کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
3055641 1186522 2012 7 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Minocycline cannot protect neurons against bilirubin-induced hyperexcitation in the ventral cochlear nucleus
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی عصب شناسی
پیش نمایش صفحه اول مقاله
Minocycline cannot protect neurons against bilirubin-induced hyperexcitation in the ventral cochlear nucleus
چکیده انگلیسی

Excitotoxicity has been suggested to play an important role in many central nervous system diseases, particularly in bilirubin encephalopathy. Minocycline treatment has been proposed to be one of the most promising potential therapies for excitotoxicity-induced neurological disorders. However, some key questions, such as the electrophysiological effect of minocycline on neuronal excitability and hyperexcitation in pathological conditions, require clarification. In this study, using patch-clamp techniques, we showed that bilirubin increased the frequency of both spontaneous excitatory postsynaptic currents (sEPSCs) and neuronal firing in isolated ventral cochlear nucleus (VCN) neurons at postnatal days 11–14 (P11–14) in rats but it did not affect the amplitude of sEPSCs or glutamate-activated (IGlu) currents. However, minocycline had no effect on sEPSC frequency or IGlu amplitude. Furthermore, minocycline pretreatment did not abolish bilirubin-induced sEPSC potentiation or neuron firing. These data suggest that minocycline does not affect excitatory synaptic transmission or hyperexcitation induced by bilirubin in VCN neurons. From these results, we propose that the neuroprotective efficacy of minocycline, if it can protect neurons against neurotoxicity induced by substances like bilirubin, is mediated by either an alternative mechanism or downstream events post neuronal hyperexcitation. Certainly, additional investigation of the neuroprotective effects of minocycline is required before embarking on further clinical trials.


► Bilirubin increased the presynaptic glutamate release and neuronal firing of VCN neurons.
► Bilirubin did not affect postsynaptic glutamate receptor sensitivity.
► Minocycline had no effect on presynaptic glutamate release, neuronal firing and postsynaptic glutamate receptor sensitivity.
► Minocycline cannot suppress the potentiation of bilirubin on presynaptic glutamate release and neuronal excitability.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Neurology - Volume 237, Issue 1, September 2012, Pages 96–102
نویسندگان
, , , , ,