VISUALISING SENSORY PROCESSING IN SYNTHETIC HIBERNATION

Some animals use the strategy, known as hibernation, to survive harsh environments by reducing metabolism and core body temperature. Even during such quiescent state, external stimuli can still rapidly restore sensorimotor response and induce arousal. However, it is unclear how the sensory signals processed in hibernation due to the difficulty of studying real hibernating animals. Recent work has shown that activation of Qrfp neurons in the preoptic area of the hypothalamus (AVPe) can induce a hibernation-like state in non-hibernators such as mice, termed Q-neuron-induced hypothermia and hypometabolism (QIH) (Takahashi et al., Nature, 2020). Interestingly, they show similar immobile behaviours to natural hibernation.
Here, we performed the in vivo calcium imaging to identify the cell type-specific manipulations in the somatosensory (S1) cortex in response to tactile stimulation while mice were awake, anaesthetized or under QIH induced by using DREADD to chemogenetically activate the Qrfp neurons. We found that the QIH mice remind response to the hind paw pinch. In vivo calcium imaging combining cell type-specific promotor-driven expression of the calcium indicator showed heterogeneous response to the hind paw pinch. Notably, astrocytes exhibited stronger calcium responses under QIH. Concurrently, glucose utilization was markedly suppressed in the cortex during QIH. Pharmacological blockade of astrocytic lactate transport attenuated stimulus-evoked neuronal activity in QIH, implicating astrocyte derived lactate as a critical metabolic substrate for sustaining sensory processing. It suggested that astrocyte is a key regulator in supporting sensory information processing during hibernation-like state.