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Neural circuitry involved in fear conditioning and odor avoidance in an animal model for Multiple Chemical Sensitivity (MCS)
Author(s) -
Cocking Davelle Leigh,
Quock Raymond Mark,
Sorg Barbara Ann
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a788
Subject(s) - odor , muscimol , freezing behavior , extinction (optical mineralogy) , psychology , basolateral amygdala , amygdala , neuroscience , prefrontal cortex , anxiety , panic disorder , fear conditioning , medicine , chemistry , psychiatry , agonist , mineralogy , receptor , cognition
A defining characteristic of the ill‐defined disorder MCS is an avoidance of odors. Another symptom, anxiety, has led some investigators to draw parallels between MCS and other disorders such as panic and posttraumatic stress. Panic disorder can be modeled in animals by fear conditioning; therefore, we fear‐conditioned animals to an odor (CS) paired with a 0.2mA footshock (US) and then tested for freezing and odor avoidance (fear responses). The underlying brain circuitry involved in these fear responses was tested via microinjection of the GABA agonists baclofen/muscimol (B/M) into either the basolateral amygdala (BLA), the central nucleus of the amygdala (CEA), or the medial prefrontal cortex (mPFC). Five minutes after drug infusion, rats were monitored for freezing behavior followed immediately by odor avoidance testing. Percent time freezing was lower in B/M‐treated rats and higher in the BLA and CEA. Odor avoidance was lower in CEA B/M‐treated rats versus controls and lower in mPFC B/M‐treated rats versus controls. Our results indicate the involvement of the CEA in odor avoidance and the involvement of the mPFC in the extinction of odor avoidance. Supported by NIH grant ES‐009135