Abstract
Cytoskeletal protein actin forms the morpho-functional platform at synapses (the communication points between neurons) and changes dynamically between monomeric globular (G-actin) and polymerized filamentous (F-actin) forms in response to neuronal activity. Such actin dynamics is essential for almost all aspects of synaptic physiology, including long-term potentiation (LTP). Synaptic dysfunction contributes to age-related cognitive decline, and agmatine supplementation attenuates memory deficits in aged rats. However, little is known how agmatine affects synaptic function.
This study investigated the effects of long-term agmatine supplementation on cytoskeletal protein actin and synaptic function in aged rats.