurons, whereas activity of ion channels modulates neuronal intrinsic excitability. However, it is unclear how excessive neuronal excitation affects intrinsic inhibition to regain homeostatic stability under physiological or pathophysiological conditions. Here, we report that a seizure-like sustained depolarization can induce short-term inhibition of hippocampal CA3 neurons via a mechanism of membrane shunting.

Emerging Role of Microglia-Mediated Neuroinflammation in Epilepsy after Subarachnoid Hemorrhage.

Epilepsy is a common and serious complication of subarachnoid hemorrhage (SAH), giving rise to increased morbidity and mortality. It's difficult to identify patients at high risk of epilepsy and the application of anti-epileptic drugs (AEDs) following SAH is a controversial topic. Therefore, it's pressingly needed to gain a better understanding of the risk factors, underlying mechanisms and the optimization of therapeutic strategies for epilepsy after SAH.

Primary central nervous system T-cell lymphoma: An analysis from the surveillance, epidemiology, and end results program.

Background: Primary central nervous system T-cell lymphoma (PCNSTCL) is a rare neoplasm with few data regarding its common features and survival characteristics.

Objective: To explore the Surveillance, Epidemiology, and End Results 18 (SEER 18) database to determine the epidemiology of PCNSTCL.

Methods: The SEER 18 registry database was queried to identify patients diagnosed with PCNSTCL from 1973 to 2014 and extract their information.

Nucleus accumbens shell: A potential target for drug-resistant epilepsy with neuropsychiatric disorders.

The nucleus accumbens (NAc) is an important component of the ventral striatum, involving motivational and emotional processes, limbic-motor interfaces. Recently, experimental and clinical data have shown that NAc, particularly NAc shell (NAcs), participates in ictogenesis and epileptogensis in drug-resistant epilepsy (DRE). Therefore, we summarize the existing literature on NAcs and potential role in epilepsy, from the bench to the clinic.

Silencing of microRNA-708 promotes cell growth and epithelial-to-mesenchymal transition by activating the SPHK2/AKT/β-catenin pathway in glioma.

Aberrant microRNA-708 (miR-708) expression is frequently reported in cancer studies; however, its role in glioma has not been examined in detail. We investigated miR-708 function in glioma and revealed that miR-708 expression was significantly down-regulated in glioma tissues and cell lines. Restoration of miR-708 inhibited glioma cell growth and invasion both in vitro and in vivo.

Effect of accumbens nucleus shell lesioning on bitemporal lobe epilepsy in rat model.

Introduction: To explore the effect of accumbens nucleus shell (ACbSh) lesioning on bitemporal lobe epilepsy.

Material And Methods: Adult Wistar rats (male) were enrolled and randomly assigned into the control group and epilepsy groups with multiple time-points. Lithium-pilocarpine was used to establish the rat epilepsy model, while the control group received an equal amount of saline.

Connectivity-based parcellation of the nucleus accumbens into core and shell portions for stereotactic target localization and alterations in each NAc subdivision in mTLE patients.

The nucleus accumbens (NAc), an important target of deep brain stimulation for some neuropsychiatric disorders, is thought to be involved in epileptogenesis, especially the shell portion. However, little is known about the exact parcellation within the NAc, and its structural abnormalities or connections alterations of each NAc subdivision in temporal lobe epilepsy (TLE) patients. Here, we used diffusion probabilistic tractography to subdivide the NAc into core and shell portions in individual TLE patients to guide stereotactic localization of NAc shell.

Blocking mPTP on Neural Stem Cells and Activating the Nicotinic Acetylcholine Receptor α7 Subunit on Microglia Attenuate Aβ-Induced Neurotoxicity on Neural Stem Cells.

β-Amyloid (Aβ) can stimulate microglia to release a variety of proinflammatory cytokines and induce neurotoxicity. Nicotine has been reported to inhibit TNF-α, IL-1, and ROS production in microglia. Mitochondrial permeability transition pore (mPTP) plays an important role in neurotoxicity as well.

Huperzine A protects neural stem cells against Aβ-induced apoptosis in a neural stem cells and microglia co-culture system.

Objectives: This study aims to explore whether Huperzine A (HupA) could protect neural stem cells against amyloid beta-peptide Aβ induced apoptosis in a neural stem cells (NSCs) and microglia co-culture system.

Methods: Rat NSCs and microglial cells were isolated, cultured and identified with immunofluorescence Assays (IFA). Co-culture systems of NSCs and microglial cells were employed using Transwell Permeable Supports.

Nicotine contributes to the neural stem cells fate against toxicity of microglial-derived factors induced by Aβ via the Wnt/β-catenin pathway.

