Neuropeptide Y Distribution in the Rat Brain

Allen, Y.S.; Adrian, Thomas E.; Allen, J.M.; Tatemoto, Kazuhiko; Crow, T J; Bloom, S.R.; Polak, J.M.

doi:10.1126/science.6136091

Cited by 1,067 publications

(340 citation statements)

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“…[166][167][168] Moreover, by using the MC4-R/GFP mice line, we identified MC4-R-positive cells coexpressing Y1-R mRNA in these forebrain sites that receive both NPY and melanocortinergic inputs. 80,107,149,150 Consequently, relevant to current discussions, 15,23 we hypothesize that the convergence of leptin/melanocortin and NPY signaling pathways likely contributes to their counterpoised relationship in energy balance regulation (Figure 4). …”

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confidence: 93%

“…[146][147][148] NPY neurons are distributed in many CNS sites, including the Arc. 149,150 Importantly, NPY-producing Arc neurons coexpress AgRP and are inhibited by leptin. 66,68,69,97,98 Of NPY receptor subtypes, the Y1-, (Y1-R), Y2-, and Y5-receptors have been implicated in the regulation ), with permission).…”

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confidence: 99%

“…182 Clearly, however, more studies are required to better understand the relation between the NPY/Y1-R and reward systems, and that between these systems and alcoholism. Nonetheless, it has been demonstrated that the Acb receives NPY inputs 149,150 and expresses Y1-R mRNA in rodents. [166][167][168] Additionally, Y1-R mRNA is faintly expressed in the mouse VTA but not at all in the rat VTA.…”

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confidence: 99%

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Body weight is regulated by the brain: a link between feeding and emotion

2005

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Regulated energy homeostasis is fundamental for maintaining life. Unfortunately, this critical process is affected in a high number of mentally ill patients. Eating disorders such as anorexia nervosa are prevalent in modern societies. Impaired appetite and weight loss are common in patients with depression. In addition, the use of neuroleptics frequently produces obesity and diabetes mellitus. However, the neural mechanisms underlying the pathophysiology of these behavioral and metabolic conditions are largely unknown. In this review, we first concentrate on the established brain machinery of food intake and body weight, especially on the melanocortin and neuropeptide Y (NPY) systems as illustration. These systems play a critical role in receiving and processing critical peripheral metabolic cues such as leptin and ghrelin. It is also notable that both systems modulate emotion and motivated behavior as well. Secondly, we discuss the significance and potential promise of multidisciplinary molecular and neuroanatomic techniques that will likely increase the understanding of brain circuitries coordinating energy homeostasis and emotion. Finally, we introduce several lines of evidence suggesting a link between the melanocortin/NPY systems and several neurotransmitter systems on which many of the psychotropic agents exert their influence. Maintaining energy homeostasis is fundamental for survival. However, obesity due to over-nutrition is an increasing worldwide public health problem. 1 In psychiatric practice, on the other hand, impaired appetite is one of the crucial issues. Anorexia and weight loss are common, for example, in patients suffering from depression. Eating disorders are medically intractable and life threatening. In addition, the so-called 'atypical' antipsychotic agents, currently and widely used to treat psychoses, often induce hyperphagia, obesity, and diabetes mellitus. [2][3][4] In the past decade, fortunately, there has been remarkable progress in understanding the molecular mechanisms of food intake and body weight. This is due in large part to increased research activity towards combating the rising incidences of obesity and associated metabolic disorders. As a result, it is now established that the central nervous system (CNS) senses and processes peripheral metabolic cues including leptin 5 and ghrelin, 6,7 resulting in coordinated energy homeostasis. However, the pathophysiology of the disequilibrium between energy intake and expenditure in psychiatric disorders remains largely unknown. Nevertheless, evidence suggests that several CNS systems regulating energy balance may be dysregulated in patients with mental illnesses, for example, eating disorders, and drug addiction. [8][9][10][11][12][13][14] In the current review, we will illustrate the neuroanatomic and molecular genetic aspects of the melanocortin and neuropeptide Y (NPY) systems residing in the CNS downstream of leptin and ghrelin, to discuss the neural bases of feeding, metabolism, and emotion. Additionally, we point the reader to...

