Neuropeptide Y attenuates anxiety- and depression-like effects of cholecystokinin-4 in mice

Desai, Sumit; Borkar, Chandrashekhar D.; Nakhate, Kartik T.; Subhedar, Nishikant K.; Kokare, Dadasaheb M.

doi:10.1016/j.neuroscience.2014.07.062

Cited by 39 publications

(25 citation statements)

References 70 publications

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“…Animal studies suggest that lower NPY levels are associated with depressive, anxiety‐like, and PTSD symptoms (Cohen et al, ; Miragaia et al, ). And, some pro‐depressant agents cause a drop in NPY (Desai, Borkar, Nakhate, Subhedar, & Kokare, ), which in turn is increased by antidepressants (Kotagale, Paliwal, Aglawe, Umekar, & Taksande, ). Of note, behavioral resilience and protective qualities to stress are strongly attributed to NPY in animal models of PTSD (Cohen et al, ; Cohen, Vainer, Zeev, Zohar, & Mathé, ).…”

Section: Discussionmentioning

confidence: 99%

Neuropeptide Y in PTSD, MDD, and chronic stress: A systematic review and meta‐analysis

Tural

Iosifescu

2020

J of Neuroscience Research

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Previous studies have suggested that neuropeptide Y (NPY) levels may be altered in patients with major depressive disorder (MDD), post‐traumatic stress disorder (PTSD) and chronic stress. We investigated, through systematic review and meta‐analysis, whether the mean levels of NPY are significantly different in patients with MDD, PTSD or chronic stress, compared to controls. The main outcome was the pooled standardized mean difference (SMD) with 95% confidence intervals between cases and controls, using the random‐effects model. Heterogeneity and publication bias were evaluated. Thirty‐five studies met eligibility criteria. Meta‐regression determined that medication and sex could explain 27% of the between‐study variance. Females and participants currently prescribed psychotropic medications had significantly higher levels of NPY. NPY levels were significantly lower in plasma and cerebrospinal fluid (CSF) in PTSD patients versus controls. Patients with MDD had significantly lower levels of NPY in plasma compared to controls, but not in the CSF. The magnitudes of the decrease in plasma NPY levels were not significantly different between PTSD and MDD. However, chronic stress patients had significantly higher plasma NPY levels compared to controls, PTSD or MDD. Our findings may imply a shared role of NPY in trauma and depression: nevertheless, it is not clear that the association is specific to these disorders. Psychotropic medications may help restore NPY levels. Further controlled studies are needed to better delineate the contribution of confounding variables such as type of depression, body mass index, appetite or sleep architecture.

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Section: Discussionmentioning

confidence: 99%

Neuropeptide Y in PTSD, MDD, and chronic stress: A systematic review and meta‐analysis

Tural

Iosifescu

2020

J of Neuroscience Research

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“…A reduction of the central NPY level and/or function was observed in experimental and clinical depression (Caberlotto et al 1999; Caberlotto and Hurd 1999), whereas central administration of NPY or Y1R agonist [Leu 31 ,Pro 34 ]-PYY produced antidepressant-like effects in rats and mice (Stogner and Holmes 2000; Redrobe et al 2002; Ishida et al 2007; Morales-Medina et al 2012a; Desai et al 2014); moreover, these effects were blocked by Y1R antagonists (Redrobe et al 2002; Ishida et al 2007; Desai et al 2014). On the other hand, antidepressant-like activity of antagonists of Y2 and Y5 receptors was also observed (Walker et al 2009; Packiarajan et al 2011; Morales-Medina et al 2012a, 2012b).…”

Section: Discussionmentioning

confidence: 99%

“…All these receptor subtypes mediate the NPY’s biological responses via the G αi signaling pathway (Michel 1991; Dumont et al 1992). There are a number of data indicating that NPY and its receptor ligands produced antidepressant-like effects in animal models of depression (Stogner and Holmes 2000; Redrobe et al 2002; Ishida et al 2007; Walker et al 2009; Packiarajan et al 2011; Morales-Medina et al 2012b; Desai et al 2014). Furthermore, significant changes in NPY-like immunoreactivity (NPY-ir) were observed not only in animal models of depressive disorders (Jiménez-Vasquez et al, 2000a,2000b; Wu et al 2011) but also in depressed patients who presented reduced levels of NPY in the cerebrospinal fluid and plasma in several studies (Widerlöv et al 1988; Westrin et al 1999; Heilig et al 2004; Soleimani et al 2014).…”

