Our data support a requirement for synaptic activity in Bortezomib serotonergic neurons during development of the flight CPG. The absence of variation in the numbers of TRHGAL4 positive but 5-HT negative neurons between fliers and non-fliers indicates that these neurons do not contribute to the flight phenotypes observed. However, at this stage we cannot completely rule out a role for TRHGAL4 positive neurons that remain 5-HT negative in Drosophila flight. Loss of serotonergic neurons in the T2 segment by TNT expression suggests that they undergo cell death. Alternately, they may cease to produce serotonin, and their cell fates are re-specified in an activity-dependent manner. Activity-dependent neurotransmitter re-specification has been shown in Xenopus larvae. However in Xenopus, increased Ca2+ spikes reduced the serotonergic cell population in the raphe, a serotonin rich region in the hindbrain while decreased Ca2+ spikes, increased the cell population. The spike activity had a converse relationship to the expression of a transcription factor, LmX1b, which is required for the maintenance of serotonin expression in the CNS. Re-specification of neurotransmitters, through altered neuronal activity, can also take place in adults, after synapse formation. This is often triggered by sensory stimuli. Thus the reduced flight in animals where synaptic activity was inhibited in adults could arise either from loss of synaptic activity affecting serotonergic modulation of flight CPG neurons during flight or it could be a consequence of re-specification of serotonergic neurons post-pupal development. This work identifies pupal development in Drosophila as a phase where serotonergic neurons of the flight circuit may be more sensitive to activity-dependent re-modelling. Identification of genes that drive this re-modelling will be of interest. Plasma lipid levels are heritable risk factors for cardiovascular disease. It has been revealed that a number of genes and pathways are involved in the pathogenesis of Mendelian dyslipidemic syndromes and also contribute to inter-individual variation in plasma lipid levels. Recent genome-wide association studies have identified genetic determinants of plasma lipids primarily, with around 100 genetic loci showing reproducible evidence of association with circulating low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and/or triglycerides. An appreciable part of the loci identified by GWA studies are in or near genes previously known to influence plasma lipid levels, whereas others are not; that is, they are located near genes not previously implicated in lipoprotein metabolism or in the intergenic regions. As these GWA studies were conducted almost exclusively in populations of European descent, studies in non-European populations will allow us to assess the relevance of the findings to other ethnic groups. Some variants may be more common in specific ethnic groups, thereby providing greater statistical power, or the effects of genetic variants on lipid levels may be enlarged in specific ethnic groups, presumably due to substantial differences in lifestyle factors. Epidemiological studies have provided evidence for association between circulating levels of plasma lipids and risk of coronary artery disease. A causal role in CAD for LDL-C has been equivocally established via clinical trials using the HMGCoA reductase inhibitor, whereas that for HDL-C and TG remains uncertain.