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Dynamically controlling terahertz (THz) wavefronts in a designable fashion is highly desired in practice. However, available methods working at microwave frequencies do not work well in the THz regime due to lacking suitable tunable elements with submicrometer sizes. Here, instead of locally controlling individual meta-atoms in a THz metasurface, we show that rotating different layers (each exhibiting a particular phase profile) in a cascaded metadevice at different speeds can dynamically change the effective Jonesmatrix property of the whole device, thus enabling extraordinary manipulations on the wavefront and polarization characteristics of a THz beam impinging on the device. After illustrating our strategy based on model calculations, we experimentally demonstrate two proof-of-concept metadevices, each consisting of two carefully designed all-silicon transmissive metasurfaces exhibiting different phase profiles. Rotating two metasurfaces inside the fabricated devices at different speeds, we experimentally demonstrate that the first metadevice can efficiently redirect a normally incident THz beam to scan over a wide solid-angle range, while the second one can dynamically manipulate both the wavefront and polarization of a THz beam. Our results pave the way to achieving dynamic control of THz beams, which is useful in many applications, such as THz radar, and bio-and chemical sensing and imaging.

The prefrontal cortex (PFC) plays a critical role in cognitive functions, including working memory, attention regulation, behavioral inhibition, as well as memory storage. The functions of PFC are very sensitive to norepinephrine (NE), and even low levels of endogenously released NE exert a dramatic influence on the functioning of the PFC. Activation of b-adrenoceptors (b-ARs) facilitates synaptic potentiation and enhances memory in the hippocampus. However, little is known regarding these processes in the PFC. In the present study, we investigate the role of b2-AR in synaptic plasticity and behavioral memory. Our results show that b2-AR selective agonist clenbuterol facilitates spike-timing-dependent long-term potentiation (tLTP) under the physiological conditions with intact GABAergic inhibition, and such facilitation is prevented by co-application with the cAMP inhibitor Rp-cAMPS. Loading postsynaptic pyramidal cells with Rp-cAMPS, the PKA inhibitor PKI 5-24 , or the G protein inhibitor GDP-b-S significantly decreases, but does not eliminate, the effect of clenbuterol. Clenbuterol suppresses the GABAergic transmission, while blocking GABAergic transmission by the GABA A receptor blocker partially mimics the effect of clenbuterol. In behavioral tests, a post-training infusion of clenbuterol into mPFC enhances 24-h trace fear memory. In summary, we observed that prefrontal cortical b2-AR activation by clenbuterol facilitates tLTP and enhances trace fear memory. The mechanism underlying tLTP facilitation involves stimulating postsynaptic cAMP-PKA signaling cascades and suppressing GABAergic circuit activities.

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