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Dysfunction in amygdala-prefrontal plasticity and extinction-resistant avoidance: A model for anxiety disorder
Jennifer E C Fragale1, Veronika Khariv2, Danielle M Gregor3
1Neurobehavioral Research Laboratory, Research Service, VA New Jersey Heath Care System, East Orange, NJ 07018, USA; Graduate School of Biomedical Sciences, New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, NJ 07103, USA.
Experimental Neurology
|November 8, 2015
Summary
Anxiety vulnerability may stem from innate dysfunction in amygdala-prefrontal cortex (PFC) connections. Impaired synaptic plasticity in WKY rats, a model for anxiety, suggests disrupted communication underlies avoidance behaviors.
Area of Science:
- Neuroscience
- Behavioral Neuroscience
- Psychiatry
Background:
- Anxiety disorders are linked to innate vulnerability and dysfunction in amygdala-prefrontal cortex (PFC) circuits.
- The precise connection between anxiety vulnerability and amygdala-PFC abnormalities remains unclear.
Purpose of the Study:
- To investigate if innate dysfunction in the amygdala to PFC projection contributes to anxiety-like behavior susceptibility.
- To examine synaptic plasticity in the basolateral amygdala (BLA) to prelimbic cortex (PL) pathway in an anxiety-vulnerable rodent model.
Main Methods:
- Utilized the Wistar Kyoto (WKY) rat, an anxiety-vulnerable model, and Sprague Dawley (SD) rats.
- Assessed synaptic plasticity, specifically long-term potentiation (LTP), in the BLA-PL projection.
- Investigated the role of NMDA receptors and tested d-cycloserine treatment.
Main Results:
- WKY rats showed normal paired-pulse plasticity but impaired LTP in the BLA-PL projection compared to SD rats.
- Lesioning the PL cortex in SD rats mimicked the extinction-resistant avoidance seen in WKY rats.
- Impaired LTP in WKY rats was linked to reduced NR2A-containing NMDA receptors in the PL cortex.
Conclusions:
- Dysfunction in amygdala-PFC synaptic plasticity is an innate characteristic of anxiety-vulnerable rats.
- This impaired plasticity may promote extinction-resistant avoidance by disrupting amygdala-PFC communication.
- Targeting NMDA receptors warrants further investigation for anxiety disorder treatment.
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