The ability of animals to respond to life-threatening stimuli is essential for survival. Although vision provides one of the major sensory inputs for detecting threats across animal species, the circuitry underlying defensive responses to visual stimuli remains poorly defined. Here, we investigate the circuitry underlying innate defensive behaviours elicited by predator-like visual stimuli in mice. Our results demonstrate that neurons in the superior colliculus (SC) are essential for a variety of acute and persistent defensive responses to overhead looming stimuli. Optogenetic mapping revealed that SC projections to the lateral posterior nucleus (LP) of the thalamus, a non-canonical polymodal sensory relay, are sufficient to mimic visually evoked fear responses. In vivo electrophysiology experiments identified a di-synaptic circuit from SC through LP to the lateral amygdale (Amg), and lesions of the Amg blocked the full range of visually evoked defensive responses. Our results reveal a novel collicular–thalamic–Amg circuit important for innate defensive responses to visual threats.

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Developing copper‐free catalysts for CO2 conversion into hydrocarbons and oxygenates is highly desirable for electrochemical CO2 reduction reaction (CO2RR). Herein, we report a cobalt phthalocyanine (CoPc) and zinc–nitrogen–carbon (Zn‐N‐C) tandem catalyst for CO2RR to CH4. This tandem catalyst shows a more than 100 times enhancement of the CH4/CO production rate ratio compared with CoPc or Zn‐N‐C alone. Density functional theory (DFT) calculations and electrochemical CO reduction reaction results suggest that CO2 is first reduced into CO over CoPc and then CO diffuses onto Zn‐N‐C for further conversion into CH4 over Zn‐N4 site, decoupling complicated CO2RR pathway on single active site into a two‐step tandem reaction. Moreover, mechanistic analysis indicates that CoPc not only generates CO but also enhances the availability of *H over adjacent N sites in Zn‐N4, which is the key to achieve the high CH4 production rate and understand the intriguing electrocatalytic behavior which is distinctive to copper‐based tandem catalysts.

Electrochemical CO2 reduction reaction (CO2RR) to multicarbon hydrocarbon and oxygenate (C2+) products with high energy density and wide availability is of great importance, as it provides a promising way to achieve the renewable energy storage and close the carbon cycle. Herein we design a Cu‐CuI composite catalyst with abundant Cu0/Cu+ interfaces by physically mixing Cu nanoparticles and CuI powders. The composite catalyst achieves a remarkable C2+ partial current density of 591 mA cm−2 at −1.0 V vs. reversible hydrogen electrode in a flow cell, substantially higher than Cu (329 mA cm−2) and CuI (96 mA cm−2) counterparts. Induced by alkaline electrolyte and applied potential, the Cu‐CuI composite catalyst undergoes significant reconstruction under CO2RR conditions. The high‐rate C2+ production over Cu‐CuI is ascribed to the presence of residual Cu+ and adsorbed iodine species which improve CO adsorption and facilitate C−C coupling.

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Temporal lobe epilepsy (TLE) is one of the most common drug-resistant forms of epilepsy in adults and usually originates in the hippocampal formations. However, both the network mechanisms that support the seizure spread and the exact directions of ictal propagation remain largely unknown. Here we report the dissection of ictal propagation in the hippocampal–entorhinal cortex (HP–EC) structures using optogenetic methods in multiple brain regions of a kainic acid-induced model of TLE in VGAT-ChR2 transgenic mice. We perform highly temporally precise cross-area analyses of epileptic neuronal networks and find a feed-forward propagation pathway of ictal discharges from the dentate gyrus/hilus (DGH) to the medial entorhinal cortex, instead of a re-entrant loop. We also demonstrate that activating DGH GABAergic interneurons can significantly inhibit the spread of ictal seizures and largely rescue behavioural deficits in kainate-exposed animals. These findings may shed light on future therapeutic treatments of TLE.

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