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We have previously shown that cholinergic agonist carbachol modulates synaptic transmission of layer 6 corticothalamic input to posteromedial nucleus of the thalamus. In rat brain slices application of carbachol depresses synaptic responses to stimulation of corticothalamic fibers but enhances their frequency facilitation. Here we show that carbachol acts via activation of muscarinic receptors, because application of muscarinic antagonist (scopolamine or atropine) abolished both: depression of corticothalamic EPSPs and increase of frequency facilitation. In contrary, high concentration (100 µM) of specific nicotinic agonist DMPP (dimethylphenylpiperazinium) neither depressed corticothalamic responses nor enhanced the frequency facilitation. Surprisingly, low concentration of DMPP (10 µM) increased corticothalamic EPSPs, but did not change the frequency facilitation of corticothalamic transmission. This research and SN were supported by the European Union Regional Development Fund through the Foundation for Polish Science within the frames of International PhD Program in Neurobiology
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p.38
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- Deptartment of Neurophysiology, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland
- Department of Clinical and Experimental Medicine, Linkoping University, Linkoping, Sweden
autor
- Deptartment of Neurophysiology, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland
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- Deptartment of Neurophysiology, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland
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- Deptartment of Clinical and Experimental Medicine, Linkoping University, Linkoping, Sweden
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- Deptartment of Neurophysiology, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland
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