Synaptic Plasticity and Memory Formation
Abstract
The purpose of the proposed research was to test and elaborate on an hypothesis regarding cellular mechanisms responsible for storing recognition memory in mammalian telencephalon. We proposed that the encoding process involves: 1) an unusual pattern of physiological activity in the relevant neural pathways, 2) influx of calcium into dendritic spines postsynaptic to the active axons, 3) activation of the calcium-sensitive protease, calpain, 4) partial degradation of spectrin, a cytoskeleton protein that regulates membrane surface chemistry and possibly spine shape, and 5) anatomical reorganization of postsynaptic structure resulting in a stable increase of postsynaptic potentials. Central to the hypothesis is the phenomenon of long-term potentiation (LTP) of synaptic transmission; much of the research conducted in the past three years has been aimed at characterizing the physiological and biochemical steps responsible for this remarkably persistent synaptic change and examining its role in memory storage. We have also hypothesized that excessive activation of the calpain system can lead to the neuronal degeneration that is associated with experimental age-related neuropathologies. Keywords: Hippocampus, Learning, Olfactory learning, Spatio-temporal activity; Synaptic plasticity, Glutamate receptors.
Document Details
- Document Type
- Technical Report
- Publication Date
- May 30, 1989
- Accession Number
- ADA211368
Entities
People
- Gary Lynch
Organizations
- University of California, Irvine