Section: Introductionmentioning

confidence: 99%

Antidepressant-like activity of the neuropeptide Y Y5 receptor antagonist Lu AA33810: behavioral, molecular, and immunohistochemical evidence

et al. 2016

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RationaleIt has recently been found that chronic treatment with the highly selective, brain-penetrating Y5 receptor antagonist, Lu AA33810 [N-[[trans-4-[(4,5-dihydro [1] benzothiepino[5,4-d] thiazol-2-yl) amino] cyclohexyl]methyl]-methanesulfonamide], produces antidepressant-like effects in the rat chronic mild stress model.ObjectiveIn the present study, we investigated the possible antidepressant-like activity of Lu AA33810 in rats subjected to glial ablation in the prefrontal cortex (PFC) by the gliotoxin L-AAA, which is an astroglial degeneration model of depression.ResultsWe observed that Lu AA33810 administered intraperitoneally at a single dose of 10 mg/kg both reversed depressive-like behavioral changes in the forced swim test (FST) and prevented degeneration of astrocytes in the mPFC. The mechanism of antidepressant and glioprotective effects of Lu AA33810 has not been studied, so far. We demonstrated the contribution of the noradrenergic rather than the serotonergic pathway to the antidepressant-like action of Lu AA33810 in the FST. Moreover, we found that antidepressant-like effect of Lu AA33810 was connected with the influence on brain-derived neurotrophic factor (BDNF) protein expression. We also demonstrated the antidepressant-like effect of Lu AA33810 in the FST in rats which did not receive the gliotoxin. We found that intracerebroventricular injection of the selective MAPK/ERK inhibitor U0126 (5 μg/2 μl) and the selective PI3K inhibitor LY294002 (10 nmol/2 μl) significantly inhibited the anti-immobility effect of Lu AA33810 in the FST in rats, suggesting that MAPK/ERK and PI3K signaling pathways could be involved in the antidepressant-like effect of Lu AA33810.ConclusionOur results indicate that Lu AA33810 exerts an antidepressant-like effect and suggest the Y5 receptors as a promising target for antidepressant therapy.

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“…The role of CCK in emotional behaviors is seen primarily through the activation of the CCK 2 receptors in limbic regions, mainly the basolateral amygdala and, to some extent, cortical areas and the hippocampus. Both human and rodents studies indicate a positive correlation of CCK levels and increased anxiety-like behavior [273][274][275]. Moreover, systemic administration of CCK-8 elevated the levels of brain-derived neurotrophic factor in the rat hippocampus, suggesting a neuroplasticity-related effect mediated by CCK [276].…”

Section: Gut Microbiota and Cck: Relevance To Anxiety And Depressionmentioning

confidence: 99%

Anxiety, Depression, and the Microbiome: A Role for Gut Peptides

et al. 2018

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The complex bidirectional communication between the gut and the brain is finely orchestrated by different systems, including the endocrine, immune, autonomic, and enteric nervous systems. Moreover, increasing evidence supports the role of the microbiome and microbiota-derived molecules in regulating such interactions; however, the mechanisms underpinning such effects are only beginning to be resolved. Microbiota-gut peptide interactions are poised to be of great significance in the regulation of gut-brain signaling. Given the emerging role of the gut-brain axis in a variety of brain disorders, such as anxiety and depression, it is important to understand the contribution of bidirectional interactions between peptide hormones released from the gut and intestinal bacteria in the context of this axis. Indeed, the gastrointestinal tract is the largest endocrine organ in mammals, secreting dozens of different signaling molecules, including peptides. Gut peptides in the systemic circulation can bind cognate receptors on immune cells and vagus nerve terminals thereby enabling indirect gut-brain communication. Gut peptide concentrations are not only modulated by enteric microbiota signals, but also vary according to the composition of the intestinal microbiota. In this review, we will discuss the gut microbiota as a regulator of anxiety and depression, and explore the role of gut-derived peptides as signaling molecules in microbiome-gut-brain communication. Here, we summarize the potential interactions of the microbiota with gut hormones and endocrine peptides, including neuropeptide Y, peptide YY, pancreatic polypeptide, cholecystokinin, glucagon-like peptide, corticotropin-releasing factor, oxytocin, and ghrelin in microbiome-to-brain signaling. Together, gut peptides are important regulators of microbiota-gut-brain signaling in health and stress-related psychiatric illnesses.

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Neuropeptide Y attenuates anxiety- and depression-like effects of cholecystokinin-4 in mice

Cited by 39 publications

References 70 publications

Neuropeptide Y in PTSD, MDD, and chronic stress: A systematic review and meta‐analysis

Neuropeptide Y in PTSD, MDD, and chronic stress: A systematic review and meta‐analysis

Antidepressant-like activity of the neuropeptide Y Y5 receptor antagonist Lu AA33810: behavioral, molecular, and immunohistochemical evidence

Anxiety, Depression, and the Microbiome: A Role for Gut Peptides

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