Torpor is a controlled and reversible state characterized by lowered metabolic rate and body temperature. In ground squirrels, torpor induces dendritic spine retraction and re-localization of synaptic proteins, which restore upon arousal (von der Ohe et al., 2007). The emergence from torpor is followed by increased sleep slow-wave activity (SWA), a well-established marker of sleep pressure. Our study aims to elucidate the structural and molecular effects of torpor and subsequent sleep in Djungarian hamsters (Phodopus sungorus), a species exhibiting daily torpor in response to a shortened photoperiod.Animals (n = 4-5/group; sex-balanced) were collected at euthermia, mid-torpor, arousal, and 2 hours post-torpor. Continuous non-invasive thermal imaging was performed to confirm torpor occurrence.First, using serial block-face scanning electron microscopy (SBEM), we examined the changes in synaptic ultrastructure in the layer 2 of the primary motor cortex during torpor. Using a linear mixed effect model, our preliminary data showed that the axon-spine interface (ASI), an indicator of synaptic strength, from the mid-torpor group (median = 0.110µm2) was significantly lower than the ASI from the euthermia group (median = 0.154µm2) (p = 0.021), suggesting torpor is associated with a marked reduction in synaptic strength.Second, using immunoblotting and immunohistochemistry, we are studying neural plasticity in the torpor-euthermia cycle by assessing the amount and localization of synaptic and cytoskeletal proteins. Our pilot data (n = 2) suggest synapse-specific differences in protein localization, likely reflecting mechanisms for fast rebuilding of synapses after torpor.This research was supported by AMED (JP21zf0127005) and Wellcome Trust (204826/Z/16/Z).