Cross talk about the role of Neuropeptide Y in CNS disorders and diseases

Bale, Rajeshwari; Doshi, Gaurav

doi:10.1016/j.npep.2023.102388

Cited by 5 publications

(2 citation statements)

References 291 publications

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“…In animal models of depression, decreased expression of NPY in the HIPP and hypothalamus [159] and reduced levels of NPY in the HIPP [160] have been observed. Furthermore, it was concluded that low NPY concentrations lead to depression, and certain antidepressants seem to increase NPY levels [161].…”

Section: Neuropeptide Ymentioning

confidence: 99%

Understanding the Biological Relationship between Migraine and Depression

Viudez-Martínez,

Torregrosa,

Navarrete

et al. 2024

Biomolecules

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Migraine is a highly prevalent neurological disorder. Among the risk factors identified, psychiatric comorbidities, such as depression, seem to play an important role in its onset and clinical course. Patients with migraine are 2.5 times more likely to develop a depressive disorder; this risk becomes even higher in patients suffering from chronic migraine or migraine with aura. This relationship is bidirectional, since depression also predicts an earlier/worse onset of migraine, increasing the risk of migraine chronicity and, consequently, requiring a higher healthcare expenditure compared to migraine alone. All these data suggest that migraine and depression may share overlapping biological mechanisms. Herein, this review explores this topic in further detail: firstly, by introducing the common epidemiological and risk factors for this comorbidity; secondly, by focusing on providing the cumulative evidence of common biological aspects, with a particular emphasis on the serotoninergic system, neuropeptides such as calcitonin-gene-related peptide (CGRP), pituitary adenylate cyclase-activating polypeptide (PACAP), substance P, neuropeptide Y and orexins, sexual hormones, and the immune system; lastly, by remarking on the future challenges required to elucidate the etiopathological mechanisms of migraine and depression and providing updated information regarding new key targets for the pharmacological treatment of these clinical entities.

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Section: Neuropeptide Ymentioning

confidence: 99%

Understanding the Biological Relationship between Migraine and Depression

Viudez-Martínez,

Torregrosa,

Navarrete

et al. 2024

Biomolecules

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“…NPY is reduced in CSF of patients with post-traumatic stress disorder (PTSD) (Sah et al, 2014) and brain tissue of rodent models of PTSD (Cohen et al, 2012). NPY also has anti-depressive properties (Andriushchenko et al, 2022;Redrobe et al, 2002bRedrobe et al, , 2002a, and lower NPY levels are found in patients with major depressive disorder (Bale and Doshi, 2023;Guilloux et al, 2012;Hashimoto et al, 1996;Tural and Iosifescu, 2020) and in rodent models of depression (Heilig, 2004;Jiménez-Vasquez et al, 2007, 2000. Multiple antidepressant treatments have been shown to increase NPY levels in rodent models (Bjørnebekk et al, 2010;Husum and Mathé, 2002;Jiménez-Vasquez et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Modulation of Temporoammonic-CA1 Synapses by Neuropeptide Y is Through Y1 Receptors

Cortes,

Bartley,

et al. 2024

Preprint

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The reduction of neuropeptide Y (NPY), an abundant neuromodulator in the brain, has been implicated in multiple neuropsychiatric disorders, such as depression and post-traumatic stress disorder (PTSD). The CA1 region of hippocampus is an important area for anxiety and highly expresses NPY. Injection of NPY into the CA1 is anxiolytic and has been shown to alleviate behavioral symptoms in a model of traumatic stress. It is known that activation of NPY Y1 receptors has anxiolytic effects and that NPY's anxiolytic effects in CA1 are blocked by an NPY Y1 receptor antagonist. However, the location of Y1 receptors mediating NPY's anxiolytic effects in CA1 is not yet known. CA1 receives inputs from entorhinal cortex through the temporammonic pathway (TA), which has been shown to be important for fear learning and sensitive to stress. Our lab previously showed that NPY reduces TA-evoked synaptic responses, however, the subtype of NPY receptor mediating this effect is not yet known. In this study, we show that Y1 receptors mediate the effects of both exogenous (bath-applied) and endogenously- released NPY in the TA pathway. This is the first demonstration of a Y1 receptor-mediated effect on synaptic function in CA1. Interestingly, chronic cell-type specific overexpression of NPY impairs the sensitivity of the TA pathway to NPY and the Y1 receptor agonist. However, the effect of NPY in the Schaffer collateral (SC) pathway, which is mediate by NPY Y2 receptors, is unaffected by NPY overexpression. There are pathway-specific differences in NPY receptors that modulate NPY's effects in CA1 and respond differently to NPY overexpression. Our results demonstrating that NPY acts at Y1 receptors in the TA pathway are consistent with the idea that the TA pathway underlies the anxiolytic effects of NPY in CA1.

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The role of NPY signaling pathway in diagnosis, prognosis and treatment of stroke

Jiang,

Zheng,

et al. 2024

Neuropeptides

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Cross talk about the role of Neuropeptide Y in CNS disorders and diseases

Cited by 5 publications

References 291 publications

Understanding the Biological Relationship between Migraine and Depression

Understanding the Biological Relationship between Migraine and Depression

Modulation of Temporoammonic-CA1 Synapses by Neuropeptide Y is Through Y1 Receptors

The role of NPY signaling pathway in diagnosis, prognosis and treatment of stroke

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