کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5844294 | 1561030 | 2016 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Antidepressant drug action - From rapid changes on network function to network rewiring
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کلمات کلیدی
5-HTRegulated in development and DNA damage responses 1Redd1SNRITrkBN-methyl-d-aspartateNMDASynaptogenesisAMPAPNNDBSmTORECTBDNF - BDNF یا فاکتور نورونزایی مشتقشده از مغز ECs - EC هاpost-traumatic stress disorder - اختلال استرس پس از ضربهPTSD - اختلال استرسی پس از ضایعه روانیamino-3-hydroxy-5-methyl-4-isoxazolepropionic acid - اسید آمینه-3-هیدروکسی-5-متیل-4-ایزوکسول پپونیکgamma-aminobutyric acid - اسید گاما آمینو بوتیریکSerotonin and noradrenaline reuptake inhibitor - بازدارنده بازگشت سراتونین و نورآدرنالینdeep brain stimulation - تحریک عمقی مغزlong-term potentiation - تقویت درازمدتLTP - تقویت طولانی مدت یا LTP Perineuronal net - خالص PerineuronalElectroconvulsive therapy - درمان با ضربه الکتریکی تشنجآور، الکتروشوک درمانیSerotonin - سروتونینelectroconvulsive shock - شوک الکتریکیAntidepressant - ضدافسردگیBrain-derived neurotrophic factor - فاکتور نوروتروفی مشتق شده از مغزSelective serotonin reuptake inhibitor - مهار کننده بازجذب سروتونین انتخابیSSRI - مهارکنندههای بازجذب سروتونینnoradrenaline - نورآدرنالین Neurotrophin - نوروتروفینmammalian target of rapamycin - هدف پستانداران رپامایسینtropomyosin-related kinase B - وابسته به tropomyosin kinase BEmotional processing - پردازش احساسیSynaptic plasticity - پلاستیسیته سیناپسیGABA - گابا
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
روانپزشکی بیولوژیکی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
There has been significant recent progress in understanding the neurobiological mechanisms of antidepressant treatments. The delayed-onset of action of monoamine-based antidepressant drugs have been associated to their ability to slowly increase synaptic plasticity and neuronal excitability via altering neurotrophic signaling (synthesis of BDNF and activation of its receptor TrkB), dematuration of GABAergic interneurons and inhibition of “breaks of plasticity”. On the other hand, antidepressants rapidly regulate emotional processing that - with the help of heightened plasticity and appropriate rehabilitation - gradually lead to significant changes on functional neuronal connectivity and clinical recovery. Moreover, the discovery of rapid-acting antidepressants, most notably ketamine, has inspired interest for novel antidepressant developments with better efficacy and faster onset of action. Therapeutic effects of rapid-acting antidepressants have been linked with their ability to rapidly regulate neuronal excitability and thereby increase synaptic translation and release of BDNF, activation of the TrkB-mTOR-p70S6k signaling pathway and increased synaptogenesis within the prefrontal cortex. Thus, alterations in TrkB signaling, synaptic plasticity and neuronal excitability are shared neurobiological phenomena implicated in antidepressant responses produced by both gradually and rapid acting antidepressants. However, regardless of antidepressant, their therapeutic effects are not permanent which suggests that their effects on neuronal connectivity and network function remain unstable and vulnerable for psychosocial challenges.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Progress in Neuro-Psychopharmacology and Biological Psychiatry - Volume 64, 4 January 2016, Pages 285-292
Journal: Progress in Neuro-Psychopharmacology and Biological Psychiatry - Volume 64, 4 January 2016, Pages 285-292
نویسندگان
Tomi Rantamäki, Ipek Yalcin,