Person: MİNBAY, FATMA ZEHRA
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MİNBAY
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FATMA ZEHRA
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Publication Glutamate receptor antagonist suppresses the activation of nesfatin-1 neurons following refeeding or glucose administration(Via Medica, 2022-01-01) Koçoğlu, S. Serter; Oy, C.; Halk, Z.; Çakır, C.; Minbay, Z.; Eyigör, O.; OY, CEREN; Halk, Z.; ÇAKIR, CİHAN; MİNBAY, FATMA ZEHRA; EYİGÖR, ÖZHAN; Tıp Fakültesi; Histoloji ve Embriyoloji Ana Bilim Dalı; 0000-0002-8332-7353; 0000-0003-3463-7483; ABQ-8779-2022; ABE-5128-2020; AAH-5249-2021; ABC-1475-2020Background: Nesfatin-1 is a newly identified satiety peptide that has regulatory effects on food intake and glucose metabolism, and is located in the hypothalamic nuclei, including the supraoptic nucleus (SON). In this study, we have investigated the hypothesis that nesfatin-1 neurons are activated by refeeding and intraperito-neal glucose injection and that the glutamatergic system has regulatory influences on nesfatin-1 neurons in the SON. Materials and methods: The first set of experiments analysed activation of nesfatin-1 neurons after refeeding as a physiological stimulus and the effective-ness of the glutamatergic system on this physiological stimulation. The subjects were randomly divided into three groups: fasting group, refeeding group and antagonist (CNQX + refeeding) group. The second set of experiments analysed activation of nesfatin-1 neurons by glucose injection as a metabolic stimulus and the effectiveness of the glutamatergic system on this metabolic stimulation. The subjects were randomly divided into three groups: saline group, glucose group and antagonist (CNQX + glucose) group. Results: Refeeding significantly increased the number of activated nesfatin-1 neurons by approximately 66%, and intraperitoneal glucose injection activated these neurons by about 55%, compared to the fasting and saline controls. The injections of glutamate antagonist (CNQX) greatly decreased the number of ac-tivated nesfatin-1 neurons. Conclusions: This study suggested that nesfatin-1 neurons were activated by peripheral and/or metabolic signals and that this effect was mediated through the glutamatergic system. (Folia Morphol 2022; 81, 2: 379-386)Publication Glutamatergic activation of A1 and A2 noradrenergic neurons in the rat brain stem(Medicinska Naklada, 2019-07-10) Gök-Yurtseven, Duygu; Kafa, İlker M.; Minbay, Zehra; Eyigör, Özhan; GÖK YURTSEVEN, DUYGU; KAFA, İLKER MUSTAFA; MİNBAY, FATMA ZEHRA; EYİGÖR, ÖZHAN; Fen Bilimleri Enstitüsü; Histoloji Bölümü ve Embriyoloji Bilim Dalı; 0000-0001-8309-0934; 0000-0003-3463-7483; AAW-4867-2021; AAG-7125-2021; ABE-5128-2020; ABC-1475-2020Aim To analyze the effects of glutamatergic agonists and antagonists on the activation of the A1 and A2 noradrenergic neurons localized in caudal ventrolateral medulla and nucleus tractus solitarii, respectively.Methods Rats were injected with glutamatergic agonists - kainic acid, alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), or N-methyl-D-aspartic acid (NMDA), and the brain sections were prepared for immunohistochemistry. Before agonist injections, antagonists - 6-cyano-7-nitroquinoxaline-2,3-dione or dizocilpine were administered. The expression of c-Fos, as the neuronal activation marker, and tyrosine hydroxylase (TH), as the marker of noradrenergic neurons was assessed with dual immunohistochemistry. The percentage of c-Fos-positive noradrenergic neurons relative to all TH-positive neurons in the respective areas of the brain stem was calculated.Results All three glutamatergic agonists significantly increased the number of the c-Fos-positive noradrenergic neurons in both the A1 and A2 area when compared with control animals. Kainic acid injection activated about 57% of TH-positive neurons in A1 and 40% in A2, AMPA activated 26% in A1 and 38% in A2, and NMDA 77% in A1 and 22% in A2. The injections of appropriate glutamatergic antagonists greatly decreased the number of activated noradrenergic neurons.Conclusion Our results suggest that noradrenergic neurons are regulated and/or activated by glutamatergic system and that these neurons express functional glutamate receptors.Publication Expression of the ionotropic glutamate receptors on neuronostatin neurons in the periventricular nucleus of the hypothalamus(Via Medica, 2022-01-01) Kocoğlu, S. Serter; Çakir, Cihan; ÇAKIR, CİHAN; Eyigör, Özhan; MİNBAY, FATMA ZEHRA; EYİGÖR, ÖZHAN; Tıp Fakültesi; Histoloji ve Embriyoloji Ana Bilim Dalı; 0000-0002-8332-7353; 0000-0003-3463-7483; ABC-1475-2020; ABE-5128-2020; AAH-5249-2021; ABQ-8779-2022Background: Neuronostatin, a newly identified peptide, is accepted as an anorex- igenic peptide since it suppresses food intake when given intracerebroventricularly. Although the effect mechanisms of neuronostatin have been shown in different studies, there are no reports in the literature describing the mechanisms controlling neuronostatin neurons. In this study, we aimed to determine the presence of the ionotropic glutamate receptor subunits (iGluRs) in neuronostatin neurons in the periventricular nucleus of the hypothalamus. Materials and methods: The presence of glutamate receptors in neuronostatin neurons was investigated by dual immunohistochemistry. Immunohistochemistry was performed on 40 mu m thick coronal brain sections with antibodies against AMPA (GluA1-4), kainate (GluK1/2/3, and GluK5), and NMDA (GluN1 and GluN2A) receptor subunits. Results: The results showed that the neuronostatin neurons expressed most of the NMDA and non-NMDA receptor subunits. The neuronostatin neurons in the anterior hypothalamic periventricular nucleus were particularly immunopositive for GluA1, GluA4, GluK1/2/3, GluK5 and GluN1 antibodies. No expression was observed for GluA2, GluA3 and GluN2A antibodies. Conclusions: For the first time in the literature, our study demonstrated that the neuronostatin neurons express glutamate receptor subunits which may form homomeric or heteromeric functional receptor complexes. Taken together, these results suggest that multiple subunits of iGluRs are responsible for glutamate transmission on neuronostatin neurons in the anterior hypothalamic periventricular nucleus.