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2017 | 77 | Suppl.1 |
Tytuł artykułu

Spinal BDNF overexpression leads to opposite effects on glutamatergic ampar and NMDAR than on muscarinic acetylcholine receptor M2 transcript level in rats with complete spinal cord transection

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Języki publikacji
EN
Abstrakty
EN
INTRODUCTION: Complete spinal cord transection (SCT) disturbs the balance between inhibitory and excitatory inputs to motoneurons increasing their excitability. However SCT causes deficiency in excitatory cholinergic input to ankle extensor motoneurons, whereas brain-derived neurotrophic factor (BDNF) overexpression below the lesion site increases markers of spinal neurotransmission and improves locomotor performance. Because glutamatergic receptors (AMPAR, NMDAR) and muscarinic acetylcholine receptor M2 play a crucial role in motoneuron excitability, we investigated if SCT and BDNF affect their expression. AIM(S): To disclose the impact of SCT and BDNF overexpression on levels of AMPAR, NMDAR and M2 mRNA transcripts 2 weeks after SCT. METHOD(S): Total RNA was isolated from L1-2 and L3-6 spinal fragments after SCT followed by intraspinal injection of PBS (n=6) or AAV-BDNF (n=7). After cDNA transcription, AMPAR (subunits GluR1, GluR2), NMDAR (subunits NR1, NR2A, NR2B), and M2 expression were measured using qRT PCR. RESULTS: In intact rats, GluR2 mRNA level was the highest, followed by NR2A/2B, while NR1 and M2 were the lowest. SCT tended to reduce levels of all mRNA transcripts, except for NR1 which tended to increase in L3-6. BDNF overexpression resulted in a significant increase of NR1 and tendency to increase of NR2A in both spinal fragments, while it led to a significant decrease of M2 in L1-2. CONCLUSIONS: BDNF overexpression slightly upregulated mRNA levels of NMDAR after SCT, not preventing deficits of M2. If M2 mRNA decrease is reflected by M2 protein levels in motoneurons, reduced contribution of M2 in modulation of motoneuron excitability may be postulated. FINANCIAL SUPPORT: 665735-Bio4Med-H2020-MSCA--COFUND-2014; National Science Centre 2013/09/B/ NZ4/03306, statutory for the Nencki Institute. This project has received funding from the European Union’s Horizon 2020 research and innovation programme under the Marie Skłodowska‑Curie grant agreement No 665735.
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Rocznik
Tom
77
Numer
Opis fizyczny
p.99
Twórcy
autor
  • Department of Neurophysiology, Laboratory of Restorative Neurobiology, Nencki Institute of Experimental Biology Polish Academy of Sciences, Warsaw, Poland
autor
  • Department of Neurophysiology, Laboratory of Restorative Neurobiology, Nencki Institute of Experimental Biology Polish Academy of Sciences, Warsaw, Poland
  • Department of Neurophysiology, Laboratory of Restorative Neurobiology, Nencki Institute of Experimental Biology Polish Academy of Sciences, Warsaw, Poland
  • Department of Neurophysiology, Laboratory of Restorative Neurobiology, Nencki Institute of Experimental Biology Polish Academy of Sciences, Warsaw, Poland
autor
  • Department of Neurophysiology, Laboratory of Restorative Neurobiology, Nencki Institute of Experimental Biology Polish Academy of Sciences, Warsaw, Poland
Bibliografia
Typ dokumentu
Bibliografia
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bwmeta1.element.agro-5372fce9-865b-4f84-923d-584f061cfcc6
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