GABAergic projections from the suprachiasmatic nucleus to the preoptic area regulate the timing of torpor in mice.

Torpor is a state of hypometabolism accompanied by a reduction in body temperature, which serves as a survival strategy enabling animals to endure harsh environments. While the circadian clock is thought to regulate the timing of torpor, the underlying neural mechanisms remain unclear. Here, we show that inhibitory neurotransmission via gamma-aminobutyric acid (GABA) in the central circadian clock, suprachiasmatic nucleus (SCN), is crucial for encoding the timing of torpor induction in female mice. Optogenetic activation of GABAergic neurons in the SCN projecting to the preoptic area (POA) suppresses torpor. These SCN neurons form monosynaptic connections with two distinct types of POA neurons: excitatory neurons that promote torpor induction, and inhibitory neurons that suppress the activity of these excitatory neurons. Furthermore, the disconnection of neural output in the SCN abolishes the timing of torpor. Retrograde tracing revealed that arginine vasopressin (Avp) neurons in the SCN innervate the POA, and selective deletion of vesicular GABA transporter in Avp neurons of the SCN leads to impaired torpor induction. This hypothalamic neuronal circuit is crucial in ensuring the survival of animals during harsh environmental conditions.