کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6271737 | 1614761 | 2016 | 29 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
High sucrose consumption induces memory impairment in rats associated with electrophysiological modifications but not with metabolic changes in the hippocampus
ترجمه فارسی عنوان
مصرف زیاد سقز باعث اختلال حافظه در موشهای صحرایی با تغییرات الکتروفیزیولوژیک میشود، اما نه با تغییرات متابولیک در هیپوکامپ
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کلمات کلیدی
HRMASHSUNaANORA1RfEPSPDPCPXFST8-Cyclopentyl-1,3-dipropylxanthine - 8-Cyclopentyl-1،3-dipropylxanthineDMSO - DMSON-Acetyl-Aspartate - N-استیل آسپارتاتAdenosine A1 receptors - آدنوزین A1 گیرندهForced swimming test - آزمون اجباری شناγ-aminobutyric acid - اسید γ-آمینوبوتیریکlong-term depression - افسردگی طولانی مدتlong-term potentiation - تقویت درازمدتLTP - تقویت طولانی مدت یا LTP Object displacement - جابجایی شیDimethylsulfoxide - دیمتیل سولفواکسیدHigh-resolution magic angle spinning - زاویه مغناطیسی با وضوح بالا چرخشHigh sucrose - سوکراس بالاNovel object recognition - شناسایی شیء رمانEntorhinal cortex - قشر انتورینالLTD - محدودOpen field - میدان بازfield excitatory postsynaptic potentials - پتانسیل پستنیپتیک تحریک پذیری میدانGABA - گابا
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
چکیده انگلیسی
High sugar consumption is a risk factor for metabolic disturbances leading to memory impairment. Thus, rats subject to high sucrose intake (HSu) develop a metabolic syndrome and display memory deficits. We now investigated if these HSu-induced memory deficits were associated with metabolic and electrophysiological alterations in the hippocampus. Male Wistar rats were submitted for 9Â weeks to a sucrose-rich diet (35% sucrose solution) and subsequently to a battery of behavioral tests; after sacrifice, their hippocampi were collected for ex vivo high-resolution magic angle spinning (HRMAS) metabolic characterization and electrophysiological extracellular recordings in slices. HSu rats displayed a decreased memory performance (object displacement and novel object recognition tasks) and helpless behavior (forced swimming test), without altered locomotion (open field). HRMAS analysis indicated a similar hippocampal metabolic profile of HSu and control rats. HSu rats also displayed no change of synaptic transmission and plasticity (long-term potentiation) in hippocampal Schaffer fibers-CA1 pyramid synapses, but had decreased amplitude of long-term depression in the temporoammonic (TA) pathway. Furthermore, HSu rats had an increased density of inhibitory adenosine A1 receptors (A1R), that translated into a greater potency of A1R in Schaffer fiber synapses, but not in the TA pathway, whereas the endogenous activation of A1R in HSu rats was preserved in the TA pathway but abolished in Schaffer fiber synapses. These results suggest that HSu triggers a hippocampal-dependent memory impairment that is not associated with altered hippocampal metabolism but is probably related to modified synaptic plasticity in hippocampal TA synapses
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 315, 19 February 2016, Pages 196-205
Journal: Neuroscience - Volume 315, 19 February 2016, Pages 196-205
نویسندگان
C. Lemos, D. Rial, F.Q. Gonçalves, J. Pires, H.B. Silva, F.C. Matheus, A.C. da Silva, J.M. Marques, R.J. Rodrigues, I. Jarak, R.D. Prediger, F. Reis, R.A. Carvalho, F.C. Pereira, R.A. Cunha,