 Gatsby Computational
Neuroscience UnitAlexandra House, 17 Queen Square, LONDON, WC1N 3AR, UK, Tel: +44 (0) 20 7679 1176, Fax +44 (0) 20 7679 1173 abla@gatsby.ucl.ac.uk, www.gatsby.ucl.ac.uk ABSTRACTS Supported by The Gatsby Foundation |Index|Objective|Attendees|Programme|Travel information|Accommodation| Acetylcholine and Memory: Beware of Dogma Mark G. Baxter It has long been thought that the neurotransmitter acetylcholine plays a critical role in memory function. Although a large body of experimental evidence is consistent with this hypothesis, some experiments find no impairment in memory after selective damage to cholinergic neurons in the basal forebrain that provide the major supply of acetylcholine to the hippocampus and neocortex. One line of research in my laboratory has focused on determining the conditions under which hippocampal (or neocortical) acetylcholine is necessary for normal memory function. We (and others) have found that although lesions of septohippocampal cholinergic neurons do not impair a wide variety of learning and memory tasks, they do impair some kinds of nonspatial stimulus-stimulus associations (social transmission of food preference) as well as some conditional associative learning tasks. Furthermore, these lesions have an effect on transfer of learning experience in conditional tasks. Taken together with work on the function of cholinergic basal forebrain neurons in other domains (for example, sensory plasticity), we would like to consider whether a general role for acetylcholine in plasticity of receptive fields in primary sensory areas might also be able to describe its function in other cortical areas. Our results also suggest that the characterization of memory tasks based on different types of cognitive demands (for example, “reference” vs. “working” memory, or spatial vs. nonspatial) likely will fail to capture the functional parameters of acetylcholine in memory. |