The context differ in several features: flat floor with wood shavings instead of the grid, cylindrical wall instead of square, and blue instead of red illumination. Then on the fourth day, they were placed in a new context and presented with 10 retention trials. On the third day, the subjects received six paired or unpaired conditioning trials with the brain stimulation CS and the footshock US (for the stimulation parameters, refer to Fig. On the second day, the baseline freezing was measured to three CS-only trials. The current levels ranged between 30 and 200 μA. Once the final current was determined, ∼80% of that level was used for the CS throughout the experiment. Stimulus intensity was set at 30 μA initially and gradually increased until the rat showed one of the orienting responses. On the first day of training, the stimulation intensity for the CS was determined by detecting observable orienting responses, such as ear pricking or head movements. ![]() The CS was produced by a pulse generator (MASTER-8 A.M.P.I.) and delivered through a stimulus isolator (ISO-Flex A.M.P.I.) to the stimulating electrode connected by a captive collar (Plastics One). In addition, our experimental design with chronically implanted stimulating electrodes allows repeated measurements of EFPs, an ideal approach for monitoring cellular changes before and after learning. Second, by using the same stimulation site for both fear conditioning and triggering EFPs in the LA, the link between acquisition of memory and changes in synaptic efficacy can be more directly evaluated. First, MGm-stimulation CS reaches the LA directly, and any influence from upstream structures can be excluded. Using direct stimulation of the MGm in fear conditioning provides several distinct advantages over conventional auditory CSs for detecting learning-induced cellular changes. Intracranial stimulation has been used as a CS to train conscious animals in eyeblink conditioning and to track converging sensory pathways ( Steinmetz et al., 1986). In the current study, we tested whether fear conditioning induces detectable changes in the LA using microstimulation of the medial division of the medial geniculate nucleus of the thalamus (MGm), an immediate afferent input to the LA, as the CS. In fact, an alternative site of critical plasticity has been proposed ( Cahill et al., 1999). ![]() None of the studies, however, can exclude the possibility that the synaptic changes observed in the LA are secondary to those in other synapses in the fear circuit. Likewise, synaptic currents in LA neurons were potentiated in brain slices prepared from fear-conditioned rats ( McKernan and Shinnick-Gallagher, 1997). In support of the hypothesis, it has been shown that fear conditioning enhances auditory CS-evoked field potentials (EFPs) in the LA ( Rogan et al., 1997) and short-latency neuronal responses in freely moving animals ( Quirk et al., 1995). Specifically, fear conditioning potentiates synaptic efficacy of some LA neurons, and the increased excitability of those neurons modifies the way CS information is transmitted. ![]() The weight of the anatomical and neurobiological evidence suggests that the amygdala, especially the lateral nucleus (LA), is where the sensory information for the CS and the US converge ( Romanski et al., 1993), and the critical cellular changes occur as a result of the convergent activation ( Fanselow and LeDoux, 1999).Ī plausible hypothesis for the cellular mechanisms of fear memory trace has been proposed to suggest that neurophysiological properties of LA neurons change as a result of learning ( Maren, 1999 Blair et al., 2001). The fast and reliable nature of fear conditioning allowed an extensive analysis of related neural components in mammalian brain ( Blanchard and Blanchard, 1972 Davis, 1992 LeDoux, 2000). As a result, the CS comes to elicit the conditioned response (CR), an orchestration of autonomic, behavioral, and endocrine responses that prepares the organism for the upcoming threat. In a typical fear conditioning, an initially neutral conditioned stimulus (CS) is contingently paired with an aversive unconditioned stimulus (US). Pavlovian fear conditioning is among a handful of learning paradigms in which well defined neural circuits have been delineated. A prerequisite for testing the SPM hypothesis, therefore, is to identify the neural circuit for the target behavior and to focus on the key sites for learning-induced synaptic plasticity. In mammalian brain, complexity of most learning tasks unavoidably demands a network of neurons, making it impossible to monitor all potentially relevant synapses. Despite the near-unanimous consensus that learning induces detectable synaptic modifications in the brain, as originally proposed by Hebb (1949) and formularized in the “synaptic plasticity and memory (SPM)” hypothesis ( Martin et al., 2000), direct evidence linking localized cellular changes with behavior has been rare.
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