Gábor Czéh

University of Pécs, Hungary, Pécs, Hungary 
"Gábor Czéh"
Mean distance: 15.7 (cluster 6)
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Varga A, Bölcskei K, Szöke E, et al. (2006) Relative roles of protein kinase A and protein kinase C in modulation of transient receptor potential vanilloid type 1 receptor responsiveness in rat sensory neurons in vitro and peripheral nociceptors in vivo. Neuroscience. 140: 645-57
Szolcsányi J, Sándor Z, Petho G, et al. (2004) Direct evidence for activation and desensitization of the capsaicin receptor by N-oleoyldopamine on TRPV1-transfected cell, line in gene deleted mice and in the rat. Neuroscience Letters. 361: 155-8
Abraham H, Losonczy A, Czéh G, et al. (2003) Potassium channel blockers tetraethylammonium and 4-aminopyridine fail to prevent microglial activation induced by elevated potassium concentration. Acta Biologica Hungarica. 54: 63-78
Szoke E, Czéh G, Szolcsányi J, et al. (2002) Neonatal anandamide treatment results in prolonged mitochondrial damage in the vanilloid receptor type 1-immunoreactive B-type neurons of the rat trigeminal ganglion. Neuroscience. 115: 805-14
Seress L, Szoke E, Czéh G. (2002) Age-related mitochondrial damage in the B-type cells of the rat trigeminal ganglia. Acta Biologica Hungarica. 53: 167-75
Balla Z, Szoke E, Czéh G, et al. (2001) Effect of capsaicin on voltage-gated currents of trigeminal neurones in cell culture and slice preparations. Acta Physiologica Hungarica. 88: 173-96
Abrahám H, Losonczy A, Czéh G, et al. (2001) Rapid activation of microglial cells by hypoxia, kainic acid, and potassium ions in slice preparations of the rat hippocampus. Brain Research. 906: 115-26
Szöke E, Balla Z, Csernoch L, et al. (2000) Interacting effects of capsaicin and anandamide on intracellular calcium in sensory neurones. Neuroreport. 11: 1949-52
Czéh B, Seress L, Czéh G. (1999) Electrophysiological characteristics and morphological properties of dentate granule--and CA3 pyramidal cells in slices cut from neonatally irradiated rats. Neurobiology (Budapest, Hungary). 7: 1-17
Czéh B, Seress L, Czéh G. (1998) Residual granule cells can maintain susceptibility of CA3 pyramidal cells to kainate-induced epileptiform discharges. Hippocampus. 8: 548-61
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