CDP-Choline Activates NUCB2/Nesfatin-1 Neurons via Cholinergic Pathways

DOI :

Hasanoglu Akbulut N.; Topal G.; Coskun N. C.; Kafa I. M.; Savci V. & Eyigor O.

Summary

Nesfatin-1 is an anorexigenic peptide that, in addition to its inhibitory effect on food intake, also plays a role in cardiovascular regulation, energy homeostasis, and the regulation of stress responses. Exogenous administration of cytidine-5’-diphosphate choline (CDP-choline) produces several effects on cardiovascular and endocrine systems. A recent study has demonstrated that CDP- choline causes an increase in the peripheral levels of nesfatin-1 peptide. In this study, we aimed to investigate the activation-inducing effect of CDP-choline application on nesfatin-1 neuronsexpressed in the supraoptic nucleus (SON) of the hypothalamus and the role of the cholinergic antagonist atropine sulfate on this activation, using c-Fos immunohistochemistry as a marker of neuronal activation. The results were evaluated as the percentage of double-labeled (activated) nesfatin-1 neurons relative to all nesfatin-1 neurons. Compared to the control group, CDP-choline administration was found to activate a statistically significant number of NUCB2/nesfatin-1 neurons in the SON (p<0.001). It has been found that intracerebroventricular administration of atropine sulfate (ATR), a muscarinic acetylcholine receptor antagonist, prior to CDP-choline, significantly inhibits neuronal activation. These findings suggest that the effects of CDP- choline may be partially mediated through acetylcholine receptors, and that the cholinergic system plays a crucial role in regulating nesfatin-1 neurons. Furthermore, it has been proposed that CDP-choline may modulate food intake via a central mechanism at the hypothalamic level.

KEY WORDS: NUCB2/nesfatin-1; Neuronal activation; CDP-choline; SON.

How to cite this article

AKBULUT, N. H.; TOPAL, G.; COSKUN, N. C.; KAFA, I. M.; SAVCI, V. & EYIGOR O. CDP-choline activates NUCB2/nesfatin- 1 neurons via cholinergic pathways. Int. J. Morphol., 44(4):1509-1515, 2026.