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Body weight is regulated by the brain: a link between feeding and emotion

2005

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“…Neuropeptide Y (NPY) is a 36-amino acid neuroactive peptide found in the cerebral cortex, hippocampus, hypothalamus, thalamus, amygdala, striatum, brainstem, and cerebellum (Allen et al, 1983;Dumont et al, 1993;Parker and Herzog, 1999;Wolak et al, 2003). NPY colocalizes with somatostatin, gamma-aminobutric acid (GABA), and nitric oxide synthase (Bidmon et al, 2001a;Kowianski et al, 2004;Kubota et al, 1994), and can modulate neuronal excitability by multiple pre-and postsynaptic mechanisms under both physiological and pathophysiological conditions.…”

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confidence: 99%

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

Kharlamov

Kelly

2007

Brain Research

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This study characterized morphological changes in the cortex and hippocampus of Sprague-Dawley rats following photothrombotic infarction and epileptogenesis with emphasis on the distribution of neuropeptide Y (NPY) expression. Animals were lesioned in the left sensorimotor cortex and compared with age-matched naïve and sham-operated controls by immunohistochemical techniques at 1, 3, 7, and 180 days post-lesioning (DPL). NPY immunostaining was assessed by light microscopy and quantified by the optical fractionator technique using unbiased stereological methods. At 1, 3, and 7 DPL, the number of NPY-positive somata in the lesioned cortex was increased significantly compared to controls and the contralateral cortex. At 180 DPL, lesioned epileptic animals with frequent seizure activity demonstrated significant increases of NPY expression in the cortex, CA1, CA3, hilar interneurons, and granule cells of the dentate gyrus. In addition to NPY immunostaining, neuronal degeneration, cell death/cell loss, and astroglial response were assessed with cell-specific markers. Nissl and NeuN staining showed reproducible infarctions at each investigated time point. FJB-positive somata were most abundant in the infarct core at 1 DPL, decreased markedly at 3 DPL, and virtually absent by 7 DPL. Activated astroglia were detected in the cortex and hippocampus following lesioning and the development of seizure activity. In summary, NPY protein expression and morphological changes following cortical photothrombosis were time-, region-and pathologic state-dependent. Alterations in NPY expression may reflect reactive or compensatory responses of the rat brain to acute infarction and to the development and expression of epileptic seizures.

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“…Neuropeptide Y is abundantly expressed throughout the CNS [1] and involved in a multitude of physiological and neuronal processes, such as feeding behavior, angiogenesis, neuronal proliferation [8,9,11] and the modulation of seizure activity. In the hippocampus, increased NPY expression is thought to be a compensatory effect of kindling and epileptogenesis [19,22,30,31], in vivo experiments in GEARS rats demonstrate that NPY suppresses absence seizures [23] and the anticonvulsant valproic acid has been proposed to act at least in part via an upregulation of NPY expression in hippocampus and nRt [2].…”

Section: Introductionmentioning

confidence: 99%

NPY signaling through Y1 receptors modulates thalamic oscillations

2007

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Neuropeptide Y is the ligand of a family of G-protein coupled receptors (Y 1 to Y 6 ). In the thalamus, exogenous and endogenously released NPY can shorten the duration of thalamic oscillations in brain slices from P13 to P15 rats, an in vitro model of absence seizures. Here, we examine which Y receptors are involved in this modulation. Application of the Y 1 receptor agonist Leu 31 Pro 34 NPY caused a reversible reduction in the duration of thalamic oscillations (−26.6 +/− 7.8%), while the Y 2 receptor agonist peptideYY and the Y 5 receptor agonist BWX-46 did not exert a significant effect. No Y receptor agonist affected oscillation period. Application of antagonists of Y 1 , Y 2 and Y 5 receptors (BIBP3226, BIIE0246 and L152,806, respectively) produced results consistent with those obtained from agonists. BIBP3226 caused a reversible disinhibition, an effect that increases oscillation duration (18.2 +/− 9.7%) while BIIE0246 and L152,806 had no significant effect. Expression of NPY is limited to neurons in the reticular thalamic nucleus (nRt), but Y 1 receptors are expressed in both nRt and adjacent thalamic relay nuclei. Thus, intra-nRt or nRt to relay nucleus NPY release could cause Y 1 receptor mediated inhibition of thalamic oscillations.

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Neuropeptide Y Distribution in the Rat Brain

Cited by 1,067 publications

References 13 publications

Body weight is regulated by the brain: a link between feeding and emotion

Body weight is regulated by the brain: a link between feeding and emotion

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

NPY signaling through Y1 receptors modulates thalamic oscillations

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