In fear conditioning, a rat is placed in a distinct environment and delivered footshock. The response to the footshock itself is called an activity burst and includes running, jumping, and vocalization. The fear conditioned to the distinct environment by the footshock elicits complete immobility termed freezing. Lesions of the ventral periaqueductal gray (vPAG) strongly attenuate freezing. However, lesions of the dorsolateral periaqueductal gray (dlPAG) increase the amount of freezing seen to conditional fear cues acquired under conditions in which intact rats do not demonstrate much fear conditioning. To examine the necessity of these regions in the acquisition and expression of fear, we performed five experiments that examined the effects of electrolytic lesions of the dlPAG and the vPAG in learned and unlearned fear. In experiment 1, lesions of the vPAG strongly attenuated, whereas lesions of the dlPAG enhanced, unconditional freezing to a cat. In experiment 2, lesions of the dlPAG made before but not after training enhanced the amount of freezing shown to conditional fear cues acquired via immediate footshock delivery. In experiment 3, vPAG lesions made either before or after training with footshock decreased the level of freezing to conditional fear cues. Neither dlPAG lesions nor vPAG lesions affected footshock sensitivity (experiment 4) or consumption on a conditioned taste aversion test that does not elicit antipredator responses (experiment 5). On the basis of these results, it is proposed that activation of the dlPAG produces inhibition of the vPAG and forebrain structures involved with defense. In contrast, the vPAG seems to be necessary for postencounter freezing defensive behavior.

The nature and mechanisms of synaptic plasticity in the amygdala and the relation of amygdaloid plasticity to behavior are exciting new areas of study in neuroscience. These issues were at the heart of presentations by Paul Chapman, Michael Fanselow, Patricia Shinnick‐Gallagher, and Michael Rogawski in a session entitled “Long‐Term Plasticity in Amygdala Synaptic Transmission” that was held at the conference featured in this volume. In this chapter, I briefly summarize these talks and give my perspective on the presentations as the session chair. I argue that we must first understand the role of the amygdala in learning and memory in order to understand the contribution of amygdaloid synaptic plasticity to behavior. Although it is generally agreed that the amygdala is involved in several forms of emotional learning and memory such as pavlovian fear conditioning, a recent debate has emerged concerning the precise role of the amygdala in learning versus performing fear responses. I discuss data from my laboratory that unravel this issue. I argue that the basolateral complex of the amygdala (BLA) normally plays an essential role in associative processes in fear conditioning. Nonetheless, rats with BLA lesions acquire and express conditional fear under some conditions. A neuroanatomical model that accounts for these data is presented.

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The present experiments compared the effects of 2 appetitive motivational states on the acquisition of Pavlovian fear conditioning in rats (Rattus norvegicus). In Experiment 1, rats were deprived of either water or food prior to contextual fear conditioning, which consisted of the delivery of a single footshock in a novel observation chamber. Conditional fear to the contextual cues of the conditioning chamber was measured by observing freezing behavior. The results revealed that water, but not food, deprivation enhanced conditional freezing to contextual stimuli paired with footshock. Experiment 2 indicated that the different impact of food or water deprivation on the acquisition of conditional freezing was not due to differential generalization decrements during extinction testing. Together, these experiments suggest that the modulation of fear conditioning by deprivation state is specific to certain motivational systems.

Emergence neophobia was assessed in an emergence apparatus that provided a choice between novel and familiar alternatives. Two weeks after emergence testing, the threshold to induce perforant-path long-term potentiation (LTP) and the magnitude of perf ora nt-path LTP in the dentate gyrus were assessed under pentobarbital anesthesia. Two measures of emergence behavior, the total duration of time spent in the alley during the I-h test and the emergence duration per entry into the novel compartment, were significantly correlated with L TP of the extracellular population excitatory postsynaptic potential (EPSP), but not with the population spike. Neophobic animals that spent relatively little time in the novel alley during the I-h test had a lower threshold to induce L TP and exhibited greater asymptotic EPSP L TP than did neophilic animals that readily entered and explored the novel alley. In a second experiment, plasma corticosterone levels in animals tested in the emergence task were also correlated with emergence duration and were generally lower in neophobic animals. Together, these data suggest that neotic behavior and LTP share a common mechanism, possibly one mediated by an interaction of glucocorticoid hormones and habituation.Long-term potentiation (LTP) is an enduring form of synaptic enhancement induced at excitatory synaptic contacts in the mammalian brain by brief episodes of rhythmic electrical stimulation (