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Nicotine has been shown to enhance multiple forms of learning and memory. However the substrates through which these effects occur are not well understood. To examine the specific substrates of nicotine's acute effects on trace fear conditioning, I infused nicotine into areas thought to support trace fear conditioning, the dorsal hippocampus, ventral hippocampus and medial prefrontal cortex. Additionally, we investigated the contributions of nicotinic acetylcholinergic signaling to trace fear conditioning by infusing the nicotinic antagonists dihydro-beta-erythroidine (DHbE) and methyllycaconitine (MLA) into these areas. Nicotine had different effects on both trace and contextual fear conditioning depending on dose and brain region, as did the nicotinic antagonists. In the dorsal hippocampus nicotine infusion enhanced both trace and contextual conditioning, although these effects were dissociable by dose and training protocol. Additionally, the high-affinity nicotinic antagonist DHbE produced selective deficits in trace conditioning, suggesting that while enhancement of nicotinic signaling can affect both contextual and trace learning, nicotinic activity in the dorsal hippocampus is critically involved in trace but not contextual conditioning. In the ventral hippocampus nicotine infusion produced deficits in both trace and contextual fear conditioning, without affecting delay conditioning, while the antagonists had no effect. This finding suggests that altered nicotinic signaling in the ventral hippocampus can suppress hippocampus dependent learning. In the mPFC nicotine selectively enhanced trace conditioning though both antagonists also enhanced trace fear conditioning. Unlike in the mPFC or dorsal hippocampus, where nicotine and antagonist induced effects occurred during training, effects in the ventral hippocampus occurred at both training and testing, suggesting that the ventral hippocampus may be able to modulate acquisition as well as expression of hippocampus dependent learning. Additionally, antagonist infusion into the mPFC during testing produced deficits in expression, suggesting that this area can modulate fear expression. Thus, the substrates of nicotinic acetylcholinergic contributions to trace and contextual fear conditioning are diverse. I put forth a multi-component model of these contributions, where trace fear conditioning is supported by dorsal hippocampus dependent maintenance of the CS during the trace interval, long-term storage in the mPFC and ventral hippocampal mediated acquisition and expression. / Psychology