Co-release of neuropeptide Y and noradrenaline from pig spleen in vivo: Importance of subcellular storage, nerve impulse frequency and pattern, feedback regulation and resupply by axonal transport

Lundberg, Jan M.; Rudehill, A.; Sollevi, Alf; Fried, Gabriel; Wallin, Gunnar

doi:10.1016/0306-4522(89)90193-0

Cited by 174 publications

(87 citation statements)

References 37 publications

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“…Because ␤-adrenoceptor agonists protect against EAE (13) and catecholamines modulate several immunological functions critical to the pathogenesis of EAE (14), the enhancement of EAE by chemical sympathectomy has largely been attributed to the depletion of catecholamines. However, although neuropeptide Y (NPY) is also released from SNS terminals innervating lymphatic tissues (16,17), no previous studies have explored the possibility that depletion of other SNS transmitters such as NPY may contribute to these findings.…”

Section: E Xperimental Autoimmune Encephalomyelitis (Eae)mentioning

confidence: 99%

Neuropeptide Y (NPY) Suppresses Experimental Autoimmune Encephalomyelitis: NPY1 Receptor-Specific Inhibition of Autoreactive Th1 Responses In Vivo

Bedoui

Miyake

Lin

et al. 2003

The Journal of Immunology

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Prior studies have revealed that the sympathetic nervous system regulates the clinical and pathological manifestations of experimental autoimmune encephalomyelitis (EAE), an autoimmune disease model mediated by Th1 T cells. Although the regulatory role of catecholamines has been indicated in the previous works, it remained possible that other sympathetic neurotransmitters like neuropeptide Y (NPY) may also be involved in the regulation of EAE. Here we examined the effect of NPY and NPY receptor subtype-specific compounds on EAE, actively induced with myelin oligodendrocyte glycoprotein 35–55 in C57BL/6 mice. Our results revealed that exogenous NPY as well as NPY Y1 receptor agonists significantly inhibited the induction of EAE, whereas a Y5 receptor agonist or a combined treatment of NPY with a Y1 receptor antagonist did not inhibit signs of EAE. These results indicate that the suppression of EAE by NPY is mediated via Y1 receptors. Furthermore, treatment with the Y1 receptor antagonist induced a significantly earlier onset of EAE, indicating a protective role of endogenous NPY in the induction phase of EAE. We also revealed a significant inhibition of myelin oligodendrocyte glycoprotein 35–55-specific Th1 response as well as a Th2 bias of the autoimmune T cells in mice treated with the Y1 receptor agonist. Ex vivo analysis further demonstrated that autoimmune T cells are directly affected by NPY via Y1 receptors. Taken together, we conclude that NPY is a potent immunomodulator involved in the regulation of the Th1-mediated autoimmune disease EAE.

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Section: E Xperimental Autoimmune Encephalomyelitis (Eae)mentioning

confidence: 99%

Neuropeptide Y (NPY) Suppresses Experimental Autoimmune Encephalomyelitis: NPY1 Receptor-Specific Inhibition of Autoreactive Th1 Responses In Vivo

Bedoui

Miyake

Lin

et al. 2003

The Journal of Immunology

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“…The detection limit is 7.8 pmol 1`and details of the method have been described and evaluated by Theodorsson-Norheim et al (1985). For characterization of NPY-LI in plasma from pig splenic venous effluent see Lundberg et al (1989b). NA was extracted by perchloric acid, followed by alumina adsorption and assayed by cation exchange high performance liquid chromatography (h.p.l.c.)…”

Section: In Vivo Experimentsmentioning

confidence: 99%

Inhibition of sympathetic vasoconstriction in pigs in vivo by the neuropeptide Y‐Y₁ receptor antagonist BIBP 3226

