Prader-Willi Syndrome (PWS) is a complex, multi-system disorder characterized by an initial 'failure to thrive', mental retardation, infertility, post-weaning hyperphagia and eventually severe obesity. Although the genetic region on human chromosome 15 that is responsible for PWS has been known for many years, how the gene or genes within this large region cause the complex clinical features of PWS is still unknown. Recent patient reports have identified that microdeletions encompassing the SNORD116 cluster on chromosome 15q11.2 manifest a phenotype substantially overlapping with PWS. This genomic cluster encodes non-coding RNAs, including long non-coding RNAs and multiple arrays of C/D box snoRNAs. However the function and physiological targets of these transcripts are poorly characterized. We aim to explore the function of these multiple non-coding RNA species from the SNORD116 locus, with the eventual goal of elucidating the molecular mechanisms linking its loss to the PWS-like phenotype. Our work shows that Snord116 snoRNAs are highly expressed throughout the brain but restricted to neurons (NeuN positive cells). Preliminary observations also suggest that fasting may regulate Snord116’s hypothalamic expression. We thus hypothesise that Snord116 may regulate the expression of a repertoire of genes impacting neuronal development and food intake control. To investigate the role of the SNORD116 locus in neural food intake pathways, we will characterise whether its brain expression pattern changes with nutritional state using in-situ hybridisation coupled with laser-capture microdissection. We further intend to determine the functional and transcriptional consequences of perturbing the expression of different Snord116 transcripts in primary neurons and Snord116-deficient mouse models. Our aim, ultimately, is to identify roles for these transcripts in responses to nutritional state and neural food intake control.