The role of the ventromedial prefrontal cortex (vmPFC) in human pavlovian threat conditioning has been relegated largely to the extinction or reversal of previously acquired stimulus-outcome ...associations. However, recent neuroimaging evidence questions this view by also showing activity in the vmPFC during threat acquisition. Here we investigate the casual role of vmPFC in the acquisition of pavlovian threat conditioning by assessing skin conductance response (SCR) and declarative memory of stimulus-outcome contingencies during a differential pavlovian threat-conditioning paradigm in eight patients with a bilateral vmPFC lesion, 10 with a lesion outside PFC and 10 healthy participants (each group included both females and males). Results showed that patients with vmPFC lesion failed to produce a conditioned SCR during threat acquisition, despite no evidence of compromised SCR to unconditioned stimulus or compromised declarative memory for stimulus-outcome contingencies. These results suggest that the vmPFC plays a causal role in the acquisition of new learning and not just in the extinction or reversal of previously acquired learning, as previously thought. Given the role of the vmPFC in schema-related processing and latent structure learning, the vmPFC may be required to construct a detailed representation of the task, which is needed to produce a sustained conditioned physiological response in anticipation of the unconditioned stimulus during threat acquisition.
Pavlovian threat conditioning is an adaptive mechanism through which organisms learn to avoid potential threats, thus increasing their chances of survival. Understanding what brain regions contribute to such a process is crucial to understand the mechanisms underlying adaptive as well as maladaptive learning, and has the potential to inform the treatment of anxiety disorders. Importantly, the role of the ventromedial prefrontal cortex (vmPFC) in the acquisition of pavlovian threat conditioning has been relegated largely to the inhibition of previously acquired learning. Here, we show that the vmPFC actually plays a causal role in the acquisition of pavlovian threat conditioning.
Although a substantial progress has been made in recent years on understanding the processes mediating extinction of learned threat, little is known about the context-dependent extinction of threat ...memories in elderly individuals. We used a 2-day differential threat conditioning and extinction procedure to determine whether young and older adults differed in the contextual recall of conditioned responses after extinction. On Day 1, conditioned stimuli were paired with an aversive electric shock in a 'danger' context and then extinguished in a different 'safe' context. On Day 2, the extinguished stimulus was presented to assess extinction recall (safe context), and threat renewal (danger context). Physiological and verbal report measures of threat conditioning were collected throughout the experiment. Skin conductance response (SCR data revealed no significant differences between age groups during acquisition and extinction of threat conditioning on Day 1. On Day 2, however, older adults showed impaired recall of extinction memory, with increased SCR to the extinguished stimulus in the 'safe' context, and reduced ability to process context properly. In addition, there were no age group differences in fear ratings and contingency awareness, thus revealing that aging selectively impairs extinction memories as indexed by autonomic responses. These results reveal that aging affects the capacity to use context to modulate learned responses to threat, possibly due to changes in brain structures that enable context-dependent behaviour and are preferentially vulnerable during aging.
Learning to recognize and respond to potential threats is crucial for survival. Pavlovian threat conditioning represents a key paradigm for investigating the neurobiological mechanisms of fear ...learning. In this review, we address the role of specific neuropharmacological adjuvants that act on neurochemical synaptic transmission, as well as on brain plasticity processes implicated in fear memory. We focus on novel neuropharmacological manipulations targeting glutamatergic, noradrenergic, and endocannabinoid systems, and address how the modulation of these neurobiological systems affects fear extinction learning in humans. We show that the administration of N-methyl-D-aspartate (NMDA) agonists and modulation of the endocannabinoid system by fatty acid amide hydrolase (FAAH) inhibition can boost extinction learning through the stabilization and regulation of the receptor concentration. On the other hand, elevated noradrenaline levels dynamically modulate fear learning, hindering long-term extinction processes. These pharmacological interventions could provide novel targeted treatments and prevention strategies for fear-based and anxiety-related disorders.
Emotions are able to impact our ability to control our behaviors. However, it is not clear whether emotions play a detrimental or an advantageous effect on action control and whether the valence of ...the emotional stimuli differently affects such motor abilities. One way to measure reactive inhibitory control is the stop-signal task (SST), which estimates the ability to cancel outright a response to the presentation of a stop signal by means of the stop signal reaction times (SSRT). Impaired as well as facilitated action control has been found when faced with emotional stimuli such as stop signals in SSTs and mixed results were observed for positive versus negative stimuli. Here, we aimed to investigate these unresolved issues more deeply. Action control capabilities were tested in 60 participants by means of a SST, in which the stop signals were represented by a fearful and a happy body posture together with their neutral counterpart. Results showed that both positive and negative body postures enhanced the ability to suppress an ongoing action compared to neutral body postures. These results demonstrate that emotional valence-independent emotional stimuli facilitate action control and suggest that emotional stimuli may trigger increased sensory representation and/or attentional processing that may have promote stop-signal processing and hence improved inhibitory performance.
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