Yan Jiao Wu

TL;DR: It is found that genetic deletion or pharmacological blockade of ASIC1a greatly reduced, but did not fully abolish, the probability of long-term potentiation (LTP) induction by either single or repeated high frequency stimulation or theta burst stimulation in the CA1 region.

TL;DR: It is reported that acid-sensing ion channel 1a (ASIC1a) is a crucial molecular regulator of fear extinction, and that this function requires ASIC1a in ventral hippocampus (vHPC), but not dorsal hippocampus, mPFC, or BLA, while genetic disruption or pharmacological inhibition in vHPC attenuated the extinction of conditioned fear, overexpression of the channel in this area promoted fear extinction.

TL;DR: The functional role of ASIC1a was found to be critical for striatum-dependent motor coordination and procedural learning by regulating the synaptic plasticity of striatal medium spiny neurons.

TL;DR: In this article , two distinct projection neuron subpopulations in physical proximity within the IC, targeting the central amygdala (CeA) and nucleus accumbens (NAc), respectively, were found to be preferentially innervated by intercortical inputs from the orbitofrontal cortex (OFC), specifically enhancing extinction to override fear memory.

TL;DR: In this paper , the authors found that sustained elevation in ambient GABA levels, by either genetic deletion or pharmacological blockade of GABA transporter-1 (GAT1), leads to synaptic scaling up of corticostriatal pathways, which underlies locomotor hyperactivity.