Publications by authors named "Heng-Sheng Chen"

Objectives: To study the effect of gap junction blockers, quinine (QUIN) and carbenoxolone (CBX), on hippocampal ripple energy expression in rats with status epilepticus (SE).

Methods: A total of 24 rats were randomly divided into four groups: model, QUIN, valproic acid (VPA), and CBX (=6 each). A rat model of SE induced by lithium-pilocarpine (PILO) was prepared.

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Objective: To study the effect of advanced maternal age (AMA) on the development of hippocampal neural stem cells in offspring rats.

Methods: Ten 3-month-old and ten 12-month-old female Sprague-Dawley rats were housed individually with 3-month-old male rats (1:1, n=20), whose offspring rats were assigned to a control group and an AMA group. A total of 40 rats were randomly selected from each group.

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BACKGROUND Subclinical epileptiform discharges (SEDs) are defined as epileptiform electroencephalographic (EEG) discharges without clinical signs of seizure in patients. The subthreshold convulsant discharge (SCD) is a frequently used model for SEDs. This study aimed to investigate the effect of levetiracetam (LEV), an anti-convulsant drug, on cognitive impairment of SCD model rats and to assess the associated mechanisms.

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Seizure-induced brain damage is age-dependent, as evidenced by the different alterations of neural physiopathology in developing and mature brains. However, little is known about the age-dependent characteristics of myelinated fiber injury induced by seizures. Considering the critical functions of oligodendrocyte progenitor cells (OPCs) in myelination and Lingo-1 signaling in regulating OPCs' differentiation, the present study aimed to explore the effects of Lingo-1 on myelin and axon in immature and adult rats after status convulsion (SC) induced by lithium-pilocarpine, and the differences between immature and adult brains.

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Objective: To analyze spectral and spatial signatures of high frequency oscillations (HFOs), which include ripples and fast ripples (FRs, >200 Hz) by quantitatively assessing average and peak spectral power in a rat model of different stages of epileptogenesis.

Methods: The lithium-pilocarpine model of temporal lobe epilepsy was used. The acute phase of epilepsy was assessed by recording intracranial electroencephalography (EEG) activity for 1 day after status epilepticus (SE).

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Dibutyl-phthalate (DBP) is a ubiquitous environmental contaminant. However, its neurotoxic effects on neonatal, immature or mature brains remain unclear. Here, we aimed to investigate the neurotoxicity of perinatal exposure of DBP on rodent offspring animals.

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Objective: To study the level of brain-derived neurotrophic factor (BDNF) in the microenvironment of the neuron-astrocyte co-culture system by Mg2+-free-induced seizure-like discharge and analyze the source of BDNF.

Methods: Hippocampal neurons (N) of fetal rats and astrocytes (AST) of neonatal rats were purified and divided into four groups, included control N (Con N) group, Mg2+-free treated N (Mg2+-free N) group, control N+AST co-culture (Con N+AST) group and Mg2+-free treated N+AST co-culture (Mg2+-free N+AST) group. The Mg2+-free treated groups were exposed to Mg2+-free media for 3 hrs to induce a repeated spontaneous seizure-like discharge.

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Objective: To develop a series of experimental animal models of myoclonus with different origins consistent with myoclonus seizure in clinic setting.

Methods: GABA(A) antagonist SR95531 was microinjected into the primary motor cortex (PMC), corpus striatum, nucleus reticular of the thalamus (NRT) to induce myoclonus (EMG burst of myoclonus View Article and Find Full Text PDF

Sodium valproate (VPA) is currently one of the major antiepileptic drugs and has been reported to impair the induction of long-term potentiation (LTP) in rat hippocampal. However, there are discrepancies when used at therapeutic dose and few researches to study the effects of VPA on the maintenance of LTP. Here we investigated the effects of VPA at therapeutic concentration on two LTP phases: induction and maintenance in CA1 region.

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Objective: To study the changes in electroencephalograph (EEG) and somatosensory evoked potential (SEP) and their relationship with neuron apoptosis in rat after ischemic insult to the brain.

Methods: Thirty-five SD rats were randomly divided into normal, sham operated and 3, 12, 24, 48, 72 hours after ischemia/reperfusion (I/R) groups with 5 rats in each group. The ischemia of brain was produced by clamping 4 vessels to the brain for various periods of time.

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