Hippocampal and Hypothalamic FBN1 Expression in an Experimental Opioid Addiction Rat Model


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Eroğlu C., Çimen Y. A. , Yıldız İ., Kurar E., Kutlu S.

4th International Congress of Turkish Neuroendocrinology Society, İstanbul, Turkey, 26 November - 28 December 2020, pp.39-40

  • Publication Type: Conference Paper / Summary Text
  • City: İstanbul
  • Country: Turkey
  • Page Numbers: pp.39-40

Abstract

Hippocampal and Hypothalamic FBN1 Expression in an Experimental Opioid Addiction Rat Model

Canan Eroglu Gunes1,2, Yasin Ali Cimen3, İbrahim Yildiz3, Ercan Kurar1,2, Selim Kutlu1,3

1Necmettin Erbakan University Neuroscience Research and Application Center (NENRC), Konya, Turkey 2Necmettin Erbakan University, Meram Faculty of Medicine, Department of Medical Biology, Konya, Turkey 3Necmettin Erbakan University, Meram Faculty of Medicine, Department of Physiology, Konya, Turkey AIM: FBN1 encodes a profibrillin and C-terminal cleavage product of this proprotein result in a fasting-induced protein hormone named Asprosin. FBN1 has critical roles in the formation of elastic fibers in connective tissues. Asprosin activates G protein-cAMP-PKA pathway and rapidly elevates serum glucose level. Asprosin can also cross blood-brain barrier and regulates hypothalamic neurons. In this study, hippocampal and hypothalamic FBN1 expression levels were investigated in an experimental opioid addiction rat model. METHODS: A total of 18 rats were randomly divided into three equal groups including control (C), morphine dependent (M) and morphine dependent+ naloxone (M+N). Experimental dependence was constituted via applying 10 mg/kg/day subcutaneous morphine injection for 7 days. M+N group received intraperitoneal 1 mg/kg naloxone 1.5 hour after morphine injections. All animals were evaluated for morphine withdrawal symptoms and compared with the other groups. Hippocampus and hypothalamus tissues were dissected and mRNA level expression of FBN1 was evaluated by using quantitative RT-PCR. RESULTS: Steady state FBN1 expressions were determined in both hippocampus and hypothalamus. Morphine treatment significantly decreased FBN1 expression in hippocampus (p<0.01). An insignificant downregulation was also observed in hypothalamus of morphine group. Naloxone treatment tends to upregulated FBN1 expression in both hippocampus and hypothalamus. However, a significant increase was determined in M+N group compared to hypothalamus of C (p<0.05) and M (p<0.01) groups. CONCLUSION: These findings suggest that asprosin and/or other possible active peptides derived from FBN1 transcript may have modulatory roles in hippocampal formation. Additionally, in morphine dependent rat, increased FBN1 levels in M+N group comparing to both control and morphine groups indicated that there is an important opioid tonic inhibition on FBN1 expression in hypothalamus.

Key words: Hypothalamus, hippocampus, opioid addiction, FBN1, asprosin.