Recent studies have demonstrated that the molecules secreted from microglias play important roles in the cell fate determination of neural stem cells (NSCs), and nicotinic acetylcholine receptor agonist treatment could reduce neuroinflammation in some neurodegenerative disease models, such as Alzheimer's disease (AD). However, it is not clear how nicotine plays a neuroprotective role in inflammation-mediated central nervous diseases, and its possible mechanisms in the process remain largely elusive. The aim of this study is to improve the survival microenvironment of NSCs co-cultured with microglias in vitro by weakening inflammation that mediated by accumulation of β-amyloid peptide (Aβ).

Stereotactic neurosurgical technique and electrophysiological study in ablating the ventromedial shell of the nucleus accumbens.

Objective: To describe in as much detail as possible the method for ablating the ventromedial shell of the nucleus accumbens (NAc) and investigate the efficacy and safety of the ablation treatment.

Methods: Sixty-five patients with drug addictions received operations within the time frame from 2004 to 2009. The ablation targets were located in the bilateral medial posterior inferior shell of the NAc.

Identification of α7 nicotinic acetylcholine receptor on hippocampal astrocytes cultured in vitro and its role on inflammatory mediator secretion.

The present study found expressions of α7 nicotinic acetylcholine receptor on hippocampal slices and hippocampal astrocytes using double immunofluorescence stainings. Expression of glial fibrillary acidic protein in the cultured hippocampal slices and hippocampal astrocytes significantly increased, and levels of macrophage inflammatory protein 1α, RANTES, interleukin-1β, interleukin-6, and tumor necrosis factor-α increased in the supernatant of cultured astrocytes following exposure to 200 nM amyloid β protein 1-42. Preconditioning of 10 μM nicotine, a nicotinic acetylcholine receptor agonist, could attenuate the influence of amyloid β protein 1-42 in inflammatory mediator secretion of cultured astrocytes.

[Effect of imatinib at different concentrations on rat C6 glioma cell apoptosis and cell cycle].

Objective: To investigate the effect of imatinib on rat C6 glioma cell apoptosis and cell cycle.

Methods: MTT assay was used to determine the OD value of C6 glioma cells following treatment with imatinib at different concentrations (0.156, 10 and 15 micromo/L) for 24, 48 and 72 h.

[Proton magnetic resonance spectroscopic imaging of the hippocampus in schizophrenia patients before and after surgery].

Objective: To explore the features of proton magnetic resonance spectroscopy (1H-MRS) of the hippocampus in schizophrenia patients before and after stereotactic neurosurgery.

Methods: 1H-MRS was performed to determine NAA/Cr and CHO/Cr ratios on the bilateral hippocampal regions before and after stereotactic neurosurgery in 20 schizophrenia patients, with 20 healthy individuals as the controls.

Results: The NAA/Cr ratio in the hippocampal regions was significantly lower and the CHO/Cr ratio significantly higher in schizophrenia patients before the surgery than in the healthy controls (P<0.

[Histomorphology of angiogenesis patterns in different areas of human astrocytomas].

Objective: To study angiogenesis patterns in the edematous area and the center of human astrocytomas by histological observation, and to reveal histological basis of vasculogenic mimicry.

Method: Tissue samples were drawn from the tumor center and the edematous area in 51 patients with human astrocytomas during operation MR and were examined by CD34 endothelial marker periodic acid-Schiff (PAS) dual staining.

Results: Vessels or capillaries stained by both PAS and CD34 were found in edematous areas of human astrocytomas.

Association of epileptiform activity with neuronal death in the CA3 subfield of the hippocampus following focally evoked limbic seizures.

OBJECTIVE: To investigate the relationnship between epileptiform activity and cell death in the CA3 subfield of hippocampus following focally evoked limbic seizures through a quantitative study. METHODS: Wistar rats used in this study received intra-amygdaloid injection of kainic acid to induce type epileptiform activity of different duration with continuous electroencephalographic (EEG) monitoring. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) was used to detect apoptotic cells.

Radiosurgical treatment of intractable epilepsy with low radiation dose.

Objective: To localize the epileptic foci with positron emission tomography (PET), and study the principles of target definition and method to determine the optimal range of exposure in radiosurgery for intractable epilepsy.

Methods: This study included 176 patients with intractable epilepsy, who received linear accelerator radiosurgery after (18)F-FDG PET for epileptic foci localization. The patients were divided according to different peripheral doses used in the treatment into Group A in which radiation dose of 9 to 11 Gy was used, Group B with 11 to 13 Gy and Group C with exposure to over 13 Gy.

[Ultrastructural features of cultured rat cortical astrocytes with stretch-induced injury].

Objective: To investigate the changes of ultrastructural features of cultured rat cortical astrocytes after stretch-induced injury.

Methods: Rat cortical astrocytes isolated from 1- to 2-day-old rats were cultured till confluency, and then plated in tissue culture wells with flexible silastic bottom after purification. A computer-controlled device was used to produce stretch-induced injury in the astrocytes with the imposed pressure of 50, 150, and 250 kPa respectively, followed by observation of the ultrastructural changes in the astrocytes with light and electron microscopy.