Neuropeptide Y modulates the antidepressant activity of imipramine in olfactory bulbectomized rats: Involvement of NPY Y1 receptors

Goyal, Sameer N.; Upadhya, Manoj A.; Kokare, Dadasaheb M.; Bhisikar, Snehal M.; Subhedar, Nishikant K.

doi:10.1016/j.brainres.2009.02.033

Cited by 31 publications

(16 citation statements)

References 69 publications

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“…Intracerebral infusion of the Y1R agonist [Leu 31 Pro 34 ]PYY, or NPY, 30 min before the test significantly increased time mice spent swimming compared to controls (Redrobe et al, 2002). Administration of [Leu 31 Pro 34 ]NPY in olfactory bulbectomized rat model of depression reduced depressive related features in open field test (Goyal et al, 2009). Moreover, Y1R deficient mice (−/−) displayed greater immobility time in FST than the +/+ wild type controls (Karlsson et al, 2008) confirming the importance of the Y1R.…”

Section: Discussionmentioning

confidence: 99%

“…In these animals, hippocampal and hypothalamic Y1 receptor mRNA levels were lower and Y1 receptor binding higher than in the control Flinders Resistant Line (Jiménez-Vasquez et al, 2007). The beneficial effect of NPY was also observed in the acute model of depression, likely mediated by the Y1 receptors (Redrobe et al, 2002; Goyal et al, 2009). Moreover, antidepressant like effects of agmatine occur via the NPYergic system and probably by stimulation of the Y1 receptor subtype (Kotagale et al, 2013).…”

Section: Introductionmentioning

confidence: 93%

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NPY1 Receptor Agonist Modulates Development of Depressive-Like Behavior and Gene Expression in Hypothalamus in SPS Rodent PTSD Model

2017

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Delivery of neuropeptide Y (NPY) to the brain by intranasal infusion soon after traumatic stress has shown therapeutic potential, and prevented development of many behavioral and neuroendocrine impairments in the single prolonged stress (SPS) animal model of PTSD. Therefore, we examined whether the Y1R preferring agonist [Leu31Pro34]NPY is sufficient to prevent development of SPS induced depressive-like behavioral changes, and hypothalamic gene expression as obtained with intranasal NPY intervention. Male Sprague-Dawely rats were given intranasal infusion of either NPY (150 μg/rat), a low (68 μg /rat), or high (132 μg/rat) dose of [Leu31Pro34]NPY or vehicle immediately following the last SPS stressor, left undisturbed for 1 week and then tested for depressive-like behavior together with naïve unstressed controls. Vehicle treated animals had elevated immobility forced swim test (FST) and reduced sucrose preference, which were not observed in animals given NPY or the higher dose of [Leu31Pro34]NPY. This dose of [Leu31Pro34]NPY, like NPY, also prevented the SPS-elicited induction of CRF mRNA in the mediobasal hypothalamus. However, [Leu31Pro34]NPY did not prevent, but rather enhanced, the SPS-triggered induction of GR and FKBP5 mRNA levels in the mediobasal hypothalamus. Thus, [Leu31Pro34]NPY may be as effective as NPY and displays therapeutic potential for preventing development of depressive-like behaviors and dysregulation of the CRF/HPA system in PTSD. However, due to its different effects compared to NPY on GR and FKBP5 a broader agonist, such as NPY, may be more desirable.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 93%

NPY1 Receptor Agonist Modulates Development of Depressive-Like Behavior and Gene Expression in Hypothalamus in SPS Rodent PTSD Model

2017

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“…Among them, neuropeptide Y (NPY) is a small peptide widely distributed throughout the brain, where it serves as a neurotransmitter and/or a modulator of several neuroendocrine functions, including cardiovascular physiology and feeding behavior [3] . Moreover, in animal models, NPY produces behavioral effects that are similar to those induced by anxiolytics [4] , antiepileptics [5] and antidepressants [6] , suggesting that its role in the CNS neurons is multifunctional.…”

Section: I S E a S E Smentioning

confidence: 98%

Neuroprotective Effect of Neuropeptide Y against Beta-Amyloid 25–35 Toxicity in SH-SY5Y Neuroblastoma Cells Is Associated with Increased Neurotrophin Production

