en عمومى General پژوهشي orginal article <p dir="ltr"><strong>Received 5 May 2015, accepted for publication 27 July 2015</strong></p> <p dir="ltr"><strong>Background & Aims</strong>: Nicotinic acetylcholine receptors (nAChRs) regulate epileptiform discharges <a name="OLE_LINK1">generated by a number of different pharmacological manipulations,</a> in the hippocampus. Functional nicotinic receptor-mediated responses are most prominently observed in hippocampal interneurons, however the pro-epileptogenic action of nAChRs appears to be independent of fast GABAergic transmission since it is resistant to the blockade of GABA_A receptors. To identify possible contribution of the GABA_B receptor in the nAChR-induced effect, a set of experiments was carried out in the presence of GABAB receptor antagonist CGP55845A.</p> <p dir="ltr"><strong>Material and Methods</strong><strong>:</strong> Hippocampal slices (400&micro;m thick) were prepared from male Wistar rats (3-4 weeks). Following a 1hr equilibration in artificial cerebrospinal fluid, slices were transferred to a submerged-type recording chamber. Extracellular field recordings were made in the Stratum pyramidale of the CA3 regions. Bath application of the convulsant compounds 4-aminopyridine (4AP) or bicuculline resulted in the development of spontaneous epileptiform bursting.</p> <p dir="ltr"><strong>Results:</strong> Slices pre-incubated with CGP55845A (GABA_B receptor antagonist) were not able to exhibit burst frequency potentiation of 4AP-induced epileptiform activity upon application of the selective nAChR agonist dimethylphenylpiperazinium iodide (DMPP -8.3 &plusmn; 7%, n=11). Similarly, in the presence of CGP55845A, slices exhibited negligible burst frequency potentiation of bicuculline-induced epileptiform activity upon DMPP application (27.6 &plusmn; 18%, n=9), in comparison to those observed in the absence of CGP55845A (248 &plusmn; 76 %, n=14). The suppression of epileptiform activity by the GABA_B receptor agonist baclofen, was partially recovered by subsequent co-application of DMPP (n=10).</p> <p dir="ltr"><strong>Conclusion:</strong> These data suggests that nAChRs may regulate the excitability of hippocampal networks at least in part through GABA_B receptor-mediated mechanisms.</p> Acetylcholine, Nicotinic, Epilepsy, GABAB, Hippocampus 27 40 http://ijrabms.umsu.ac.ir/browse.php?a_code=A-10-53-1&slc_lang=en&sid=1 Shiva Roshan-Milani shivamilani@umsu.ac.ir 1003194753284600240 1003194753284600240 Yes Department of Physiology, Neurophysiology Research Center, Medical Faculty, Urmia University of Medical Science, Urmia, Iran Morteza Motazakker motazakker@umsu.ac.ir 1003194753284600241 1003194753284600241 No Department of Microbiology, Medical Faculty, Urmia University of Medical Science, Urmia, Iran Ehsan saboory saboory@umsu.ac.ir 1003194753284600242 1003194753284600242 No Department of Physiology, Neurophysiology Research Center, Medical Faculty, Urmia University of Medical Science, Urmia, Iran Stuart Cobb stuart.cobb@glasgow.ac.uk 1003194753284600243 1003194753284600243 No Division of Neuroscience and Biomedical Systems, IBLS, University of Glasgow, Glasgow, G12 8QQ, UK