Abstract
A neurally oriented conceptual and computational model of fear conditioning manifested by freezing behavior (FRAT), which accounts for many aspects of delay and context conditioning, has been constructed. Conditioning and extinction are the result of neuromodulation-controlled LTP at synapses of thalamic, cortical, and hippocampal afferents on principal cells and inhibitory interneurons of lateral and basal amygdala. The phenomena accounted for by the model (and simulated by the computational version) include conditioning, secondary reinforcement, blocking, the immediate shock deficit, extinction, renewal, and a range of empirically valid effects of pre- and post-training ablation or inactivation of hippocampus or amygdala nuclei.
Highlights
Cues that predict the imminent onset of pain or danger as well as the situational contexts in which such events occur come to evoke fear
There is considerable evidence that the acquisition of conditional fear can be substantially attributed to forms of long-term potentiation at synapses of cortical, thalamic, and hippocampal afferents on cells of the basolateral region of the amygdala (BLA; Blair et al, 2001)
While for modeling purposes we focused on freezing, the model is expected to generalize to other commonly used measures such as fear-potentiated startle, autonomic arousal, conditioned suppression, and inhibitory avoidance, with the greatest differences being in response generation circuitry downstream from the BLA (Hitchcock and Davis, 1986; LeDoux et al, 1988; Tomaz et al, 1993; Amorapanth et al, 1999)
Summary
Cues that predict the imminent onset of pain or danger as well as the situational contexts in which such events occur come to evoke fear In laboratory animals this has a variety of manifestations including freezing, cardiac responses, and analgesia (Bolles and Fanselow, 1980). There is not yet consensus on the locus of extinction, a variety of lines of work, both behavioral and neurophysiological, have established that under most circumstances extinction is at least in part due to learned inhibition of activity in fear-producing pathways and not primarily to erasure of the changes that caused the original conditioning (Bouton, 1993, 2004). While these are major advances, there are many conspicuous properties of fear learning for which we neither know the mechanisms nor have hypotheses of a kind that invite physiological testing
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