| While much is known about biochemical mechanisms of enduring synaptic plasticity and long-term memory, relatively little information is available about the machinery involved in rapid synaptic enhancement and short-term memory. The present thesis experiments set out to identify and investigate the role of key candidate proteins that may be involved in the rapid synaptic alterations necessary for short-term memory, and ultimately long-lasting synaptic modification and memory, to take place. The NR2B subunit of the N-methyl-D-aspartate (NMDA) receptor, the Ca2+/Calmodulin Dependent Protein Kinase II (CaMKII), and the Group I metabotropic glutamate receptor, mGluR5 were experimental targets chosen for their unique properties. The techniques of immunohistochemistry, electrophysiology, and fear conditioning were used to conduct these investigations, with a focus on the lateral nucleus of the amygdala (LA), a crucial site for learning and plasticity. The present experiments confirmed that NR2B, CaMKII, and mGluR5 are expressed abundantly in the LA, necessary for the induction of LTP in the LA, and vital for the acquisition of short-term, and long-term, fear memories. |
