کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6274338 | 1614823 | 2013 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Adolescent chronic mild stress alters hippocampal CB1 receptor-mediated excitatory neurotransmission and plasticity
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کلمات کلیدی
multivariate ANOVACCKCMSPTXDSIaCSFeCBs2-AG2-arachidonoyl-glycerolCRSTBSPNDAEADMSO - DMSOPTSD - اختلال استرسی پس از ضایعه روانیchronic mild stress - استرس مزمن مزمنChronic restraint stress - استرس مهلک مزمنStress - استرس یا فشار روانیDepression - افسردگیendocannabinoids - اندوکانبایوئید هاTheta-burst stimulation - تحریک حباب تتاanalysis of variance - تحلیل واریانسANOVA - تحلیل واریانس Analysis of varianceLTP - تقویت طولانی مدت یا LTP Dimethyl sulfoxide - دیمتیل سولفواکسیدpost natal day - روز تولدartificial cerebrospinal fluid - مایع مغزی نخاعی مصنوعیHPA - میلی بار یا هکتوپاسکالhypothalamic–pituitary–adrenal - هیپوتالاموس-هیپوفیز-آدرنالHippocampus - هیپوکامپ Picrotoxin - پیکروتوکسینCannabinoid - کانابینوئیدcholecystokinin - کولهسیستوکینینGlucocorticoid - گلوکوکورتیکوئیدهاCB1 receptor - گیرنده CB1
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Adolescent chronic mild stress alters hippocampal CB1 receptor-mediated excitatory neurotransmission and plasticity Adolescent chronic mild stress alters hippocampal CB1 receptor-mediated excitatory neurotransmission and plasticity](/preview/png/6274338.png)
چکیده انگلیسی
Endocannabinoids (eCBs) are involved in the stress response and alterations in eCB signaling may contribute to the etiology of mood disorders. Exposure to chronic mild stress (CMS), a model of depression, produces downregulation of the cannabinoid 1 (CB1) receptor in the hippocampus of male rats. However, it is unknown how this stress-induced change in CB1 levels affects eCB-mediated neurotransmission. In vitro, field potential recordings from CMS-exposed (21-days) rats were performed to assess the effects of stress on eCB-regulated glutamatergic neurotransmission in/on hippocampal area CA1. We observed that application of the CB1 agonist, WIN 55,212-5 (1 μM), in stress animals resulted in a â¼135% increase in excitatory neurotransmission, whereas CB1 activation in non-stress animals leads to a â¼30% decrease. However, during blockade of GABA(A) neurotransmission with picrotoxin, CB1 activation yielded a â¼35% decrease in stress animals. These findings indicate that CMS does not directly affect glutamatergic neurotransmission. Rather, CMS sensitizes CB1 function on GABAergic terminals, leading to less inhibition and an increase in excitatory neurotransmission. This finding is reinforced in that induction of weak long-term-potentiation (LTP) is enhanced in CMS-exposed animals compared to controls and this enhancement is CB1-dependent. Lastly, we observed that the LTP-blocking property of WIN 55,212-5 shifts from being glutamate-dependent in non-stress animals to being GABA-dependent in stress animals. These results effectively demonstrate that CMS significantly alters hippocampal eCB-mediated neurotransmission and synaptic plasticity.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 253, 3 December 2013, Pages 444-454
Journal: Neuroscience - Volume 253, 3 December 2013, Pages 444-454
نویسندگان
C.G. Reich, G.R. Mihalik, A.N. Iskander, J.C. Seckler, M.S. Weiss,