While sleep is conserved across evolution, the function or functions of sleep remain unknown. Notably, sleep loss impairs learning and memory throughout the animal kingdom. Previous work strongly suggests that sleep is required for maintenance of neural and behavioral plasticity, although mechanisms remain elusive. In this body of work, I present two studies (Chapters 2, 3) that characterize cell-type-specific changes in synapse abundance after sleep deprivation, first in the Drosophila Mushroom bodies (MB), an associative learning center. Then, I describe neurotransmitter cell type specific changes in synapse abundance throughout the entire central brain. The first study is published in Current Biology, while the second study will soon be submitted to eLife. Additionally, Chapter 1 is published in Frontiers in Behavioral Neuroscience.In Chapter 1, I introduce roles for sleep in the maintenance of neural and behavioral plasticity in the contexts of development and memory acquisition and consolidation. Then, I discuss individual variations in response to sleep loss due to intrinsic and environmental factors. In Chapter 2, I show that sleep loss results in a net increase in synapse abundance in the MB using a genetic reporter of the presynaptic active zone protein Bruchpilot (BRP). Additionally, sleep induction reduces BRP abundance throughout the MB lobes. For the first time, I then characterize cell-type-specific changes in synaptic abundance throughout the MB, finding that increased BRP abundance can be attributed to cholinergic Kenyon cells (KCs). Finally, using a fluorescent reporter for synaptic contacts, I show that KC output connections are not uniformly scaled by sleep loss, but depend on the identity of the postsynaptic partner. These changes in synapse abundance and connectivity may underlie learning and memory deficits induced by sleep loss. In Chapter 3, I examine unclear whether the same cell-type specific trends in plasticity that we observe in the memory encoding MBs can be generalized to other neuropil regions of the central brain. This study examines changes in BRP abundance after sleep loss in each neuropil region in different neurotransmitter cell types. Consistent with my findings in the MB, I find that sleep deprivation upscales excitatory cholinergic synapses throughout each neuropil region, whereas other neurotransmitter cell types are less sensitive to sleep loss. Notably, BRP abundance is similarly affected within each neuropil region for a given neurotransmitter class. Our results are consistent with previous findings that excitatory and inhibitory neurons can be differentially affected by sleep loss. Sleep deprivation may therefore disrupt excitatory/inhibitory balance (E/I balance) in the brain, which may underlie some of the cognitive and behavioral consequences of insufficient sleep. In sum, this work seeks to elucidate alterations in synaptic plasticity after sleep loss in the Drosophila brain. As sleep is evolutionarily conserved, our findings may inform the function(s) of sleep in animal models and humans. Here, I find that sleep loss does not uniformly affect synapse abundance across cell types. Certain cell types are especially vulnerable to the effects of sleep deprivation, which may underlie consequences of prolonged waking.