کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9425392 | 1295867 | 2005 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Acute effects of ethanol on hippocampal long-term potentiation and long-term depression are mediated by different mechanisms
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کلمات کلیدی
aCSFd,l-2-amino-5-phosphonovalerateAPVIfenprodilNMDARsEPSPsEthanol - اتانولPopulation spike - افزایش جمعیتlong-term depression - افسردگی طولانی مدتlong-term potentiation - تقویت درازمدتLTP - تقویت طولانی مدت یا LTP Blackouts - خاموشیpostnatal day - روز پس از زایمانartificial cerebrospinal fluid - مایع مغزی نخاعی مصنوعیLTD - محدودHippocampus - هیپوکامپ excitatory postsynaptic potentials - پتانسیل های پست پراکنده تحریک پذیرSynaptic plasticity - پلاستیسیته سیناپسیPicrotoxin - پیکروتوکسینN-Methyl-d-aspartate receptors - گیرنده های N-methyl-d-aspartate
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Acute effects of ethanol on hippocampal long-term potentiation and long-term depression are mediated by different mechanisms Acute effects of ethanol on hippocampal long-term potentiation and long-term depression are mediated by different mechanisms](/preview/png/9425392.png)
چکیده انگلیسی
To determine potential mechanisms contributing to ethanol-induced cognitive impairment, we examined acute effects of ethanol on hippocampal N-methyl-d-aspartate receptors and forms of synaptic plasticity thought to underlie memory processing. In the CA1 region of rat hippocampal slices, ethanol partially inhibited N-methyl-d-aspartate receptor-mediated synaptic responses at concentrations up to 180mM. The block of synaptic N-methyl-d-aspartate receptors by 60mM ethanol occluded the effects of 10μM ifenprodil, an agent that has relative selectivity for N-methyl-d-aspartate receptors expressing NR1 and NR2B subunits. Ethanol did not occlude the effects of a low concentration of 2-amino-5-phosphonovalerate, an antagonist with less N-methyl-d-aspartate receptor subtype selectivity. Recent studies indicate that ifenprodil and other NR2B-selective antagonists inhibit N-methyl-d-aspartate receptor-dependent long-term depression but not long-term potentiation. We found that ethanol reversibly inhibited long-term depression in a manner consistent with its effects on synaptic N-methyl-d-aspartate receptors. Ethanol also inhibited the induction of N-methyl-d-aspartate receptor-dependent long-term potentiation, but the actions on long-term potentiation were complex and largely irreversible over the time course of our experiments. Furthermore, ethanol inhibited a form of long-term potentiation induced by very high frequency stimulation that does not depend on N-methyl-d-aspartate receptor activation. The effects of ethanol on both forms of long-term potentiation, but not on long-term depression, were at least partially reversed by block of GABA type A receptors with picrotoxin. These results indicate that pharmacologically relevant concentrations of ethanol exert preferential effects on a subtype of synaptic N-methyl-d-aspartate receptors in the CA1 hippocampal region. Inhibition of synaptic N-methyl-d-aspartate receptors appears to contribute strongly to ethanol-mediated long-term depression inhibition, but effects on long-term potentiation are complex, involving, at least partially, changes in GABAergic transmission.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 136, Issue 2, 2005, Pages 509-517
Journal: Neuroscience - Volume 136, Issue 2, 2005, Pages 509-517
نویسندگان
Y. Izumi, K. Nagashima, K. Murayama, C.F. Zorumski,