Publication:
Immunohistochemical determination of the excitatory and inhibitory axonal endings contacting nucb2/nesfatin-1 neurons

dc.contributor.buuauthorGÖK YURTSEVEN, DUYGU
dc.contributor.buuauthorAghayeva, Aynura
dc.contributor.buuauthorHASANOĞLU AKBULUT, NURSEL
dc.contributor.buuauthorAkbulut, Nursel Hasanoglu
dc.contributor.buuauthorEyigör, Özhan
dc.contributor.buuauthorEYİGÖR, ÖZHAN
dc.contributor.departmentBursa Uludağ Üniversitesi/Tıp Fakültesi/Histoloji ve Embriyoloji Anabilim Dalı.
dc.date.accessioned2024-09-25T06:06:56Z
dc.date.available2024-09-25T06:06:56Z
dc.date.issued2023-12-28
dc.description.abstractNesfatin-1 is an anorexigenic peptide suppressing food intake and is synthesized and secreted by neurons located in the hypothalamus. Our study was aimed to demonstrate the effect of excitatory and inhibitory neurotransmitters on NUCB2/nesfatin-1 neurons. In this context, dual peroxidase immunohistochemistry staining was performed using NUCB2/nesfatin-1 primary antibody with each of the primary antibodies of vesicular transporter proteins applied as markers for neurons using glutamate, acetylcholine, and GABA as neurotransmitters. In double labeling applied on floating sections, the NUCB2/nesfatin-1 reaction was determined in brown color with diaminobenzidine, while vesicular carrier proteins were marked in black. Slides were analyzed to determine the ratio of nesfatin-1 neurons in the three hypothalamic nucleus in contact with a relevant vesicular carrier protein. The ratios of NUCB2/nesfatin-1 neurons with the innervation were compared among neurotransmitters. In addition, possible gender differences between males and females were examined. The difference in the number of VGLUT2-contacting NUCB2/nesfatin-1 neurons was significantly higher in males when compared to females. When both genders were compared in different nuclei, it was seen that there was no statistical significance in terms of the percentage of NUCB2/nesfatin-1 neuron apposition with VGLUT3. The statistical evaluation showed that number of NUCB2/nesfatin-1 neurons receiving GABAergic innervation is higher in males when compared to females (*p <= 0.05; p = 0.045). When the axonal contact of vesicular neurotransmitter transporter proteins was compared between the neurotransmitters, it was determined that the most prominent innervation is GABAergic. In the supraoptic region, no contacts of VAChT-containing axons were found on NUCB2/nesfatin-1 neurons in both female and male subjects. In conclusion, it is understood that both excitatory and inhibitory neurons can innervate the NUCB2/nesfatin-1 neurons and the glutamatergic system is effective in the excitatory innervation while the GABAergic system plays a role in the inhibitory mechanism.
dc.identifier.doi10.1016/j.npep.2023.102401
dc.identifier.issn0143-4179
dc.identifier.urihttps://doi.org/10.1016/j.npep.2023.102401
dc.identifier.urihttps://hdl.handle.net/11452/45182
dc.identifier.volume103
dc.identifier.wos001166190000001
dc.indexed.wosWOS.SCI
dc.language.isoen
dc.publisherElsevier
dc.relation.bapTTU-2021-376
dc.relation.journalNeuropeptides
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectSubunit messenger-rnas
dc.subjectParaventricular nucleus
dc.subjectImmunoreactive neurons
dc.subjectFood-intake
dc.subjectNesfatin-1
dc.subjectGlutamate
dc.subjectReceptor
dc.subjectAnxiety
dc.subjectOxytocin
dc.subjectVasopressin
dc.subjectNesfatin-1
dc.subjectVesicular neurotransmitter transporter protein
dc.subjectHypothalamic nuclei
dc.subjectGaba
dc.subjectGlutamate
dc.subjectScience & technology
dc.subjectLife sciences & biomedicine
dc.subjectEndocrinology & metabolism
dc.subjectNeurosciences
dc.subjectNeurosciences & neurology
dc.titleImmunohistochemical determination of the excitatory and inhibitory axonal endings contacting nucb2/nesfatin-1 neurons
dc.typeArticle
dspace.entity.typePublication
relation.isAuthorOfPublicationcab61234-84e8-4496-8002-16427421ba6b
relation.isAuthorOfPublication57503bab-1719-45f6-a0e0-df41bd5cd569
relation.isAuthorOfPublication.latestForDiscoverycab61234-84e8-4496-8002-16427421ba6b

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