Abstract
Long-lasting, activity-dependent changes in the efficacy of synaptic transmission are considered to be of fundamental importance for the storage of information and for the development of neural circuitry. The leading experimental model for such a change has been long-term potentiation (LTP), a long-lasting increase in synaptic strength. Intensive experimental analysis of LTP in the hippocampus has resulted in a detailed description of the initial steps responsible for its generation. Recently, a form of long-term depression (LTD) in the hippocampus has been described and examined. It shares several mechanistic features with LTP and appears to be able to reverse LTP. The intracellular second messenger systems that are required to generate and maintain LTP and LTD have been difficult to identify definitively. Leading candidates include diffusible intercellular messengers as well as protein kinases and protein phosphatases, the activities of which may converge at the level of specific phosphoproteins. In addition to delineating the cellular mechanisms under lying LTP and LTD, investigators also are beginning to clarify the roles they play in real learning and memory. The Neuroscientist 1:35-42, 1995