Neuropeptide Y and Cardiovascular Function

Morris, Margaret J.

doi:10.1007/978-3-642-18764-3_11

Cited by 5 publications

(3 citation statements)

References 222 publications

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“…In addition to anti-seizure activity, NPY is anxiolytic, a potent appetite stimulant, and has cardiovascular effects after both central and peripheral administration (Zini et al, 1984;Cabrele et al, 2000;Morris, 2004). However, the orexigenic effects of NPY are predominantly mediated through Y 1 and Y 5 receptors (Gerald et al, 1996;Cabrele et al, 2000;Chaffer & Morris, 2002).…”

Section: Discussionmentioning

confidence: 97%

Neuropeptide Y suppresses absence seizures in a genetic rat model primarily through effects on Y₂ receptors

Morris

Gannan

Stroud

et al. 2007

Eur J of Neuroscience

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Neuropeptide Y (NPY) potently suppresses absence seizures in a model of genetic generalized epilepsy, genetic absence epilepsy rats of Strasbourg (GAERS). Here we investigated the Y-receptor subtype(s) on which NPY exerts this anti-absence effect. A dual in vivo approach was used: the cumulative duration of seizures was quantified in adult male GAERS in 90-min electroencephalogram recordings following intracerebroventricular (i.c.v.) injection of: (i) subtype-selective agonists of Y1 ([Leu31Pro34]NPY, 2.5 nmol), Y2 (Ac[Leu(28,31)]NPY24-36, 3 nmol), Y5 receptors [hPP1(-17),Ala31,Aib32]NPY, 4 nmol), NPY (3 nmol) or vehicle; and following (ii) i.c.v. injection of antagonists of Y1 (BIBP3226, 20 nmol), Y2 (BIIE0246, 20 nmol) and Y5 (NPY5RA972, 20 nmol) receptors or vehicle, followed by NPY (3 nmol). Injection of the Y1- and Y5-selective agonists resulted in significantly less mean seizure suppression (37.4% and 53.9%, respectively) than NPY (83.2%; P < 0.05), while the Y2 agonist had similar effects to NPY (62.3% suppression, P = 0.57). Food intake was not increased following injection of the Y2 agonist, while significant increases in food intake were seen following NPY and the other Y-subtype agonists. Compared with vehicle, NPY injection suppressed seizures following the Y1 and Y5 antagonists (45.3% and 80.1%, respectively, P < 0.05), but not following the Y2 antagonist (5.1% suppression, P = 0.46). We conclude that NPY Y2 receptors are more important than Y1 and Y5 receptors in mediating the effect of NPY to suppress absence seizures in a genetic rat model. Y2 receptor agonists may represent targets for novel drugs against genetic generalized epilepsies without resulting in appetite stimulation.

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Section: Discussionmentioning

confidence: 97%

Neuropeptide Y suppresses absence seizures in a genetic rat model primarily through effects on Y₂ receptors

Morris

Gannan

Stroud

et al. 2007

Eur J of Neuroscience

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“…There have been similar reports of higher NPY levels in several tissues such as the median preoptic and arcuate nucleus [30]; ventromedial hypothalamic nucleus and locus coeruleus [31]; mesenteric and femoral artery, jugular vein and vena cava [22]; urinary bladder, urethra and prostate [32] of SHR compared to Wistar-Kyoto (WKY). On the other hand, there have also been reports of lower NPY levels compared to normotensive controls, especially in the CNS and spinal cord.…”

Section: Npy Tissue Levels and Innervationmentioning

confidence: 76%

“…The purpose of the present paper is to discuss and summarize data suggesting an involvement of NPY and sympathetic control of vascular tone in hypertension. The reader is also referred to several recent reviews which address various aspects of the topic [17][18][19][20][21][22].…”

Section: Introductionmentioning

confidence: 99%

Neuropeptide Y and sympathetic control of vascular tone in hypertension

Westfall

Experientia Supplementum

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Presynaptic Neuropeptide Receptors

Schlicker

Kathmann

2008

Handbook of Experimental Pharmacology

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Presynaptic receptors for four families of neuropeptides will be discussed: opioids, neuropeptide Y, adrenocorticotropic hormone (ACTH), and orexins. Presynaptic receptors for the opioids (micro, delta, kappa, and ORL(1)) and neuropeptide Y (Y(2)) inhibit transmitter release from a variety of neurones, both in the peripheral and central nervous systems. These receptors, which were also identified in human tissue, are coupled to G(i/o) proteins and block voltage-dependent Ca(2+) channels, activate voltage-dependent K(+) channels, and/or interfere with the vesicle release machinery. Presynaptic receptors for ACTH (MC(2) receptors) have so far been identified almost exclusively in cardiovascular tissues from rabbits, where they facilitate noradrenaline release; they are coupled to G(s) protein and act via stimulation of adenylyl cyclase. Presynaptic receptors for orexins (most probably OX(2) receptors) have so far almost exclusively been identified in the rat and mouse brain, where they facilitate the release of glutamate and gamma-aminobutyric acid (GABA); they are most probably linked to G(q) and directly activate the vesicle release machinery or act via a transduction mechanism upstream of the release process. Agonists and antagonists at opioid receptors owe at least part of their therapeutic effects to actions on presynaptic receptors. Therapeutic drugs targeting neuropeptide Y and orexin receptors and presynaptic ACTH receptors so far are not available.

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Neuropeptide Y and Cardiovascular Function

Cited by 5 publications

References 222 publications

Neuropeptide Y suppresses absence seizures in a genetic rat model primarily through effects on Y₂ receptors

Neuropeptide Y suppresses absence seizures in a genetic rat model primarily through effects on Y₂ receptors

Neuropeptide Y and sympathetic control of vascular tone in hypertension

Presynaptic Neuropeptide Receptors

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Neuropeptide Y and Cardiovascular Function

Cited by 5 publications

References 222 publications

Neuropeptide Y suppresses absence seizures in a genetic rat model primarily through effects on Y2 receptors

Neuropeptide Y suppresses absence seizures in a genetic rat model primarily through effects on Y2 receptors

Neuropeptide Y and sympathetic control of vascular tone in hypertension

Presynaptic Neuropeptide Receptors

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Neuropeptide Y suppresses absence seizures in a genetic rat model primarily through effects on Y₂ receptors

Neuropeptide Y suppresses absence seizures in a genetic rat model primarily through effects on Y₂ receptors