Optogenetic manipulation of the prelimbic cortex during fear memory reconsolidation alters fear extinction in a preclinical model of comorbid PTSD/AUD

Author(s):  
C. E. Smiley ◽  
J. T. McGonigal ◽  
K. E. Nimchuk ◽  
J. T. Gass
2013 ◽  
Vol 244 ◽  
pp. 137-141 ◽  
Author(s):  
Fabricio H. Do Monte ◽  
Rimenez R. Souza ◽  
Ting T. Wong ◽  
Antonio de Padua Carobrez

2013 ◽  
Vol 21 (1) ◽  
pp. 753-759 ◽  
Author(s):  
C. A. J. Stern ◽  
L. Gazarini ◽  
A. C. Vanvossen ◽  
M. S. Hames ◽  
L. J. Bertoglio

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Thiago Rodrigues da Silva ◽  
Ana Maria Raymundi ◽  
Leandro José Bertoglio ◽  
Roberto Andreatini ◽  
Cristina A. Stern

2014 ◽  
Vol 24 ◽  
pp. S322 ◽  
Author(s):  
C.A. Stern ◽  
L. Gazarmi ◽  
A.C. Vanvossen ◽  
A.W. Zuardi ◽  
F.S. Guimarães ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Leonardo Santana Novaes ◽  
Letícia Morais Bueno-de-Camargo ◽  
Carolina Demarchi Munhoz

AbstractThe persistence of anxiety and the deficit of fear memory extinction are both phenomena related to the symptoms of a trauma-related disorder, such as post-traumatic stress disorder (PTSD). Recently we have shown that single acute restraint stress (2 h) in rats induces a late anxiety-related behavior (observed ten days after stress), whereas, in the present work, we found that the same stress impaired fear extinction in animals conditioned ten days after stress. Fourteen days of environmental enrichment (EE) prevented the deleterious effect of stress on fear memory extinction. Additionally, we observed that EE prevented the stress-induced increase in AMPA receptor GluA1 subunit phosphorylation in the hippocampus, but not in the basolateral amygdala complex and the frontal cortex, indicating a potential mechanism by which it exerts its protective effect against the stress-induced behavioral outcome.


2015 ◽  
Vol 594 ◽  
pp. 1-5 ◽  
Author(s):  
Yu Hou ◽  
Liyan Zhao ◽  
Genai Zhang ◽  
Lixiang Ding

Author(s):  
Lucas A. Marcondes ◽  
Jociane de C. Myskiw ◽  
Eduarda G. Nachtigall ◽  
Rodrigo F. Narvaes ◽  
Ivan Izquierdo ◽  
...  

2017 ◽  
Vol 2 (2) ◽  
pp. 158-169 ◽  
Author(s):  
Valerio Rizzo ◽  
Khalid Touzani ◽  
Bindu L. Raveendra ◽  
Supriya Swarnkar ◽  
Joan Lora ◽  
...  

Author(s):  
Masoomeh Dadkhah ◽  
◽  
Abbas Ali Vafaei ◽  
Ali Rashidy-Pour ◽  
Parnia Trahomi ◽  
...  

Purpose: The basolateral amygdala (BLA) and infralimbic area (IL) of medial prefrontal cortex (mPFC) are two inter-connected brain structures that mediate both fear memory expression and extinction. Besides the well-known role of the BLA in the acquisition and expression of fear memory, projections from IL to BLA inhibit fear expression and have a critical role in fear extinction. However, the details of IL-BLA interaction remain unclear. Here, we aimed to investigate the role of functional reciprocal interactions between BLA and IL in mediating fear memory extinction. Methods: Using lidocaine (LID), male rats underwent unilateral or bilateral inactivation of the BLA and then unilateral intra-IL infusion of CORT, prior to extinction training of auditory fear conditioning paradigm. Freezing behavior was reported as an index for the measurement of conditioned fear. Infusions were performed before the extinction training, allowing to examine the effects on fear expression and also further extinction memory. Experiments 1-3 investigated the effects of left or right infusion of CORT into IL, and LID unilaterally into BLA on fear memory extinction. Results: Results showed that intra-IL infusion of CORT in the right hemisphere reduced freezing behavior when administrated before the extinction training. Auditory fear memory extinction was impaired by asymmetric inactivation of BLA and CORT infusion in the right IL; however, the same effect was not observed with symmetric inactivation of BLA. Conclusion: It is concluded that that the IL-BLA neural circuit may provide additional evidence to contribution of this circuit in auditory fear extinction. This study demonstrate dissociable roles for right or left BLA in subserving the auditory fear extinction. Our finding also raise the possibility that left BLA-IL circuitry may contribute in mediating auditory fear memory extinction via underlying mechanisms, however further research is required.


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