This novel study investigated the effects of intracerebroventricular (ICV) injection α- klotho and its interaction with neuropeptide Y (NPY) receptors on food intake in broiler chicken. This study included 4 experiments with 4 groups in each with 11 replicates per group. Birds were feed deprived 3 h prior injection, following injection returned to their cage and food provided. In experiment 1, group 1 received ICV injection of the saline and groups 2 to 4 received ICV injection of the α-klotho (1, 2, and 4 µg), respectively. In experiment 2, chicken received ICV injection of the saline, B5063 (NPY receptor antagonist, 1.25 µg), α-klotho (4 µg) and co-injection of the B5063 + α-klotho. In experiments 3 and 4, SF22 (NPY receptor antagonist, 1.25 µg), and SML0891 (NPY receptor antagonist, 1.25 µg) were injected instead of the B5063. Then consumed food was measured at 30, 60, and 120 min post the injection. Based on results, ICV injection of the α-klotho (2 and 4 µg) significantly decreased food intake (P < 0.05). Co-injection of the B5063 + α-klotho significantly amplified hypophagic effect of the α-klotho (P < 0.05). α-klotho-induced hypophagia was not influenced by SF22 or SML0891. These results suggest that α-klotho-induced hypophagia is mediated via NPY receptors in broiler chicken.
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http://dx.doi.org/10.1016/j.psj.2024.104166 | DOI Listing |
Alzheimers Dement
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National Council of Scientific and Technical Research (CONICET/UNLP), La Plata, Argentina.
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View Article and Find Full Text PDFAlzheimers Dement
December 2024
National Council of Scientific and Technical Research (CONICET/UNLP), La Plata, Argentina.
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View Article and Find Full Text PDFAlzheimers Dement
December 2024
Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Milano, Italy.
Background: The role of oligomeric forms of various proteins as direct responsible of neuronal dysfunction in neurodegenerative disorders has been supported by numerous findings at experimental level and, more recently, by histological examinations in human material. The cellular prion protein (PrP) has been proposed to mediate the neurotoxicity of β-amyloid, α-synuclein and tau oligomers. We demonstrated that although amyloid-β oligomers (AβOs) bind with high affinity to PrP, the memory deficit induced by intracerebroventricular (ICV) administration of AβOs in mice was not mediated by PrP.
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Ivane Beritashvili Center of Experimental Biomedicine, Tbilisi, Georgia.
Background: Alzheimer's disease (AD) is a neurodegenerative disease that causes progressive cognitive decline over age 65. Individuals suffering from this disease suffer memory loss, and histological examination of the brains. Okadaic acid (OA), is a potent and selective inhibitor of protein phosphatases 1 and 2A.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Michigan State University, Grand Rapids, MI, USA.
Background: A recent study of familial Alzheimer's disease identified a mutation in the RELN gene that appeared to delay the onset of dementia. It was hypothesized that this RELN-COLBOS variant protected against dementia by enhanced signaling at reelin receptors. We previously developed a secreted, bio-active reelin fragment (R36) and packaged it into AAV.
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