Acid-sensing ion channel 1a regulates the specificity of reconsolidation of conditioned threat responses.

Recent research on altering threat memory has focused on a reconsolidation window. During reconsolidation, threat memories are retrieved and become labile. Reconsolidation of distinct threat memories is synapse dependent, whereas the underlying regulatory mechanism of the specificity of reconsolidation is poorly understood. We designed a unique behavioral paradigm in which a distinct threat memory can be retrieved through the associated conditioned stimulus. In addition, we proposed a regulatory mechanism by which the activation of acid-sensing ion channels (ASICs) strengthens the distinct memory trace associated with the memory reconsolidation to determine its specificity. The activation of ASICs by CO2 inhalation, when paired with memory retrieval, triggers the reactivation of the distinct memory trace, resulting in greater memory lability. ASICs potentiate the memory trace by altering the amygdala-dependent synaptic transmission and plasticity at selectively targeted synapses. Our results suggest that inhaling CO2 during the retrieval event increases the lability of a threat memory through a synapse-specific reconsolidation process.

Post-stroke neuronal circuits and mental illnesses.

Stroke is one of the leading causes of death in the United States. It is also associated with severe mental illnesses, such as depression and anxiety, that hinder the rehabilitation of surviving patients. Thus, a better understanding of how stroke causes mental illnesses is crucial, but little is known about the neurological mechanisms involved. In this review, we summarized the most common mental illnesses developed after stroke, as well as the underlying mechanisms at the neuronal circuit level.

Labeling Aversive Memory Trace in Mouse Using a Doxycycline-inducible Expression System.

A memory trace, also known as a memory engram, is theorized to be a mechanism for physical memory storage in the brain ( Silva et al., 2009 ; Josselyn, 2010) and memory trace is associated with a specific population of neurons ( Liu et al., 2012 ; Ramirez et al., 2013 ). Labeling and stimulating those neurons will activate the memory trace ( Liu et al., 2012 ; Ramirez et al., 2013 ). Memory appears to be spread over different regions of the brain rather than being localized to one area. Therefore, the methods used to trace memory have the ability to improve our understanding of neuronal circuits. In this protocol, we introduce a doxycycline-inducible expression system to label the specific neurons associated with the original memory trace.