Changes in neuropeptide Y protein expression following photothrombotic brain infarction and epileptogenesis

Kharlamov, Elena A.; Kharlamov, Alexander; Kelly, Kenneth G.

doi:10.1016/j.brainres.2006.09.107

Cited by 32 publications

(22 citation statements)

References 59 publications

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“…60) The NPY neurons in the arcuate nucleus project axons to orexin neurons in the LHA, 61,62) and the projections are involved in the regulation of feeding behavior 63,64) and arousal. 65) Although it remains unclear whether the projections of NPY neurons to the hypothalamus from the arcuate nucleus are related to the onset of an antidepressant-like effect, our previous study demonstrated that i.c.v.…”

Section: Discussionmentioning

confidence: 99%

Involvement of Neuropeptide Y Signaling in the Antidepressant-Like Effect and Hippocampal Cell Proliferation Induced by Kososan, a Kampo Medicine, in the Stress-Induced Depression-Like Model Mice

Ito

Hori

Yabe

et al. 2012

Biological & Pharmaceutical Bulletin

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Neuropeptide Y (NPY) and Orexin-A (OX-A1) Thus, NPY plays pivotal roles in a variety of physiological processes, including food intake, 2,3) gastrointestinal function, 4) circadian rhythm, 5) cognition, 6,7) seizure, 8) and anxiety. 9,10) Numerous studies also indicate that NPY could be involved in the pathogenesis of depression and in the effects of antidepressant therapies. In preclinical studies, hippocampal NPY levels have been decreased in animals exposed to chronic mild stress, 11) inescapable stress, 12) and maternal separation, 13,14) all of which are known as stress-based models of depression. Flinders Sensitive Line and Fawn Hooded rats, two genetic models of depression, also have significantly decreased hippocampal NPY levels compared to control rats. [15][16][17][18][19][20] In addition, it has been reported that the reduced hippocampal NPY levels in animal models of depression were restored by treatment with antidepressants, 12,15,21) electroconvulsive stimuli, [16][17][18][19] and running. 22) Moreover, additional evidence has shown that NPY per se exhibits antidepressantlike activity via the Y1 receptor [23][24][25][26] and promotes the proliferation of hippocampal neural progenitor cells.27-31) These findings suggest that the upregulation of hippocampal cell proliferation and neurogenesis, the downregulation of which is inversely associated with the pathology of depression, 32,33) could be required for NPY-induced antidepressant-like effects.In clinical studies, some reports have suggested that NPY levels in the cerebrospinal fluid are decreased in patients with major depression [34][35][36][37] and that the NPY levels are improved by electroconvulsive therapy 38) and treatment with an antidepressant. 39) Improvement in the dysfunction of the NPY system might alleviate some afflictions in patients with major depression.Similarly to NPY, several findings have indicated that orexin-A (OX-A), which is a neuropeptide produced especially in the lateral hypothalamic area (LHA), not only regulates food intake 40) but could be also involved in the pathology of depression. [41][42][43] Moreover, OX-A signaling is associated with the onset of antidepressant-like activity in mice. [44][45][46] These evidences suggest that NPY and OX-A could be key mediators in the pathology of depression and in antidepressant-like effects.Kososan, a Kampo (Japanese herbal) medicine (Xiang-Su-San in Chinese), is composed of five herbs (Cyperi Rhizoma, Perillae Herba, Aurantii Nobilis Pericarpium, Glycyrrhizae Radix, and Zingiberis Rhizoma) and is clinically applied in the treatment of depression-like symptoms associated with the initial stage of the common cold, anorexia, food-related allergic urticaria, irritable bowel syndrome, chronic fatigue syndrome, insomnia, and autonomic imbalance. It has been also clinically suggested that kososan can alleviate depression induced by interferon (IFN)-α therapy for hepatitis C. 47) Our previous studies using two animal models of depression, stress-and IFN-α-induced depressionlike mode...

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Section: Discussionmentioning

confidence: 99%

Involvement of Neuropeptide Y Signaling in the Antidepressant-Like Effect and Hippocampal Cell Proliferation Induced by Kososan, a Kampo Medicine, in the Stress-Induced Depression-Like Model Mice

Ito

Hori

Yabe

et al. 2012

Biological & Pharmaceutical Bulletin

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“…NPY-producing neurons are distributed not only in the arcuate nucleus, but also in the hippocampus (in interneurons of the hilus and in CA1-3 regions). 20) Several studies have also shown that the levels of NPY in the cerebrospinal fluid are decreased in patients with major depression, [21][22][23] that NPY exhibits an antidepressive-like activity via the Y1 receptor in vivo, 24) and that NPY exerts a proliferative activity in neural …”

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confidence: 99%

A Possible Mechanism Underlying an Antidepressive-Like Effect of Kososan, a Kampo Medicine, via the Hypothalamic Orexinergic System in the Stress-Induced Depression-Like Model Mice