Croce

Dinallo²,

Ricci

et al. 2011

Neurodegener Dis

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Background: In the central nervous system, several neuropeptides are believed to be involved in the pathophysiology of Alzheimer’s disease (AD). Among them, neuropeptide Y (NPY) is a small peptide widely distributed throughout the brain, where it serves as a neurotransmitter and/or a modulator of several neuroendocrine functions. More recently, NPY has generated interest because of its role in neuroprotection against excitotoxicity and modulation of neurogenesis. Interestingly, these effects are also influenced by neurotrophins, critical molecules for the function and survival of neurons that degenerate in AD. Objective: Our purpose was to investigate whether NPY might be a neuroprotective agent in AD and whether neurotrophins are involved in NPY-induced neuroprotection. Methods: To test this hypothesis, we exposed the SH-SY5Y neuroblastoma cell line to toxic concentrations of β-amyloid (Aβ) peptide fragment 25–35 (Aβ_25–35) and measured cell survival and neurotrophin expression before and after a preincubation with NPY in the growth medium. Results: Our results demonstrated that preincubation with NPY prevented cell loss due to the toxic effect of Aβ_25–35. Moreover, while intracellular production of nerve growth factor and brain-derived neurotrophic factor were reduced by Aβ, NPY restored or even increased neurotrophin protein and mRNA in SH-SY5Y cells. Conclusion: In conclusion, this study demonstrates that NPY increases the survival of SH-SY5Y neuroblastoma cells and counteracts the toxic effect of Aβ. In addition, NPY restores the neurotrophin levels in these cells. Although preliminary, these observations might be useful to understand the pathology of Alzheimer’s and/or develop new therapeutic strategies.

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“…Taken together, these studies suggest that anxiolytic-like effects of NPY are mediated via Y1 receptors. It seems that NPY, acting via NPY-Y1 receptors, may modulate the noradrenergic and serotonergic systems and influence cortical and limbic functions (Goyal et al, 2009).…”

Section: Introductonmentioning

confidence: 99%

The Neuropeptide Y (NPY)-ergic System is Associated with Behavioral Resilience to Stress Exposure in an Animal Model of Post-Traumatic Stress Disorder

Cohen

Liu

Kozlovsky

et al. 2011

Neuropsychopharmacol

243

190

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Converging evidence implicates the regulatory neuropeptide Y (NPY) in anxiety-and depression-related behaviors. The present study sought to assess whether there is an association between the magnitude of behavioral responses to stress and patterns of NPY in selected brain areas, and subsequently, whether pharmacological manipulations of NPY levels affect behavior in an animal model of PTSD. Animals were exposed to predator-scent stress for 15 min. Behaviors were assessed with the elevated plus maze and acoustic startle response tests 7 days later. Preset cutoff criteria classified exposed animals according to their individual behavioral responses. NPY protein levels were assessed in specific brain regions 8 days after the exposure. The behavioral effects of NPY agonist, NPY-Y1-receptor antagonist, or placebo administered centrally 1 h post-exposure were evaluated in the same manner. Immunohistochemical technique was used to detect the expression of the NPY, NPY-Y1 receptor, brain-derived neurotrophic factor, and GR 1 day after the behavioral tests. Animals whose behavior was extremely disrupted (EBR) selectively displayed significant downregulation of NPY in the hippocampus, periaqueductal gray, and amygdala, compared with animals whose behavior was minimally (MBR) or partially (PBR) disrupted, and with unexposed controls. One-hour post-exposure treatment with NPY significantly reduced prevalence rates of EBR and reduced trauma-cue freezing responses, compared with vehicle controls. The distinctive pattern of NPY downregulation that correlated with EBR as well as the resounding behavioral effects of pharmacological manipulation of NPY indicates an intimate association between NPY and behavioral responses to stress, and potentially between molecular and psychopathological processes, which underlie the observed changes in behavior. The protective qualities attributed to NPY are supported by the extreme reduction of its expression in animals severely affected by the stressor and imply a role in promoting resilience and/or recovery.

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Neuropeptide Y modulates the antidepressant activity of imipramine in olfactory bulbectomized rats: Involvement of NPY Y1 receptors

Cited by 31 publications

References 69 publications

NPY1 Receptor Agonist Modulates Development of Depressive-Like Behavior and Gene Expression in Hypothalamus in SPS Rodent PTSD Model

NPY1 Receptor Agonist Modulates Development of Depressive-Like Behavior and Gene Expression in Hypothalamus in SPS Rodent PTSD Model

Neuroprotective Effect of Neuropeptide Y against Beta-Amyloid 25–35 Toxicity in SH-SY5Y Neuroblastoma Cells Is Associated with Increased Neurotrophin Production

The Neuropeptide Y (NPY)-ergic System is Associated with Behavioral Resilience to Stress Exposure in an Animal Model of Post-Traumatic Stress Disorder

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