Age-related change in short-term synaptic plasticity intrinsic to excitatory striatal synapses.

Aging disrupts the expression of synaptic plasticity in many central nervous system (CNS) structures including the striatum. We found age differences in paired-pulse plasticity to persist at excitatory striatal synapses following block of gamma aminobutyric acid (GABA)A and GABA(B) receptors, a property that was independent of the number of afferents activated. High Mg2+/low Ca2+ artificial cerebral spinal fluid (ACSF) reduced release probability and consequently the size of the evoked excitatory post-synaptic potential (EPSP). High Mg2+/low Ca2+ ACSF also increased the expression of paired-pulse facilitation and eliminated the age difference seen previously in normal ACSF. These data suggest that age differences in paired-pulse plasticity reflect an alteration in release probability at excitatory striatal synapses. In support of this hypothesis, we found age differences in another presynaptic form of plasticity referred to as synaptic augmentation. Examination of the synaptic depression that developed during the conditioning tetanus also revealed an age-related increase in synaptic depression. These data indicate that age-related changes in facilitation may be due in part to a reduction in the readily releasable pool of synaptic vesicles. Dendritic structure (spine density and dendritic length) was correlated with short-term synaptic plasticity, but these relationships depended upon the variance associated with age (hierarchical regression). Post-hoc within-age group regressions demonstrated relationship between spine density and paired-pulse plasticity. No other age-specific correlations were found. These findings imply an age-dependent association between altered dendritic morphology and changes in synaptic plasticity.