Abstract

Shock, immobilization, and exposure to predator-related stimuli have all been used to study fear conditioning in rodents, but they have never been used in conjunction in a single study. Experiment 1 compared the effects of these three reinforcers, alone and in various combinations, on the expression of long-term conditioned fear memory and extinction in adult male rats. Whereas foot shock conditioning, alone, was rapidly extinguished; the combination of immobilization and cat exposure, or all 3 stimuli together, produced a significant increase in the magnitude of fear conditioning and greater resistance to extinction, which persisted for at least 5 weeks post-training (p < 0.05). Experiment 2 assessed the role of the hippocampus in predator-based context and cued fear conditioning. Pharmacological suppression of hippocampal activity during fear conditioning produced a selective impairment of contextual, but not cued, fear memory. Experiment 3 investigated the effects of sleep deprivation prior to fear conditioning on the expression of fear memory. This experiment demonstrated that pre-training sleep deprivation blocked the expression of contextual (hippocampal-dependent), but not cued (hippocampal-independent), fear memory. Overall, this series of experiments has extended the use of predator exposure in conjunction with conventional reinforcers, such as foot shock and immobilization, to advance our understanding of the neurobiology of traumatic memory.

Highlights

  • Fear associations to environmental stimuli are part of an evolutionary defensive behavior system that protects individuals from danger [1]-[4]

  • Planned comparisons showed that muscimol infused prior to the cat procedure significantly reduced (p < 0.03) freezing compared to aCSF (Figure 3)

  • Previous work has shown that lesions or inactivation of the dorsal hippocampus prior to foot shock conditioning block the expression of contextual, but not cued, fear memory [23] [30]-[34]

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Summary

Introduction

Fear associations to environmental stimuli are part of an evolutionary defensive behavior system that protects individuals from danger [1]-[4]. Fear conditioning paradigms in a broad range of species [5]-[7] have investigated how environmental stimuli become associated with aversive events [8] [9], and the neural mechanisms underlying associative learning have been studied [10] [11]. Lesions of the amygdala block Pavlovian fear conditioning [17] and prevent freezing expressed to contexts and cues associated with foot shock [18]-[23]. Lesions of the amygdala made one week before or up to one month after training can block memory-related (freezing) behavior [19]. More recent work targeting the molecular biology of amygdala neurons has confirmed the crucial role of the lateral and basolateral subdivisions of the amygdala in the formation and expression of fear memories [24]-[27]

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