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The NSF introduces the elicitation of endogenous fear through the perception of novel, anxiogenic spaces, as added variable.
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The approach, therefore, seems ill-suited to capture cases where endogenous epidemics of fear inspire widespread adaptations unrelated to prevalence.
In addition, pharmacological blockade of Y1 receptors in the BLA inhibited extinction, suggesting a facilitating role of endogenous NPY on fear extinction by acting on Y1 receptors in the BLA.
However, a facilitatory role of endogenous cortisol on fear memory consolidation is observed only in male subjects and in subjects with high cortisol levels (Zorawski et al. 2006), suggesting a rather minor impact of this factor in our (random female) sample.
Endogenous cannabinoids also influence fear responding.
Additionally, the endogenous aetiologies of dental fear were considered as general anxiety and depressive disorders, especially multiple phobias and depressive personality [ 41– 41].
CB1 receptor knockout-impaired fear extinction and endogenous cannabinoid levels were increased in the BLA after extinction training (Marsicano et al., 2002).
Modulation of fear and anxiety by the endogenous cannabinoid system.
The intracellular location of epitope-tagged proteins can be identified in immunofluorescence experiments in a similarly well-controlled manner, without fear of cross-reactivity with the endogenous protein.
Endogenous co-agonists of the NMDA receptor modulate contextual fear in trace conditioning.
The aim of the present study was to characterize the role of endogenous NPY in acquisition, expression and extinction of conditioned fear, and to investigate the participation of individual NPY receptors in these processes.
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