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Although most analyses of amnesia have focused on the loss of explicit declarative and episodic memories following hippocampal-region damage, considerable insights into amnesia can also be realised by studying hippocampal function in simple procedural, or habit-based, associative learning tasks. Although many simple forms of associative learning are unimpaired by hippocampal damage, more complex tasks which require sensitivity to unreinforced stimuli, configurations of multiple stimuli, or contextual information are impaired by hippocampal damage. In several recent papers we have developed a computational theory of hippocampal function which argues that this brain region plays a critical role in the formation of new stimulus representations during learning (Gluck & Myers, 1993, 1995; Myers & Gluck, 1996; Myers, Gluck, & Granger, 1995). We have applied this theory to a broad range of empirical data from studies of classical conditioning in both intact and hippocampal-lesioned animals, and the model correctly accounts for these data. The classical conditioning paradigm can be adapted for use in humans, and similar results for acquisition are obtained in both normal and hippocampal-damaged humans. More recently, we have begun to address an important set of category learning studies in both normals and hippocampal-damaged amnesics. This work integrates experimental studies of amnesic category learning (Knowlton, Squire, & Gluck, 1994) with theoretical accounts of associative learning, and builds on previously established behavioural correspondences between animal conditioning and human category learning (Gluck & Bower, 1988a). Our work to date illustrates some initial progress towards a more integrative understanding of hippocampal function in both animal and human learning, which may be useful in guiding further empirical and theoretical research in human memory and amnesia.

Previously we have shown that Gluck and Myers's (1993) corticohippocampal model could be extended to incorporate Hasselmo and Schnell's (1994) hypothesis that septohippocampal cholinergic processes regulate the amount of information storage in hippocampus. The generalized model could account for the effect of the anticholinergic drug scopolamine in delaying onset of eyeblink conditioning . Here, we show that the model also accounts for additional eyeblink results, including quick recovery after scopolamine is removed, preserved latent inhibition, learned irrelevance and extinction under scopolamine, and no effect of systemic scopolamine after hippocampal lesion. Additionally, the model is consistent with data concerning localized scopolamine iI\iections to the medial septum, the lateral septum, and the hippocampus and their effect on eyeblink conditioning.

Anterior communicating artery (ACoA) aneurysm rupture can lead to an anterograde amnesia syndrome similar to that observed after damage to the hippocampus and medial temporal lobes (MT). It is currently believed that ACoA amnesia results from basal forebrain damage that disrupts hippocampal processing without direct hippocampal damage. Converging evidence from animal studies and computational modeling suggests that qualitative differences may exist in the pattern of memory impairment after basal forebrain or MT damage. For example, animals with basal forebrain but not hippocampal damage are impaired at delay eyeblink classical conditioning (EBCC). In this study, individuals with ACoA amnesia were shown to be impaired at delay EBCC compared with matched controls; this contrasts with the spared delay EBCC previously observed in MT amnesia. This finding suggests the beginning of a possible dissociation between the memory impairments in MT versus ACoA amnesia.