title: Gastrodin suppresses the amyloid β-induced increase of spontaneous discharge in the entorhinal cortex of rats.
abstract: 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 Aβ(1-42) on the discharge properties of EC neurons, using in vivo extracellular single unit recordings. The protective effects of gastrodin (GAS) were also investigated against Aβ(1-42)-induced alterations in EC neuronal activities. The results showed that the spontaneous discharge of EC neurons was increased by local application of soluble Aβ(1-42) and that GAS can effectively reverse Aβ(1-42)-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 Aβ(1-42)-elicited inward currents in EC neurons. Our study suggested that GAS may provide neuroprotective effects on Aβ(1-42)-induced hyperactivity in EC neurons of rats.
authors.affiliation: Department of Physiology, Third Military Medical University, Chongqing 400038, China.
authors.forename: Peng-zhi
authors.initials: PZ
authors.lastname: Chen
authors.affiliation: Department of Physiology, Third Military Medical University, Chongqing 400038, China.
authors.forename: Hui-hui
authors.initials: HH
authors.lastname: Jiang
authors.affiliation: Department of Physiology, Third Military Medical University, Chongqing 400038, China.
authors.forename: Bo
authors.initials: B
authors.lastname: Wen
authors.affiliation: Department of Physiology, Third Military Medical University, Chongqing 400038, China.
authors.forename: Shuan-cheng
authors.initials: SC
authors.lastname: Ren
authors.affiliation: School of Acupuncture and Tuina, Chengdu University of Traditional Chinese Medicine, Chengdu 611130, China.
authors.forename: Yang
authors.initials: Y
authors.lastname: Chen
authors.affiliation: Department of Chemistry, Third Military Medical University, Chongqing 400038, China.
authors.forename: Wei-gang
authors.initials: WG
authors.lastname: Ji
authors.affiliation: Department of Physiology, Third Military Medical University, Chongqing 400038, China.
authors.forename: Bo
authors.initials: B
authors.lastname: Hu
authors.affiliation: Department of Physiology, Third Military Medical University, Chongqing 400038, China.
authors.forename: Jun
authors.initials: J
authors.lastname: Zhang
authors.affiliation: Department of Physiology and Pharmacology, The Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, Calgary, Canada T2N 4N1.
authors.forename: Fenglian
authors.initials: F
authors.lastname: Xu
authors.affiliation: Department of Physiology, Third Military Medical University, Chongqing 400038, China.
authors.forename: Zhi-ru
authors.initials: ZR
authors.lastname: Zhu
mesh_terms: D000200:Action Potentials / Q000187:drug effects; D016229:Amyloid beta-Peptides / Q000494:pharmacology*; D000818:Animals; D001592:Benzyl Alcohols / Q000494:pharmacology*; D018728:Entorhinal Cortex / Q000187:drug effects* / Q000502:physiology*; D005960:Glucosides / Q000494:pharmacology*; D008297:Male; D009474:Neurons / Q000187:drug effects* / Q000502:physiology*; D018696:Neuroprotective Agents / Q000494:pharmacology*; D010446:Peptide Fragments / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D016229:Amyloid beta-Peptides; D001592:Benzyl Alcohols; D005960:Glucosides; D018696:Neuroprotective Agents; D010446:Peptide Fragments; C075222:amyloid beta-protein (1-42); C045345:gastrodin