Functions:
Neuropeptide F is one of the many neuropeptides in the body; they are a group of quite diverse signal molecules that contribute to a wide range of different behaviours. NPF functions affect many different behaviours including:
- Feeding behaviour
- Stress response
- Alcohol sensitivity, and
- Modulate aggression
Drosophila NPF (dNPF) is localized in the neuronal network of the central nervous system, dNPF neurons are found on the “dorsal surface of the brain and in subesophageal ganglia” (Wu, et. al., 2003). NPF in flatworms is localized to the central and peripheral nervous systems, “mainly in the dorsal and ventral nerve plexi” (Dougan, et. al., 2002), a network of intersecting nerves.
Effects on different systems:
In Drosophila larvae that eat well have been shown to have high NPF gene expression, whereas older larvae, which are known to not eat as much, are shown to have decreased NPF gene expression. These larvae also show “increased mobility, food-dependent clumping and cooperative burrowing” (Wu, et. al., 2003). Transgenic larvae that are experimentally deficient in NPF have been shown to display the same behaviours as the older larvae (Wu, et. al., 2003).
Even when faced with stressful situations such as being placed in extremely cold temperatures that can lead to death, NPF is required for “cold-resistant feeding behaviour of fasted larvae” (Lingo, P.R. et. al., 2007). The overexpression of the NPF receptor (NPFR1) in fed larvae triggered this cold resistant feeding activity, which is normally seen in fasted larvae. I believe that if the receptor expression is increased, NPF will be able to have a greater effect because it has more binding sites, therefore triggering the cold resistant feeding. It can be concluded that the NPF pathway is critical for responses to stressors of a thermal, gustatory or mechanical form (Lingo, P.R. et. al., 2007).
Furthermore, studies have shown the NPF and its receptor NPFR1 can have a mild affect on alcohol sensitivity. If Drosophila were deficient in NPF/NPFR1 signalling then there is a significant decrease in alcohol sensitivity. For example, when flies had their NPF/NPFR1 signalling pathways disrupted they showed a significant resistance in ethanol sedation (Wen, et. al., 2005). Coincidentally, flies that overexpress NPF pathways display the opposite phenotype. The neural circuits and pathways that are affected by alcohol are still somewhat uncertain, if these can be fully understood then further experimentation on this topic can be accomplished.
NPF is also important for sexual dimorphism in adult Drosophila (Lee, et. al., 2006). This study shows that male flies lacking NPF expression also lack male sexual behaviours.
Pathologies:
Neuropeptides act as neuroregulators along the central nervous system, if a problem arises within the regulatory system then diseases and consequences will be the outcome.
Neuropeptide Y (vertebrate homologue of NPF) has been linked to neurodegenerative diseases such as Alzheimer’s disease and Huntington’s disease. Studies have shown that concentrations on NPY are reduced in the cerebral cortex of Alzheimer’s patients, and this may be correlated to a loss of its’ corresponding (nonpyramidal) neurons (Dr. Flint Beal, M., & Dr. Martin, J.B., 2008 and Dr. Kowall, N.W., & Dr. Flint Beal, M. 1988). In Huntington’s disease, studies have shown an increase in the amount of NPY, which has been correlated to the preservation of the associated neurons (Flint Beal, M., et. al., 1986).
Future developments:
All these studies are on complex systems and neuronal pathways that are not yet completely understood. I believe if we are to reliably know the role of NPY in vertebrates and NPF in invertebrates then we have to understand these complicated systems first. After we posses that knowledge, we can further analyze these neuropeptides to gain a complete understanding of their effects and capabilities.
REFERENCES
1) Dougan, P.M., Mair, G.R., Halton, D.W., Curry, W.J., Day, T.A., & Maule, A.G. (2002). Gene Organization and Expression of a Neuropeptide Y Homolog from the Land Planarian Arthurdendyus triangulates. The journal of comparative neurology. 454; 58-64.
2) Dr. Flint Beal, M., & Dr. Martin, J.B. (2008). Neuropeptides in neurological disease. Annals of Neurology. 20(5); 547-565.
3) Dr. Kowall, N.W., & Dr. Flint Beal, M. (1988). Cortical somatostatin, neuropeptides Y, and NADPH diaphorase neurons: Normal anatomy and alterations in Alzheimer’s disease. Annals of Neurology. 23(2); 105-114.
4) Flint Beal, M., Kowall, N.W., Ellison, D.W., Mazurek, M.F., Swartz, J.K., & Martin, J.B. (1986). Replication of the neurochemical characteristics of Huntington’s disease by quinolinic acid. Nature. 321; 168-171.
5) Lee, G., Bahn, J.H., & Park, J.H. (2006). Sex- and clock-controlled expression of the neuropeptide F gene in Drosophila. PNAS. 103(33); 12580-12585.
6) Lingo, P.R., Zhao, Z., & Shen, P. (2007). Co-regulation of Cold-Resistant Food Acquisition by insulin- and Neuropeptide Y-like Systems in Drosophila melanogaster. Neuroscience. 148(2): 371-374.
7) Wen, T., Parrish, C., Wu, D., & Shen, P. (2005). Drosophila neuropeptide F and its receptor, NPFR1, define a signaling pathway that acutely modulates alcohol sensitivity. PNAS. 102(6); 2141-2146.
8) Wu, Q., Wen, T., Lee, G., Park, J.H., Cai, H.N., & Shen, P. (2003). Developmental Control of Foraging and Social Behaviour by the Drosophila Neuropeptide Y-like System. Neuron. 39; 147-161.
