Thy1-Expressing Neurons in the Basolateral Amygdala May Mediate Fear Inhibition

• DOI: 10.1523/jneurosci.5539-12.2013
• Publication Date: 2013-06-19T16:18:44Z
• Authors: A. M. Jasnow; D. E. Ehrlich; D. C. Choi; J. Dabrowska; M. E. Bowers; K. M. McCullough; D. G. Rainnie; K. J. Ressler
• Keywords: Basolateral amygdala; Extinction (optical mineralogy); Freezing behavior; Stimulus (psychology); Channelrhodopsin

Research has identified distinct neuronal circuits within the basolateral amygdala (BLA) that differentially mediate fear expression versus inhibition; however, molecular markers of these populations remain unknown. Here we examine whether optogenetic activation a cellular subpopulation, which may correlate with physiologically extinction neurons in BLA, would support conditioning inhibition/extinction. We first molecularly characterized Thy1-channelrhodopsin-2 (Thy1-ChR2-EYFP)-expressing as subpopulation glutamatergic pyramidal BLA. Optogenetic stimulation inhibited medial central and shunted excitation from lateral amygdala. Brief during training disrupted later memory male mice. unreinforced stimulus exposure enhanced retention, but had no effect on expression, locomotion, or open-field behavior. Together, data suggest Thy1-expressing BLA provide an important pharmacological target for inhibiting enhancing furthering our understanding mechanisms processing.