Spinal BDNF overexpression partially protects synaptic machinery of neuromuscular junction from disintegration after complete spinal cord transection in adult rats: Neurochemical and morphological changes evaluated by histochemical techniques

• Autorzy: Glowacka A. , Gajewska-Wozniak O. , Bernadzki K.M. , Czarkowska-Bauch J. , Skup M.
• Języki publikacji: EN

Abstrakty

EN

INTRODUCTION: Complete spinal cord transection (SCT) leads to loss of motor control due to disruption of supraspinal tracts and altered functioning of both central and peripheral synapses. We showed that SCT at low thoracic segments causes deficiency in cholinergic input to ankle extensor (soleus) motoneurons, whereas brain-derived neurotrophic factor (BDNF) overexpression below the lesion site increases markers of spinal neurotransmission and improves locomotor performance. These findings raise the question if SCT impairs also integrity of peripheral synapses in soleus muscle and if BDNF can counteract lesion effects. AIM(S): To disclose the impact of SCT and BDNF overexpression on pre- (VAChT and S-100) and postsynaptic (nAChR) components of neuromuscular junction (NMJ) in soleus muscle. METHOD(S): VAChT and S-100 were detected immunohistochemically and acetylcholine receptors were visualized with fluorescently labeled bungarotoxin on free‑floating muscle fibers 2 weeks after SCT and intraspinal injection of PBS (n=6) or BDNF (n=7). Images acquired on Zeiss confocal microscope were deconvoluted with Huygens Professional and analyzed with 3D Imaris Software to evaluate NMJ morphology. RESULTS: SCT reduced the number of contacts of normal morphology to 39% which was accompanied by decrease in NMJs size. BDNF overexpression resulted in preservation of 73% of normal contacts, but did not prevent NMJ shrinkage. VAChT-labeled synaptic vesicles marking motoneuron terminals were visibly more dispersed after SCT than in controls. BDNF did not affect this dispersion. CONCLUSIONS: Spinal BDNF overexpression partially prevents NMJs from denervation, albeit does not counteract the reduced size of NMJ. It needs further investigation whether motor improvement is the effect of direct neuroprotective role of BDNF on NMJs or the result of altered signaling at central synapses. FINANCIAL SUPPORT: National Science Centre 2013/09/B/NZ4/03306, statutory for the Nencki Institute.

• Wydawca: -
• Czasopismo: Acta Neurobiologiae Experimentalis
• Rocznik: 2017
• Tom: 77
• Numer: Suppl.1
• Opis fizyczny: p.79

Twórcy

autor

Glowacka A.

• Department of Neurophysiology, Nencki Institute of Experimental Biology Polish Academy of Sciences, Warsaw, Poland

autor

Gajewska-Wozniak O.

• Department of Neurophysiology, Nencki Institute of Experimental Biology Polish Academy of Sciences, Warsaw, Poland

autor

Bernadzki K.M.

• Department of Cell Biology, Nencki Institute of Experimental Biology Polish Academy of Sciences, Warsaw, Poland

autor

Czarkowska-Bauch J.

• Department of Neurophysiology, Nencki Institute of Experimental Biology Polish Academy of Sciences, Warsaw, Poland

autor

Skup M.

• Department of Neurophysiology, Nencki Institute of Experimental Biology Polish Academy of Sciences, Warsaw, Poland