All paradigms consisted of both a fear-conditioning session and a fear-expression test at different post conditioning intervals, i.e. presenting the CS to the animals for a short duration.
This observation is in accordance with our current experiments revealing an increased fear expression in NPY KO mice.
The first analysis examined responses to morphs that included a degree of fear expression.
Using fear-potentiated startle as a measure in rats, Broqua et al. (1995) showed that intracerebroventricular application of the Y1 receptor-preferring agonist LeuProNPY results in a reduction of fear expression.
The study focused on 28 volunteers who, in response to being prompted, made the wide-eyed fear expression, a neutral facial expresson, or an expression of disgust.
They find that upon reinstatement of fear c-Fos labeling is reduced in the infralimbic cortex (IL) and the connected ITC but increased in the central nucleus of the amygdala (CEM), which is a key nucleus of fear expression.
In brief, following fear expression, a wave of gene transcription, akin to that following CBT-based fear extinction (see the 'Quantifying fear and fear extinction in pre-clinical animal models' section above), is required to (re consolidate the recently retrieved fear memory, which has been transferred into a labile short-term memory, into a stable long-term memory.
The IL inhibits the medial subdivision of the central nucleus of the amygdala (CeM), a key region for fear expression (Wilensky et al., 2006; Ciocchi et al., 2010), partly through intercalated amygdala neurons (ITCs) (Likhtik et al., 2008; Amano et al., 2010), which are also necessary for extinction.
Individuals can also acquire fear from a social context, such as through observing the fear expression of a conspecific.
This species-specific defense response can be reliably acquired in a single conditioning trial, making it a widely used model for fear expression and learning and memory.
