Browsing by Author "Xu, Fenglian"

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    Gastrodin Suppresses the Amyloid β-Induced Increase of Spontaneous Discharge in the Entorhinal Cortex of Rats
    (2014-10-30) Chen, Peng-zhi; Jiang, Hui-hui; Wen, Bo; Ren, Shuan-cheng; Chen, Yang; Ji, Wei-gang; Hu, Bo; Zhang, Jun; Xu, Fenglian; Zhu, Zhi-ru
    Accumulated soluble amyloid beta- (Aβ-) induced aberrant neuronal network activity may directly contribute to cognitive deficits, which are the most outstanding characteristics of Alzheimer’s disease (AD). The entorhinal cortex (EC) is one of the earliest affected brain regions in AD. Impairments of EC neurons are responsible for the cognitive deficits in AD. However, little effort has been made to investigate the effects of soluble Aβ on the discharge properties of EC neurons in vivo. The present study was designed to examine the effects of soluble Aβ1−42 on the discharge properties of EC neurons, using in vivo extracellular single unit recordings. The protective effects of gastrodin (GAS) were also investigated against Aβ1−42-induced alterations in EC neuronal activities. The results showed that the spontaneous discharge of EC neurons was increased by local application of soluble Aβ1−42 and that GAS can effectively reverse Aβ1−42-induced facilitation of spontaneous discharge in a concentration-dependent manner. Moreover, whole-cell patch clamp results indicated that the protective function of GAS on abnormal hyperexcitability may be partially mediated by its inhibitory action on Aβ1−42-elicited inward currents in EC neurons. Our study suggested that GAS may provide neuroprotective effects on Aβ1−42-induced hyperactivity in EC neurons of rats.
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    Mercury-induced toxicity of rat cortical neurons is mediated through N-Methyl-D-Aspartate receptors
    (BioMed Central Ltd., 2012-09-14) Xu, Fenglian; Farkas, Svetlana; Kortbeek, Simone; Chen, Lina; Zhang, Fangxiong; Zamponi, Gerald W.; Syed, Naweed I.
    Mercury is a well-known neurotoxin implicated in a wide range of neurological or psychiatric disorders including autism spectrum disorders, Alzheimer's disease, Parkinson's disease, epilepsy, depression, mood disorders and tremor. Mercury-induced neuronal degeneration is thought to invoke glutamate-mediated excitotoxicity, however, the underlying mechanisms remain poorly understood. Here, we examine the effects of various mercury concentrations (including pathological levels present in human plasma or cerebrospinal fluid) on cultured, rat cortical neurons.
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    The Effects of General Anesthetics on Neuron Structure and Function
    (2016) Armstrong, Ryden J; Syed, Naweed Imam; Xu, Fenglian; Shutt, Timothy; Dobson, Gary; Shearer, Jane
    Recent studies have implicated general anesthetic exposure to long-lasting cognitive impairments in children. However, the mechanisms that underlie anesthetic toxicity remain controversial. Here, I used an in vitro primary neuron culture to determine the effects of two volatile general anesthetics – sevoflurane and desflurane – on neuron development. To this end, I first quantified how general anesthetics affect neuron structural development. I show that sevoflurane and desflurane impair neurite growth, neuron polarization, and mitochondrial morphology. Next, I determined the functional impact of general anesthetics on neuronal synaptogenesis and spontaneous synaptic activity. I demonstrate that both sevoflurane and desflurane impair synaptogenesis and spontaneous synaptic current frequency. Finally, I examined a promising mitochondrial protective compound – Mdivi-1 – and found it to reverse many of the noxious effects of sevoflurane and desflurane. These results show, for the first time, several subcellular impacts of sevoflurane and desflurane, which may underlie the learning and memory deficits seen clinically.