Design of a Neurally Plausible Model of Fear Learning

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.

Hebbian and neuromodulatory mechanisms interact to trigger associative memory formation

“…One possibility is that activation of β-ARs, which are Gs protein-coupled receptors, modulates Hebbian, calcium-dependent processes through direct interactions in intracellular signaling networks (17). This type of mechanism has been elegantly identified in invertebrates (3,11,16) and in studies of mammalian synaptic plasticity (7,13,14,18,19) and could serve both to facilitate plasticity induction and learning and to enhance long-term memory consolidation through synergistic action occurring within LA glutamatergic projection neurons (for reviews see refs. 4,11,12,17).…”

“…Findings from in vitro and in vivo physiological studies suggest that Hebbian processes control synaptic strengthening (2-10). However, other results and theories suggest that Hebbian mechanisms alone are not normally sufficient for producing synaptic plasticity and that synaptic strengthening mediating memory formation involves interactions between Hebbian and neuromodulatory mechanisms (3,4,7,(11)(12)(13)(14)(15)(16)(17)(18)(19). Although molecules that may mediate Hebbian processes in memory formation have been identified (3,11,16,17,(20)(21)(22), it has been difficult to directly test whether Hebbian plasticity alone or in combination with neuromodulation is necessary and sufficient to produce neural plasticity and memories in behaving animals (especially in mammals).…”

Computational Models of the Amygdala in Acquisition and Extinction of Conditioned Fear

“…With the advance of neurophysiology, we now know the amygdala can be divided into several functionally distinct nuclei in the processing of CS/US information (reviewed above). In keeping with new emerging neurobiological data, recent connectionist models of fear learning have started to model finer details of the amygdala circuitry and evolved from modeling only one or two brain structures to multiple regions and their interactions [33,34,72,78]. For example, to understand the cognitive-emotional interaction mediating flexible behaviors, John et al [34] developed an amygdala circuit model that consists of three subnetworks: (1) the BLA subnetwork; (2) the ITC subnetwork; and (3) the central output subnetwork.…”

Auditory Fear Circuits in the Amygdala – Insights from Computational Models

“…The model revealed how the two populations might encode contextual specificity of fear and extinction memories. Krasne et al (2011) report a model of the amygdala and hippocampus where fear conditioning and extinction memories 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 model was developed using a firing rate framework and was able to reproduce several known features of fear learning and make testable predictions.…”