Assessment of the activation of nesfatin-1 and neuronostatin neurons and the effect of glutamatergic system in different stress models by histological techniques

In this study, the perception mechanisms of the nesfatin-1 and neuronostatin neurons that suppress nutrient intake for stress signals, the possible activating effect of stress on these neurons and the role of the glutamatergic system in this activation were investigated. In order to demonstrate the perception of stress-related signals, glucocotricoid (GR), mineralocorticoid (MR) and corticotrophin-releasing factor receptor (CRFR) proteins were evaluated and corticotropin-releasing factor expressions were evaluated in nerve endings on neurons. The results of these studies showed that the nesfatin-1 neurons express GR and MR proteins in order to receive peripheral stress signals. It was also demonstrated that the nesfatin-1 neurons possess CRF receptors. Neuronostatin neurons express only GR protein. The effect of different types of stress applications (immobilization, swimming forced stress, acute inflammatory stres) on nesfatin-1 and neuronostatin neurons was investigated by dual immunohistochemical staining, it was found that after immobilization and swimming stress, activation of nesfatin-1 neurons in paraventricular and arcuate nuclei increased significantly but there was no change in neuronostatin neurons. In addition, inflammatory stress effected the activation of the nesfatin-1 neurons only localized in the supraoptic nuclei. The effectiveness of the glutamatergic system in stress-induced activation was examined in subjects treated with pre-stress glutamate receptor antagonists and showed that its activation was significantly suppressed. It is suggested that the glutamatergic system and the glutamate receptors play a role in the activation of nesfatin-1 neurons after receiving stress signals and that the higher centers in the brain which use the glutamate as a neurotransmitter participate in this regulatory mechanism. In conclusion in this study we were able to determine that, the neurons which suppress the food intake synthesize the receptor proteins in order to receive the peripheral stress signals, nesfatin-1 neurons can participate in the attenuation of food intake during stress and the glutamatergic system plays an important role in the activation of nesfatin-1 neurons following acute stress. It is suggested that these new findings will shed light on planning clinical studies in order to understand the molecular mechanisms of the eating disorders during stress as well as the treatment of such disorders.