کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8951021 | 1645807 | 2018 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Phrenic long-term facilitation following intrapleural CTB-SAP-induced respiratory motor neuron death
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کلمات کلیدی
CTBPaCO2PaO2PetCO2AIHPhrenic long-term facilitationpLTFamyotrophic lateral sclerosis - اسکلروز جانبی آمیوتروفیکALS - بیماری اسکلروز جانبی آمیوتروفیکNeurodegenerative disease - بیماری های نوروژنیکcholera toxin B - تومور مثانه BBreathing - نفس کشیدنacute intermittent hypoxia - هیپوکسی متناوب حادEnd-tidal PCO2 - پایان PCO2 جزر و مدVentilatory control - کنترل تهویه
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
فیزیولوژی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Amyotrophic lateral sclerosis (ALS) is a devastating disease leading to progressive motor neuron degeneration and death by ventilatory failure. In a rat model of ALS (SOD1G93A), phrenic long-term facilitation (pLTF) following acute intermittent hypoxia (AIH) is enhanced greater than expected at disease end-stage but the mechanism is unknown. We suggest that one trigger for this enhancement is motor neuron death itself. Intrapleural injections of cholera toxin B fragment conjugated to saporin (CTB-SAP) selectively kill respiratory motor neurons and mimic motor neuron death observed in SOD1G93A rats. This CTB-SAP model allows us to study the impact of respiratory motor neuron death on breathing without many complications attendant to ALS. Here, we tested the hypothesis that phrenic motor neuron death is sufficient to enhance pLTF. pLTF was assessed in anesthetized, paralyzed and ventilated Sprague Dawley rats 7 and 28â¯days following bilateral intrapleural injections of: 1) CTB-SAP (25â¯Î¼g), or 2) un-conjugated CTB and SAP (control). CTB-SAP enhanced pLTF at 7 (CTB-SAP: 162â¯Â±â¯18%, nâ¯=â¯8 vs. Control: 63â¯Â±â¯3%; nâ¯=â¯8; pâ¯<â¯0.05), but not 28â¯days post-injection (CTB-SAP: 64â¯Â±â¯10%, nâ¯=â¯10 vs. Control: 60â¯Â±â¯13; nâ¯=â¯8; pâ¯>â¯0.05). Thus, pLTF at 7 (not 28) days post-CTB-SAP closely resembles pLTF in end-stage ALS rats, suggesting that processes unique to the early period of motor neuron death enhance pLTF. This project increases our understanding of respiratory plasticity and its implications for breathing in motor neuron disease.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Respiratory Physiology & Neurobiology - Volume 256, October 2018, Pages 43-49
Journal: Respiratory Physiology & Neurobiology - Volume 256, October 2018, Pages 43-49
نویسندگان
Nicole L. Nichols, Taylor A. Craig, Miles A. Tanner,