کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4328062 | 1614159 | 2009 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Impaired glial buffering hampers antidromic conduction of CA1 neurons during hypoxia
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کلمات کلیدی
PRVADSCSDDPCPXfEPSP1,3-Dipropyl-8-cyclopentylxanthine - 1،3-Dipropyl-8-cyclopentylxanthineAPs - AP هاOPs - OP هاSpike - اسپایکevoked potential - بالقوه را تحریک می کندHippocampal slice - برش هیپوکامپConduction block - بلوک هدایتcurrent source density - تراکم منبع فعلیExtracellular potassium - پتاسیم غیر سلولیField excitatory postsynaptic potential - پتانسیل پستنیپتیک مزمن تحریک پذیر
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Increased potassium conductance during hypoxia causes membrane hyperpolarization and a resultant increase in extracellular potassium concentration ([K+]o). In addition, glial buffering of [K+]o is the key mechanism for clearing excess K+ and is important for neuronal function and survival. Here, we studied the effect of glial buffering of [K+]o on neural impulse conduction during hypoxia using a potassium-selective electrode and evoked potential recording in rat hippocampal slices. The increase in [K+]o during hypoxia was modest and there were no significant differences between the layers. The [K+]o during hypoxia was significantly elevated by addition of barium (1Â mM), especially in the stratum pyramidale and stratum oriens. Although synaptic transmission was depressed during hypoxia, the presynaptic volley and antidromic population spike mostly remained unchanged. With the addition of barium, antidromic conduction was more profoundly affected than the presynaptic volley. When presynaptic inhibition was precluded by including a selective A1 adenosine receptor blocker to restore synaptic transmission, blockade of the antidromic conduction became more evident compared with the blockade of other recorded field potentials. These findings are compatible with regional differences in the increase of [K+]o and suggest that glial buffering of high [K+]o is important in antidromic conduction during hypoxia.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Brain Research - Volume 1280, 14 July 2009, Pages 90-97
Journal: Brain Research - Volume 1280, 14 July 2009, Pages 90-97
نویسندگان
Youn-Kwan Park, Seok-Joon Kim,