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Browsing by Author "0000-0001-5757-8450"
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Item Glutamate and orexin neurons(Academic Press Elsevier Science, 2012) Litwack, G.; Eyigör, Özhan; Minbay, Zehra; Kafa, İlker Mustafa; Uludağ Üniversitesi/Tıp Fakültesi/Histoloji ve Embriyoloji Anabilim Dalı.; Uludağ Üniversitesi/Tıp Fakültesi/Anatomi Anabilim Dalı.; 0000-0001-5757-8450; 0000-0003-3463-7483; ABE-5128-2020; AAG-7125-2021; ABC-1475-2020; 6603109907; 8220935200; 8450193200Orexin neurons are localized in the lateral hypothalamus and regulate many functions including sleep wake states. Substantial number of neurotransmitters and neuromodulators has been proposed to influence orexinergic system. Glutamate, as the major excitatory amino acid neurotransmitter in the hypothalamus, was shown to mediate orexin neurons in the regulation of wakefulness and feeding. Glutamate is readily present in the Lateral hypothalamus, and glutamate receptors are expressed by the neurons of this region. Glutamate agonists initiate excitatory postsynaptic currents in orexin neurons, and this can be blocked by specific antagonists of the glutamate receptors. It is reported that both NMDA and non-NMDA receptors contribute the glutamatergic neurotransmission which affects orexinergic functions. Glutamatergic axon terminals are demonstrated to make contacts with the orexin neurons, as revealed by the presence of vesicular glutamate transporter proteins in the terminals, and these contacts were ultrastructurally confirmed to establish synapses on orexin neurons. This chapter reviews the literature on the glutamatergic regulation of orexin neurons including the data from our laboratory.Item Immunohistochemical evidence for glutamatergic regulation of nesfatin-1 neurons in the rat hypothalamus(MDPI, 2020-09-07) Serter Kocaoğlu, Sema; Gök, Duygu Yurtseven; Minbay, Zehra; Ezigör, Özhan; Bursa Uludağ Üniversitesi/Tıp Fakültesi/Histoloji ve Embriyoloji Anabilim Dalı.; 0000-0001-5757-8450; 0000-0003-3463-7483; ABE-5128-2020; ABC-1475-2020; AAW-4867-2021; 57193760779; 8220935200; 6603109907Nesfatin-1, identified as an anorexigenic peptide, regulates the energy metabolism by suppressing food intake. The majority of nesfatin-1-synthesizing neurons are concentrated in various hypothalamic nuclei, especially in the supraoptic (SON), arcuate (ARC) and paraventricular nuclei (PVN). We tested the hypothesis that the glutamatergic system regulates nesfatin-1 neurons through glutamate receptors. Therefore, the first aim of the proposed studies was to examine effects of different glutamate agonists in the activation of nesfatin-1 neurons using c-Fos double immunohistochemical labeling. Experimental groups were formed containing male and female rats which received intraperitoneal injections of glutamate agonists kainic acid, alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-D-aspartate (NMDA) while the control rats received vehicle. The significant increase in the number of c-Fos-expressing nesfatin-1 neurons after agonist injections were observed both in female and male subjects and some of these effects were found to be sexually dimorphic. In addition, treatment with specific glutamate antagonists 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) or dizocilpine (MK-801) before each of the three agonist injections caused a statistically significant reduction in the number of activated nesfatin-1 neurons in the hypothalamic nuclei including supraoptic, paraventricular and arcuate nuclei. The second aim of the study was to determine the expression of glutamate receptor subunit proteins in the nesfatin-1 neurons by using a double immunofluorescence technique. The results showed that the glutamate receptor subunits, which may form homomeric or heteromeric functional receptor channels, were expressed in the nesfatin-1 neurons. In conclusion, the results of this study suggest that nesfatin-1 neurons respond to glutamatergic signals in the form of neuronal activation and that the glutamate receptors that are synthesized by nesfatin-1 neurons may participate in the glutamatergic regulation of these neurons.Item Neuroprotective effects of uridine in a rat model of neonatal hypoxic-ischemic encephalopathy(Elsevier Ireland, 2013-05) Cansev, Mehmet; Minbay, Zehra; Gören, Bülent; Yaylagül, Esra Örenlili; Çetinkaya, Merih; Köksal, Nilgün; Alkan, Tülin; Uludağ Üniversitesi/Fen-Edebiyat Fakültesi/Biyoloji Bölümü.; Uludağ Üniversitesi/Tıp Fakültesi/Histoloji ve Embriyoloji Anabilim Dalı.; Uludağ Üniversitesi/Tıp Fakültesi/Fizyoloji Bölümü.; Uludağ Üniversitesi/Tıp Fakültesi/Farmakoloji Anabilim Dalı.; Uludağ Üniversitesi/Tıp Fakültesi/Neonatoloji Anabilim Dalı.; 0000-0001-6466-5042; 0000-0002-5206-1185; 0000-0002-5206-1185; 0000-0001-5757-8450; AAH-1792-2021; AAH-1718-2021; ABC-1475-2020; AAG-8393-2021; V-4209-2018; M-9071-2019; ABH-4915-2020; 8872816100; 8220935200; 6602543716; 55618956600; 23994946300; 7003323615; 6601953747Neonatal hypoxic ischemic encephalopathy (HIE) is a major cause of neurological disability requiring newer therapeutic strategies. Uridine is the principal circulating pyrimidine in humans and a substrate for nucleotides and membrane phospholipids. The objective of this study was to investigate the effects of uridine in a neonatal rat model of HIE. Rat pups subjected to hypoxic ischemic insult on postnatal day 7 were injected intraperitoneally with either saline or uridine (100, 300 or 500 mg/kg) for three consecutive days and brains were collected for evaluation of brain infarct volume and apoptosis. Compared with Control group, uridine at 300 and 500 mg/kg doses significantly reduced percent infarct volume, TUNEL(+) cell ratio and active Caspase-3 immunoreactivity in the cortex, as well as in CA1 and CA3 regions of the hippocampus. Uridine (300 and 500 mg/kg) also decreased active Caspase-3 expression in the ipsilateral hemisphere. These data indicate that uridine dose-dependently reduces brain injury in a rat model of neonatal HIE by decreasing apoptosis.