Neural circuits underlying auditory fear conditioning have been extensively studied. Here we identified a previously unexplored pathway from the lateral amygdala (LA) to the auditory cortex (ACx), and found that selective silencing of this pathway using chemo-and optogenetic approaches impairs fear memory retrieval. Dual-color in vivo two-photon imaging of mouse ACx showed pathwayspecific increases in the formation of LA axon boutons, dendritic spines of ACx layer-5 pyramidal cells, and putative LA-ACx synaptic pairs after auditory fear conditioning. Furthermore, co-imaging of pre-and postsynaptic structures showed that essentially all new synaptic contacts were made by adding new partners to existing synaptic elements. Together, these findings identify an amygdalocortical projection that plays an important role in fear memory expression and is selectively modified by associative fear learning, and unravel a distinct architectural rule for synapse formation in the adult brain. 2 IntroductionAssociative learning enables an animal to adapt to and survive in a complex environment. In classical auditory fear conditioning, animals learn to associate a neutral stimulus (a sound) with a foot-shock, and exhibit fear responses to the sound presentation. Amygdala is critical for the formation of auditory fear memory 1 .Previous studies have also shown that the auditory cortex (ACx) is required for auditory fear learning [2][3][4] , and that fear conditioning could induce rapid and long-term changes in neuronal responses and spine dynamics in ACx. However, which synapses in ACx underwent modification remain unclear.Long-term in vivo two-photon imaging has been used to monitor structural remodeling of synaptic connectivity, as was shown by changes in presynaptic boutons or postsynaptic spines that represent the formation or elimination of synapses.Previous studies have shown that sensory experience and learning can induce changes in the turnover of presynaptic axon boutons 9 and postsynaptic dendritic spines. To further explore synaptic dynamics in specific pathways, concurrent imaging of preand post-synaptic structures in identified connections is required. This approach, although successfully applied in studying synaptic dynamics in hippocampal slices 16 , has not been used for in vivo imaging of the neocortex.In this study, combining tracing methods with electron microscopy (EM), we identified a projection to ACx that originates from lateral amygdala (LA), the major 3 input region of the amygdala. Chemo-and optogenetic silencing of LA axons in ACx during fear recall test greatly reduced animals' fear responses, suggesting that the LAACx pathway plays an important role in the expression of fear memory. By coimaging labeled axons originating from brain regions projecting to ACx and apical dendrites of pyramidal neurons in ACx, we were able to monitor the dynamics of putative synaptic pairs in specific pathways in vivo. We observed a selective increase in bouton and spine formation at LA-ACx connections after fear con...

Wakefulness, rapid eye movement (REM) sleep, and non–rapid eye movement (NREM) sleep are characterized by distinct electroencephalogram (EEG), electromyogram (EMG), and autonomic profiles. The circuit mechanism coordinating these changes during sleep-wake transitions remains poorly understood. The past few years have witnessed rapid progress in the identification of REM and NREM sleep neurons, which constitute highly distributed networks spanning the forebrain, midbrain, and hindbrain. Here we propose an arousal-action circuit for sleep-wake control in which wakefulness is supported by separate arousal and action neurons, while REM and NREM sleep neurons are part of the central somatic and autonomic motor circuits. This model is well supported by the currently known sleep and wake neurons. It can also account for the EEG, EMG, and autonomic profiles of wake, REM, and NREM states and several key features of their transitions. The intimate association between the sleep and autonomic/somatic motor control circuits suggests that a primary function of sleep is to suppress motor activity.