AMELIORATION OF AGE-RELATED DEFICITS IN THE STIMULATION OF SYNAPSIN PHOSPHORYLATION

In a previous report we demonstrated that aged (24-26 month) rats have deficits in long-term potentiation, a form of synaptic enhancement th at is dependent on protein phosphorylation (Moore et al., Hippocampus, 3:57-66; 1993). In the present study we demonstrate that aged rats ha ve a deficit in the phosphorylation of the synaptic vesicle associated protein synapsin I. Specifically, aged animals exhibit defective phor bol ester-induced stimulation of synapsin phosphorylation at its calci um/calmodulin dependent protein kinase II sites. We also examined the effects of caloric restriction and antioxidant therapy on this age-rel ated deficit. We found that either life-long caloric restriction or tr eatment with 16 mg/kg N-tert-butyl-alpha-phenylnitrone (PEN) for 2 wee ks can at least partially ameliorate the age-related deficit in the ph orbol ester stimulation of synapsin phosphorylation. (C) 1997 Elsevier Science Inc.