Individual differences |
Methods | Statistics | Clinical | Educational | Industrial | Professional items | World psychology |
Biological: Behavioural genetics · Evolutionary psychology · Neuroanatomy · Neurochemistry · Neuroendocrinology · Neuroscience · Psychoneuroimmunology · Physiological Psychology · Psychopharmacology (Index, Outline)
NPY has been associated with a number of physiologic processes in the brain, including the regulation of energy balance, memory and learning, and epilepsy (Colmers, W.F. Epilepsy Curr. 2003 March;3(2):53-58).
Role in regulation of feeding[edit | edit source]
NPY's role in regulating energy balance is well known. It forms part of the "lipostat" system along with leptin and corticotropin-releasing hormone (CRH). High NPY levels in the cerebrospinal fluid are associated with high food intake and decreased physical activity. Leptin, produced by adipocytes in response to high fat levels is detected by the arcuate nucleus in the hypothalamus. Increased arcuate nucleus activity acts on the paraventricular nucleus to inhibit the production of NPY at that site, thus reducing feeding behaviour. Arcuate nucleus activity also stimulates the release of CRH which further decreases feeding and increases energy expenditure.
Receptors[edit | edit source]
The receptor protein that NPY operates on is a G-protein coupled receptor in the rhodopsin like GPCR family. These receptors are metabotropic, causing metabolic changes in the target cell rather than directly opening ion channels. The protein contains seven membrane spanning domains and six subtypes have been identified at this time. Subtypes Y1 and Y5 have known roles in the regulation of feeding. This receptor family is one of the most highly conserved between species yet found.
See also[edit | edit source]
References[edit | edit source]
- Carlson, N. R., Physiology of behaviour 6th edn., 1998, pp.393-398
[edit | edit source]
|This page uses Creative Commons Licensed content from Wikipedia (view authors).|