Literature DB >> 20138163

Arcuate nucleus destruction does not block food deprivation-induced increases in food foraging and hoarding.

Megan J Dailey1, Timothy J Bartness.   

Abstract

The mechanisms underlying the control of food intake are considerably better understood than those underlying the appetitive ingestive behaviors of foraging and hoarding of food, despite the prevalence of the latter across species including humans. Neuropeptide Y (NPY) and Agouti-related protein (AgRP), two orexigenic neuropeptides known to stimulate food intake in a variety of species, applied centrally to Siberian hamsters increases foraging and especially hoarding with lesser increases in food intake. Both are expressed in the arcuate nucleus (Arc) and their synthesis increases with food deprivation, a naturally-occurring stimulus that markedly increases foraging and hoarding in Siberian hamsters. Therefore, we tested whether destruction of Arc neurons blocks these ingestive behaviors. This was accomplished either by microinjecting NPY conjugated to saporin (NPY-SAP) bilaterally into the Arc to kill NPY receptor-bearing neurons or via neonatal monosodium glutamate (MSG) treatment. For both methods, Arc cresyl violet staining (cell density) and NPY and Y1 receptor-immunoreactivity (ir) were significantly decreased. Although baseline foraging and food hoarding were not affected, food deprivation-induced increased food hoarding was surprisingly exaggerated approximately 100% with both types of Arc destruction. We found a substantial amount of remaining NPY-ir fibers, likely emanating from the brainstem, and a significant up-regulation of Y1 receptors in Arc NPY projections areas (hypothalamic paraventricular nucleus and perifornical area) after Arc denervation and their activation may have accounted for the exaggerated increases. The converging evidence from both Arc destruction methods suggests an intact Arc is not necessary for food deprivation-induced increases in food foraging and hoarding. Copyright 2010 Elsevier B.V. All rights reserved.

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Year:  2010        PMID: 20138163      PMCID: PMC2896996          DOI: 10.1016/j.brainres.2010.01.078

Source DB:  PubMed          Journal:  Brain Res        ISSN: 0006-8993            Impact factor:   3.252


  70 in total

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