Yazar "Bal, Ramazan" seçeneğine göre listele

Listeleniyor 1 - 2 / 2
  • Küçük Resim
    Öğe
    Modulation of excitability of stellate neurons in the ventral cochlear nucleus of mice by atp-sensitive potassium channels
    (Springer, 2018) Bal, Ramazan; Öztürk, Gürkan; Önalan Etem, Ebru; Him, Aydın; Cengiz, Nurettin; Kulo?lu, Tuncay; Tuzcu, Mehmet; Yıldırım, Caner; Tektemur, Ahmet
    Major voltage-activated ionic channels of stellate cells in the ventral part of cochlear nucleus (CN) were largely characterized previously. However, it is not known if these cells are equipped with other ion channels apart from the voltage-sensitive ones. In the current study, it was aimed to study subunit composition and function of ATP-sensitive potassium channels (K-ATP) in stellate cells of the ventral cochlear nucleus. Subunits of K-ATP channels, Kir6.1, Kir6.2, SUR1, and SUR2, were expressed at the mRNA level and at the protein level in the mouse VCN tissue. The specific and clearly visible bands for all subunits but that for Kir6.1 were seen in Western blot. Using immunohistochemical staining technique, stellate cells were strongly labeled with SUR1 and Kir6.2 antibodies and moderately labeled with SUR2 antibody, whereas the labeling signals for Kir6.1 were too weak. In patch clamp recordings, K-ATP agonists including cromakalim (50 A mu M), diazoxide (0.2 mM), 3-Amino-1,2,4-triazole (ATZ) (1 mM), 2,2-Dithiobis (5-nitro pyridine) (DTNP) (330 A mu M), 6-Chloro-3-isopropylamino- 4H-thieno[3,2-e]-1,2,4-thiadiazine 1,1-dioxide (NNC 55-0118) (1 A mu M), 6-chloro-3-(methylcyclopropyl)amino-4H-thieno[3,2-e]-1,2,4-thiadiazine 1,1-dioxide (NN414) (1 A mu M), and H2O2 (0.88 mM) induced marked responses in stellate cells, characterized by membrane hyperpolarization which were blocked by K-ATP antagonists. Blockers of K-ATP channels, glibenclamide (0.2 mM), tolbutamide (0.1 mM) as well as 5-hydroxydecanoic acid (1 mM), and catalase (500 IU/ml) caused depolarization of stellate cells, increasing spontaneous action potential firing. In conclusion, K-ATP channels seemed to be composed dominantly of Kir 6.2 subunit and SUR1 and SUR2 and activation or inhibition of K-ATP channels regulates firing properties of stellate cells by means of influencing resting membrane potential and input resistance.
  • Küçük Resim
    Öğe
    Modulation of the excitability of stellate neurons in the ventral cochlear nucleus of mice by TRPM2 channels
    (Elsevier, 2020) Bal, Ramazan; Öztürk, Gürkan; Önalan Etem, Ebru; Eraslan, Ersen; Özaydın, Seda
    Oxidative stress-induced Ca2+ permeable transient receptor potential melastatin 2 (TRPM2) channels are expressed at high levels in the brain, appear to link neuronal excitability to cellular metabolism, and are involved in the pathogenesis of neurodegenerative disorders. We aimed to study the electrophysiological properties of TRPM2 channels in stellate cells of the mouse ventral cochlear nucleus (VCN) using molecular, immunohistochemical and electrophysiological approaches.In the present study, the real time PCR analysis revealed the presence of the TRPM2 mRNA in the mouse VCN tissue. Cell bodies of stellate cells were moderately labeled with TRPM2 antibodies using immunohistochemical staining.Stellate cells were sensitive to intracellular ADP-ribose (ADPR), a TRPM2 agonist. Upon the application of ADPR, the resting membrane potential of the stellate cells was significantly depolarized, shifting from -61.2 +/- 0.9 mV to-57.0 +/- 0.8 mV (P < 0.001; n = 21), and the firing rate significantly increased (P < 0.001, n = 6). When the pipette solution contained ADPR (300 mu M) and the TRPM2 antagonists flufenamic acid (FFA) (100 mu M), N-(p-amylcinnamoyl) anthranilic acid (ACA) (50 mu M) and 8-bromo-cADP-Ribose (8Br-cADPR) (50 mu M), the membrane potential shifted in a hyperpolarizing direction. ADPR did not significantly change the resting membrane potential and action potential firing rate of stellate cells from TRPM2-/- mice.In conclusion, the results obtained using these molecular, immunohistochemical and electrophysiological approaches reveal the expression of functional TRPM2 channels in stellate neurons of the mouse VCN. TRPM2 might exert a significant modulatory effect on setting the level of resting excitability.