If fear memory is expressed by a long-term potentiation (LTP) of synaptic transmission in the amygdala, then reversal of LTP (depotentiation) in this area of the brain may provide an important mechanism for amelioration of anxiety and post-traumatic stress disorder. Herein, we show that low-frequency stimulation (LFS) of the external capsule elicits a depotentiation in the lateral nucleus of the amygdala. The induction of depotentiation requires activation of N-methyl-D-aspartate receptors and voltage-dependent calcium channels but is independent of adenosine A 1 and metabotropic glutamate group II receptors. Extracellular perfusion or loading cells with protein phosphatase (PP) 2B (calcineurin) inhibitors prevents depotentiation. The same stimulating protocol applied to the amygdala in vivo attenuates the expression of fear memory measured with fearpotentiated startle and reduces conditioning-elicited phosphorylation of Akt and mitogen-activated protein kinase (MAPK). This is paralleled by an increase in the activity of calcineurin. In addition, application of calcineurin inhibitor blocks LFS-induced extinction of fear memory and MAPK dephosphorylation. Taken together, this study characterizes the properties of LFS-induced depotentiation in the amygdala and suggests an involvement of calcineurin cascade in synaptic plasticity and memory storage.The prevention of fear development or, more importantly, the erasure of fear memory is a major challenge to neuroscientists and psychiatrists today. Fear conditioning is the process by which a cue comes to induce an elevated startle when it is consistently paired with an aversive stimulus, such as a foot shock (Pavlov, 1927;Davis, 2000;LeDoux, 2000). It represents not only an animal model of fear and anxiety but also a model of long-term neural plasticity and memory because, once conditioned, animals can be left untrained for at least 1 month without a loss of startle susceptibility (Campeau and Davis, 1995). Previous studies suggested that LTP of synapses from auditory thalamus and cortex to the LA underlay the encoding of fear memory (McKernan and Shinnick-Gallagher, 1997;Rogan et al., 1997). If this is true, then depotentiation in these synapses may result in an attenuation of fear memory. In an analogous situation, it has been shown that administration of LFS to the amygdala in vivo blocked the development and expression of kindled seizures, a phenomenon termed quenching (Weiss et al., 1995). A recent report demonstrated that depotentiation could be induced at the EC-basolateral amygdala synapse (AroniadouAnderjaska et al., 2001); however, the underlying mechanism was not elucidated.In the present study, we first show that depotentiation occurs in the amygdala that is capable of reversing tetanusinduced LTP. Depotentiation is dependent on N-methyl-Daspartate (NMDA) receptor and VDCC activation and requires postsynaptic phosphatase activity. By behavioral assessment, we further demonstrate that administration of LFS to the EC or LA using depotentiation-like pa...

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Bi Fe O 3 (BFO) thin films produced with varied film thicknesses ranging from 100to230nm were fabricated on BaPbO3(BPO)∕Pt∕Ti∕SiOx∕Si substrates by rf-magnetron sputtering. Saturated polarization–electrical field hysteresis loops, polarization response by pulse measurement, and retention properties were obtained for BFO films with various thicknesses on BPO. The retention behaviors of BFO demonstrate logarithmic time dependence and stretched exponential law. When the thicknesses of BFO films increase, the contribution of logarithmic time dependence to retention, the stretched exponential law becomes dominant. BFO films with thinner thickness exhibit better retention properties but possess smaller remnant polarization.