@article {2326,
	title = {Correction of amygdalar dysfunction in a rat model of fragile X syndrome.},
	journal = {Cell Rep},
	volume = {37},
	year = {2021},
	month = {2021 Oct 12},
	pages = {109805},
	abstract = {<p>Fragile X syndrome (FXS), a commonly inherited form of autism and intellectual disability, is associated with emotional symptoms that implicate dysfunction of the amygdala. However, current understanding of the pathogenesis of the disease is based primarily on studies in the hippocampus and neocortex, where FXS defects have been corrected by inhibiting group I metabotropic glutamate receptors (mGluRs). Here, we observe that activation, rather than inhibition, of mGluRs in the basolateral amygdala reverses impairments in a rat model of FXS. FXS rats exhibit deficient recall of auditory conditioned fear, which is accompanied by a range of in\&nbsp;vitro and in\&nbsp;vivo deficits in synaptic transmission and plasticity. We find presynaptic mGluR5 in the amygdala, activation of which reverses deficient synaptic transmission and plasticity, thereby restoring normal fear learning in FXS rats. This highlights the importance of modifying the prevailing mGluR-based framework for therapeutic strategies to include circuit-specific differences in FXS pathophysiology.</p>
},
	issn = {2211-1247},
	doi = {10.1016/j.celrep.2021.109805},
	author = {Fernandes, Giselle and Mishra, Pradeep K and Nawaz, Mohammad Sarfaraz and Donlin-Asp, Paul G and Rahman, Mohammed Mostafizur and Hazra, Anupam and Kedia, Sonal and Kayenaat, Aiman and Songara, Dheeraj and Wyllie, David J A and Schuman, Erin M and Kind, Peter C and Chattarji, Sumantra}
}
@article {1584,
	title = {Extinction recall of fear memories formed before stress is not affected despite higher theta activity in the amygdala.},
	journal = {Elife},
	volume = {7},
	year = {2018},
	month = {2018 08 13},
	abstract = {<p>Stress is known to exert its detrimental effects not only by enhancing fear, but also by impairing its extinction. However, in earlier studies stress exposure preceded both processes. Thus, compared to unstressed animals, stressed animals had to extinguish fear memories that were strengthened by prior exposure to stress. Here, we dissociate the two processes to examine if stress specifically impairs the acquisition and recall of fear extinction. Strikingly, when fear memories were formed before stress exposure, thereby allowing animals to initiate extinction from comparable levels of fear, recall of fear extinction was unaffected. Despite this, we observed a persistent increase in theta activity in the BLA. Theta activity in the mPFC, by contrast, was normal. Stress also disrupted mPFC-BLA theta-frequency synchrony and directional coupling. Thus, in the absence of the fear-enhancing effects of stress, the expression of fear during and after extinction reflects normal regulation of theta activity in the mPFC, not theta hyperactivity in the amygdala.</p>
},
	keywords = {Amygdala, Animals, Extinction, Psychological, Fear, Male, Memory, Mental Recall, Prefrontal Cortex, Rats, Sprague-Dawley, Stress, Physiological, Theta Rhythm},
	issn = {2050-084X},
	doi = {10.7554/eLife.35450},
	author = {Rahman, Mohammed Mostafizur and Shukla, Ashutosh and Chattarji, Sumantra}
}