Ito

Yabe

Nagai

et al. 2009

Biological & Pharmaceutical Bulletin

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Kososan, a Kampo (Japanese herbal) medicine (Xiang-SuSan in Chinese), is composed of five herbs (Cyperi Rhizoma, Perillae Herba, Aurantii Nobilis Pericarpium, Glycyrrhizae Radix, and Zingiberis Rhizoma) and is clinically used to treat the depression-like symptoms associated with the initial stage of the common cold, anorexia, food-related allergic urticaria, irritable bowel syndrome, chronic fatigue syndrome, insomnia, and autonomic imbalance. It has been also clinically suggested that kososan can alleviate the depression induced by interferon (IFN)-a therapy for hepatitis C. 1) Our previous studies using two animal models of depression, stress-and IFN-a-induced depression-like model mice, demonstrated that oral administration of kososan leads to an antidepressive-like effect via the normalization of the dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis, which is strongly associated with the pathogenesis of depression.2,3) These findings provide supporting evidence that kososan may be beneficial in the treatment of depression.Depressive disorder is thought to reflect maladaptive changes in stress-responsive systems.4) Numerous studies have reported that excessive exposure to stressful life events induces the onset of depression, which is accompanied by a decrease in neurogenesis in the dentate gyrus of the hippocampus. [5][6][7][8] Therefore, disruption of neurogenesis plays a crucial role in the mechanism by which stress facilitates depression.9,10) Furthermore, chronic treatment with antidepressants increases neurogenesis in the rat hippocampus 11) and adult hippocampal neurogenesis is required for the behavioral recovery effects of antidepressants.12) Thus, neurogenesis-inducing compounds may directly and/or indirectly produce antidepressive-like effects.Recent studies have reported that orexin-A (OX-A), which is a neuropeptide produced especially in the lateral hypothalamic area (LHA) and in the posterior hypothalamus, 13,14) is involved in the pathology of depression. A decrease in the number and size of OX-A-producing neurons in the LHA was observed in male Wistar-Kyoto rats, which exhibit a hyper-responsiveness of the HPA axis, a characteristic of depression. 15) Suicidal patients with major depression exhibit significantly lower OX-A levels in the cerebrospinal fluid when compared with patients who suffer from adjustment disorder and dysthymia.16) In addition, our previous study demonstrated that intracerebroventricular administration of OX-A induces an antidepressive-like effect via hippocampal cell proliferation in mice.17) The orexin receptor 1 (OXR1), which is a subtype of the orexin receptor, is expressed in the granule cell layer, hilus, and CA1-3 regions of the hippocampus.18) In addition, orexin-producing neurons also project to the hippocampus, in which neurogenesis occurs. Therefore, hippocampal neurogenesis may, at least in part, be regulated by a change in OX-A expression in the LHA. The neuropeptide Y (NPY) is implicated in the stimulation of feeding behavior 19) and its effect ...

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“…Additionally, NPY is a plasma biomarker that can indicate stroke, although its expression does not differ based on the type (ischemic vs. hemorrhagic) of stroke (19). Studies in animal models have demonstrated that NPY increases around brain lesions, and that administration of NPY following stroke increases infarct volume and decreases reperfusion (14,20). Therefore, NPY is an important contributor in stroke biology.…”

Section: Resultsmentioning

confidence: 99%

“…Because these diseases underlie the pathological changes leading to ischemic stroke, NPY itself may act as a risk factor for ischemic stroke. In fact, in animal models of cerebral infarction, NPY expression levels are increased in cortical and subcortical tissues around the lesions (14). Furthermore, Lee et al (15) reported that two polymorphisms in NPY, 4112C/T and 6411A/C, significantly increase the risk of ischemic stroke.…”

Section: Introductionmentioning

confidence: 99%

Neuropeptide Y Gene Promoter -399T/C Polymorphism Increases Risk of Ischemic Stroke

Fu¹,

Zhang²,

Wang³

et al. 2013

Balkan Med J

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Background: Several genetic factors underlying ischemic stroke have been identified. Variants of Neuropeptide Y (NPY), whose product plays diverse roles in modulating physiological functions, have been associated with an increased risk of ischemic stroke in South Korean individuals.Aims: We explored the association between a polymorphism in the NPY gene promoter at position -399 and the risk of ischemic stroke in Han Chinese.Study Design: Case-control study. Methods:The polymorphism -399T/C in the promoter of NPY was analysed in 500 patients with ischemic stroke and 500 healthy individuals by amplification and sequencing of this region. Non-conditional logistic regression was used to analyse association between genotypes and the risk of ischemic stroke.Results: Genotype and allele frequencies differed significantly between the ischemic stroke and control groups (P<0.05). Additionally, compared to stroke patients with the TT genotype, those with the CC genotype had a 1.7-times higher risk of ischemic stroke (OR=1.739, 95%CI=1.201-2.520, P=0.003), especially for those who were over 60 years old or male. Individuals with the TC genotype did not have an increased risk of ischemic stroke (P>0.05). Conclusion:The -399T/C polymorphism of the NPY gene is associated with ischemic stroke in Han Chinese individuals, and the CC genotype may be a risk factor for ischemic stroke.

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Changes in neuropeptide Y protein expression following photothrombotic brain infarction and epileptogenesis

Cited by 32 publications

References 59 publications

Involvement of Neuropeptide Y Signaling in the Antidepressant-Like Effect and Hippocampal Cell Proliferation Induced by Kososan, a Kampo Medicine, in the Stress-Induced Depression-Like Model Mice

Involvement of Neuropeptide Y Signaling in the Antidepressant-Like Effect and Hippocampal Cell Proliferation Induced by Kososan, a Kampo Medicine, in the Stress-Induced Depression-Like Model Mice

A Possible Mechanism Underlying an Antidepressive-Like Effect of Kososan, a Kampo Medicine, via the Hypothalamic Orexinergic System in the Stress-Induced Depression-Like Model Mice

Neuropeptide Y Gene Promoter -399T/C Polymorphism Increases Risk of Ischemic Stroke

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