Akademik Veri Yönetim Sistemi
20th Turkish Neuroscience Congress, İstanbul, Türkiye, 19 - 23 Ekim 2022, (Yayınlanmadı)
Bengisu Arslantaş1 , Güzide Şatır Başaran2 1 Genome and Stem Cell Research Center, Erciyes University, Kayseri Türkiye; 2 Department of Biochemistry, Faculty of Pharmacy, Erciyes University, Kayseri ,Türkiye Objective: Acute intermittent hypoxia (AIH) causes long-term facilitation (LTF), known as a persistent increase in the amplitude of the ventilatory motor output response. LTF, requires motor neuron activation. furthermore, pro-inflammatory signal-induced glial cell activation has a role in LTF. In this study, it was hypothesized that COX-2 inhibition plays a role in ventilatory plasticity. Methods: In our study, divided into 2 groups as control (CON) and ibuprofen (IBU), 6 adult male, 3-month-old Spraque Dawley rats were used in each group were exposed to AIH. During the protocol, subjects were exposed to AIH and ventilation(V) measured. After that, tissue perfusion was performed and 20μ thick transverse medulla oblongata sections were taken. cFOS was used to show neuron activation, and GFAP, Iba-1/CD11b primary antibodies were used to show glial cell activation by immunofluorescence staining. The nucleus tractus solitarius (NTS) region on the medulla oblongata was visualized with a confocal microscope and density analyzes were performed. 2-way ANOVA tests were used for group comparison. p<0.05 was determined as a statistical significance level. Results: Baseline ventilation at 60th (666±35, p=0.0150) and 90th (658±35, p=0.0217) minutes after intermittent hypoxia increased significantly in CON group compared to baseline ventilation (549±16). There was no significant increase in IBU group. Expression of cFOS in NTS was significantly decreased in IBU group compared to CON group (p<0.05). There was no significant difference in expression of GFAP/Iba-1 and GFAP/CD11b in IBU group compared to CON group. Conclusion: Although LTF requires neuron activation, proinflammatory signaling pathway-dependent glial cell activation may also be required. Our data showed that ventilation was increased due to increased neuron activation in NTS. In addition, the absence of a significant increase in glial cell activation, but COX-2 inhibition causing depression in ventilation may result from this depression without and/or the initiation of glial cell activation. In conclusion, we think that COX-2 inhibition may block the LTF mechanism without glial cell activation after short-term intermittent hypoxia.
Keywords: Acute intermittent hypoxia, ventilatory long-term facilitation, NSAID, COX-2