Lundberg

Modin

1995

British J Pharmacology

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4 High frequency stimulation of the sympathetic trunk in control pigs caused a biphasic vasoconstrictor response in nasal mucosa, hind limb and skin: there was an immediate, peak response, followed by a long-lasting vasoconstriction. BIBP 3226 (1 and 3 mg kg-1) reduced the second phase by about 50% but had no effect on the-peak response. In the spleen, kidney and mesenteric circulation (which lack the protracted response) BIBP 3226 was likewise without effect on the maximal vasoconstriction, and did not influence noradrenaline overflow from spleen and kidney. pressure (by about 5 and 15 mmHg at 1 mg kg-' and 3 mg kg-', respectively), accompanied by splenic and mesenteric vasodilatation, suggesting that this effect was unrelated to Y, receptor blockade. 6 The peptide YY (PYY)-and NPY-evoked vasoconstriction in the kidney of reserpine-treated pigs was markedly reduced (by 95%) by BIBP 3226 while the vasoconstrictor effect in the spleen was attenuated by only 20%. BIBP 3226 did not influence stimulation-evoked NPY release. The vasoconstrictor response in reserpine-treated pigs to single impulse stimulation, which is observed only in nasal mucosa and hind limb, was unchanged regarding maximal amplitude and the integrated effect was only moderately reduced (by about 25%) in the presence of BIBP 3226 (1 mg kg-'). BIBP 3226 (1 mg kg-') markedly reduced (by 55-70%) the long-lasting vascular response (total integrated blood flow reduction) evoked by sympathetic nerve stimulation at high frequency (40 impulses at 20 Hz) in spleen, kidney, nasal mucosa and hind limb. Furthermore, the maximal amplitude of the vasoconstriction was reduced mainly in the kidney (by 60%) and also in the spleen (by 40%). 7 It is concluded that BIBP 3226 can act as a selective Y, receptor antagonist in the pig. Endogenous NPY via Y, receptor activation may play a role in evoking the long-lasting vasoconstriction seen in nasal mucosa, hind limb and skin after high frequency stimulation of sympathetic nerves in control pigs. Furthermore, NPY via Y, receptor mechanisms seems to be of major importance for the long-lasting component of the reserpine resistant sympathetic vasoconstriction in many vascular beds, and for the maximal vasoconstrictor response in the kidney. Circulating NPY and PYY induce splenic vasoconstriction via Y2-receptors in contrast to neuronally released NPY which mainly activates Y1 receptors.

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“…After sympathetic nerve activation, epinephrine activates various physiological processes (Lundberg et al 1989). Adipogenesis is the reverse process of lipolysis.…”

Section: Introductionmentioning

confidence: 99%

Impact of stress hormone on adipogenesis in the 3T3-L1 adipocytes

Pandurangan

Ravikumar

2013

Cytotechnology

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Stress hormone is known to play a vital role in lipolysis and adipogenesis in fat cells. The present study was carried out to evaluate the effect of epinephrine on adipogenesis in the 3T3-L1 cells. The investigation on adipogenesis was done in both mono and co-cultured 3T3-L1 cells. 3T3-L1 preadipocytes and C2C12 cells were grown independently on transwell plates and transferred to differentiation medium. Following differentiation, C2C12 cells transferred to 3T3-L1 plate and treated with medium containing 10 lg/ml of epinephrine. Adipogenic markers such as fatty acid binding protein 4, peroxisome proliferator activating receptor, CCAAT/ enhancer-binding protein, adiponectin, lipoprotein lipase and fatty acid synthase mRNA expressions were evaluated in the 3T3-L1 cells. Epinephrine treatment reduced adipogenesis, evidenced by reducing adipogenic marker mRNA expression in the 3T3-L1 cells. In addition, glycerol accumulation and oil red-O staining supported the reduced rate of adipogenesis. Taking all together, it is concluded that the stress hormone, epinephrine reduces the rate of adipogenesis in the mono and co-cultured 3T3-L1 cells. In addition, the rate of adipogenesis is much reduced in the co-cultured 3T3-L1 cells compared monocultured 3T3-L1 cells.

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Co-release of neuropeptide Y and noradrenaline from pig spleen in vivo: Importance of subcellular storage, nerve impulse frequency and pattern, feedback regulation and resupply by axonal transport

Cited by 174 publications

References 37 publications

Neuropeptide Y (NPY) Suppresses Experimental Autoimmune Encephalomyelitis: NPY1 Receptor-Specific Inhibition of Autoreactive Th1 Responses In Vivo

Neuropeptide Y (NPY) Suppresses Experimental Autoimmune Encephalomyelitis: NPY1 Receptor-Specific Inhibition of Autoreactive Th1 Responses In Vivo

Inhibition of sympathetic vasoconstriction in pigs in vivo by the neuropeptide Y‐Y₁ receptor antagonist BIBP 3226

Impact of stress hormone on adipogenesis in the 3T3-L1 adipocytes

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Co-release of neuropeptide Y and noradrenaline from pig spleen in vivo: Importance of subcellular storage, nerve impulse frequency and pattern, feedback regulation and resupply by axonal transport

Cited by 174 publications

References 37 publications

Neuropeptide Y (NPY) Suppresses Experimental Autoimmune Encephalomyelitis: NPY1 Receptor-Specific Inhibition of Autoreactive Th1 Responses In Vivo

Neuropeptide Y (NPY) Suppresses Experimental Autoimmune Encephalomyelitis: NPY1 Receptor-Specific Inhibition of Autoreactive Th1 Responses In Vivo

Inhibition of sympathetic vasoconstriction in pigs in vivo by the neuropeptide Y‐Y1 receptor antagonist BIBP 3226

Impact of stress hormone on adipogenesis in the 3T3-L1 adipocytes

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Inhibition of sympathetic vasoconstriction in pigs in vivo by the neuropeptide Y‐Y₁ receptor antagonist BIBP 3226