Adenosine receptor activation is responsible for prolonged depression of synaptic transmission after spreading depolarization in brain slices
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چکیده
منابع مشابه
Electrophysiological characteristics of hippocampal CA1 neurons after spreading depression-triggered epileptic activity in brain slices
Introduction: A close link between spreading depression (SD) and several neurological diseases such as epilepsy could be demonstrated in many experimental studies. Epilepsy is among the most common brain disorders. Despite a large number of investigations, its mechanisms have not been yet well elucidated. Hippocampus is one of the important structures involved in seizures. The aim of this st...
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Both brain-derived neurotrophic factor (BDNF) and adenosine influence neuronal plasticity. We now investigated how adenosine influences the action of BDNF on synaptic transmission in the CA1 area of the rat hippocampal slices. Alone, BDNF (20-100 ng/ml) did not significantly affect field EPSPs (fEPSPs). However, a 2 min pulse of high-K(+) (10 mm) 46 min before the application of BDNF (20 ng/ml)...
متن کاملelectrophysiological characteristics of hippocampal ca1 neurons after spreading depression-triggered epileptic activity in brain slices
introduction: a close link between spreading depression (sd) and several neurological diseases such as epilepsy could be demonstrated in many experimental studies. epilepsy is among the most common brain disorders. despite a large number of investigations, its mechanisms have not been yet well elucidated. hippocampus is one of the important structures involved in seizures. the aim of this study...
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We have examined the interaction between synapsin I, the major phosphoprotein on the membrane of small synaptic vesicles, and brain spectrin. Using recombinant peptides we have localized the synapsin I attachment site upon the beta-spectrin isoform betaSpIISigmaI to a region of 25 amino acids, residues 211 through 235. This segment is adjacent to the actin binding domain and is within the regio...
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ژورنال
عنوان ژورنال: Neuroscience
سال: 2012
ISSN: 0306-4522
DOI: 10.1016/j.neuroscience.2012.07.053