ICLM Journal Club
This Week - 24 March 2017 (9:30 a.m., Gonda 2nd Floor Conference Room)
Speaker: Abha Rajbhandari
Title: Deletion of PAC1 Receptors From the Medial Intercalated Cells of the Amygdala Enhances Fear Generalization and Decreases Fear Extinction Whereas Deletion From the Basolateral Amygdala Decreases Fear Acquisition
https://www.ncbi.nlm.nih.gov/pubmed/24516127 https://www.ncbi.nlm.nih.gov/pubmed/21350482
Post-traumatic stress disorder (PTSD) involves inappropriate inhibitory control over fear after exposure to life-threatening traumatic experiences. Previous studies have linked the neuropeptide pituitary adenylate cyclase activating peptide (PACAP) and its G-coupled receptor PAC1 to PTSD diagnosis and symptom severity. PACAP and PAC1 are expressed in the neural circuitry of fear and regulate conditioned fear behaviors. Using mice expressing green fluorescent protein (GFP) in PACAP containing neurons we found that PACAP-containing neurons in the basolateral portion of the amygdala project into the medial intercalated cells (mICCs). mICCs are crucial for modulating fear extinction and express PAC1 receptors. Therefore, we investigated whether deletion of PAC1 receptors from the mICCs alters fear acquisition, generalization or extinction via AAV-driven Cre-recombinase infusion in PAC1 floxed mice. The results indicate that deletion of PAC1 receptors from the intercalated cells enhances fear generalization and reduces fear extinction potentially by decreasing feed-forward inhibition into the CeA. Deletion of these receptors from the BLA leads to deficit in fear acquisition. These results indicate that PACAP/PAC1 may play differential role in fear depending on the site of action in the fear circuitry. The finding that the mICCs modulate fear generalization is a novel and interesting as studies have focused on the role of ICCs in fear extinction, but not generalization.
About Us
Introduction
The Integrative Center for Learning and Memory (ICLM) is a multidisciplinary center of UCLA labs devoted to understanding the neural basis of learning and memory and its disorders. This will require a unified approach across different levels of analysis, including;
1. Elucidating the molecular cellular and systems mechanisms that allow neurons and synapses to undergo the long-term changes that ultimately correspond to 'neural memories'.
2. Understanding how functional dynamics and computations emerge from complex circuits of neurons, and how plasticity governs these processes.
3. Describing the neural systems in which different forms of learning and memory take place, and how these systems interact to ultimately generate behavior and cognition.
History of ICLM
The Integrative Center for Learning and Memory formally LMP started in its current form in 1998, and has served as a platform for many interactions and collaborations within UCLA. A key event organized by the group is the weekly ICLM Journal Club. For more than 10 years, graduate students, postdocs, principal investigators, and invited speakers have presented on topics ranging from the molecular mechanisms of synaptic plasticity, through computational models of learning, to behavior and cognition. Dean Buonomano oversees the ICLM journal club with help of student/post doctoral organizers. For other events organized by ICLM go to http://www.iclm.ucla.edu/Events.html.
Current Organizers:
Walt Babiec (O'Dell Lab) & Helen Motanis (Buonomano Lab)
Current Faculty Advisor:
Past Organizers:
i) Anna Matynia(Aug 2004 - Jun 2008) (Silva Lab)
ii) Robert Brown (Aug 2008 - Jun 2009) (Balleine Lab)
iii) Balaji Jayaprakash (Aug 2008 - Nov 2011) (Silva Lab)
iv) Justin Shobe & Thomas Rogerson (Dec 2011 - June 2013) (Silva Lab)
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