The role of the hippocampus in memory is commonly investigated by comparing fear conditioning paradigms that differ in their reliance on the hippocampus. For example, the dorsal (septal) portion of the hippocampus is involved in trace, but not delay fear conditioning, two Pavlovian paradigms in which only the relative timing of stimulus presentation is varied. However, a growing literature implicates the ventral (temporal) portion of the hippocampus in the expression of fear, irrespective of prior training. The current experiments evaluated the relative contributions of the dorsal and ventral portions of the hippocampus to trace fear conditioning specifically vs. the expression of conditioned fear in general. Lesions restricted to the dorsal hippocampus blocked acquisition of trace fear conditioning. Larger lesions, also including an adjacent portion of the ventral hippocampus, were required to impair retrieval of trace fear conditioning. Delay fear conditioning was not disrupted in either case. In contrast, lesions that encompassed almost the entire dorsal and ventral hippocampus disrupted expression of both trace and delay fear conditioning. The current data suggest distinct roles in fear conditioning for three regions of the hippocampus: the septal zone is required for acquisition of trace fear conditioning, a larger portion of the hippocampus is critical for memory retrieval, and a region including the temporal zone is required for expression of both trace and delay fear conditioning. These findings are consistent with evidence suggesting the neuroanatomical and functional segregation of the hippocampus into three zones along its septal-temporal axis.

In two experiments, the time course of the expression of fear in trace (hippocampus-dependent) versus delay (hippocampus-independent) conditioning was characterized with a high degree of temporal specificity using fear-potentiated startle. In experiment 1, groups of rats were given delay fear conditioning or trace fear conditioning with a 3-or 12-sec trace interval between conditioned stimulus (CS) offset and unconditioned stimulus (US) onset. During test, the delay group showed fear-potentiated startle in the presence of the CS but not after its offset, whereas the trace groups showed fear-potentiated startle both during the CS and after its offset. Experiment 2 compared the time course of fear expression after trace conditioning with the time course in two delay conditioning groups: one matched to the trace conditioning group with respect to CS duration, and the other with respect to ISI. In all groups, fear was expressed until the scheduled occurrence of the US and returned to baseline rapidly thereafter. Thus, in both trace and delay fear conditioning, ISI is a critical determinant of the time course of fear expression. These results are informative as to the possible role of neural structures, such as the hippocampus, in memory processes related to temporal information.Although in Pavlovian delay conditioning presentations of the conditioned stimulus (CS) and the unconditioned stimulus (US) overlap, in trace conditioning a temporal gap or "trace" interval is interposed between the CS and the US. Even though eyeblink (i.e., skeletal) and fear (i.e., emotional) conditioning rely upon different neural substrates, the hippocampus has been shown to be critically involved in trace conditioning in both preparations (Moyer Jr. et al. 1990;McEchron et al. 1998;Quinn et al. 2002). Thus, the hippocampus is unlikely to be involved simply in the expression of the motoric or emotional responses associated with trace conditioning. Rather, given that trace (hippocampally dependent) and delay (hippocampally independent) conditioning differ solely with respect to the relative timing of CS and US presentation, the hippocampus would appear to be critically involved in mnemonic processes related to encoding the temporal relationship between the CS and the US. To understand hippocampal function, it is important, therefore, to characterize how the timing of conditioned responses in delay and trace conditioning relates to the timing of occurrences of the CS and US in training (see Quinn et al. 2002). In the current studies, this issue was addressed by using the acoustic startle reflex to assess the time course of the expression of conditioned fear after trace and delay conditioning.Some evidence supporting the contention that the hippocampus is involved in the temporal aspects of memory for trace conditioning is derived from the finding that hippocampal lesions sometimes simply cause a diminution in the latency and amplitude of conditioned eyeblink responses, rather than an outright block of trace eyeblink conditioning (Port et al...

Although contextual fear conditioning emerges later in development than explicit-cue fear conditioning, little is known about the stimulus parameters and biological substrates required at early ages. The current experiments adapted methods for investigating hippocampus function in adult rodents to identify determinants of contextual fear conditioning in developing rats. Experiment 1 examined the duration of exposure required by weanling rats at postnatal day (PND) 23 to demonstrate contextual fear conditioning. This experiment demonstrated that 30 s of context exposure is sufficient to support conditioning. Furthermore, preexposure enhanced conditioning to an immediate footshock, the context preexposure facilitation effect (CPFE), but had no effect on contextual conditioning to a delayed shock. Experiment 2 demonstrated that NMDA receptor inactivation during preexposure impairs contextual learning at PND 23. Thus, the conjuctive representations underlying the CPFE are NMDA-dependent as early as PND23 in the rat.

Two methods assessed the use of experimenter-given directional cues by a New World monkey species, cotton top tamarins (Saguinus oedipus). Experiment 1 used cues to elicit visual co-orienting toward distal objects. Experiment 2 used cues to generate responses in an object-choice task. Although there were strong positive correlations between monkey pairs to co-orient, visual co-orienting with a human experimenter occurred at a low frequency to distal objects. Human hand pointing cues generated more visual co-orienting than did eye gaze to distal objects. Significant accurate choices of baited cups occurred with human point and tap cues and human look cues. Results highlight the importance of head and body orientation to induce shared attention in cotton top tamarins, both in a task that involved food getting and a task that did not.

Long-term memory for fear of an environment (contextual fear conditioning) emerges later in development (postnatal day; PD 23) than long-term memory for fear of discrete stimuli (PD 17). As contextual, but not explicit cue, fear conditioning relies on the hippocampus; this has been interpreted as evidence that the hippocampus is not fully developed until PD 23. Alternatively, the hippocampus may be functional prior to PD 23, but unable to cooperate with the amygdala for fearful learning. The current experiments investigate this by separating the phases of conditioning across developmental stages. Rats were allowed to learn about the context on one day and to form the fearful association on another. Rats exposed to the context on PD 17 exhibited significant fear only when trained and tested a week later (PD 23, 24), but not on consecutive days (PD 18, 19), demonstrating that rats can learn about a context as early as PD 17. Further experiments clarify that it is associative mechanisms that are developing between PD 18 and 23. Finally, the hippocampus was lesioned prior to training to ensure the task is being solved in a hippocampus-dependent manner. These data provide compelling evidence that the hippocampus is functional for contextual learning as early as PD 17, however, its connection to the amygdala or other relevant brain structures may not yet be fully developed.Research in recent decades has yielded a great deal of information regarding the neural substrates of cognitive processes, such as emotional expression and learning and memory in adult organisms, but relatively little regarding the neural substrates underlying these processes in developing organisms. Pavlovian fear conditioning has proven a useful tool for studying cognition in adult organisms (Malenka and Nicoll 1997;Anagnostaras et al. 2001;Maren 2001) and ought to be an especially powerful tool to help uncover the neural substrates of various cognitive processes in adolescent organisms due to its reliance on relatively basic sensory, motor, and affective systems (Campbell and Spear 1972). Indeed, several behavioral and toxicological studies have already adapted methods pioneered in the adult for use in developing animals with great success (Rudy