AGE-RELATED CHANGE IN SHORT-TERM SYNAPTIC PLASTICITY INTRINSIC TO EXCITATORY STRIATAL SYNAPSES

Aging disrupts the expression of synaptic plasticity in many central n ervous system (CNS) structures including the striatum. We found age di fferences in paired-pulse plasticity to persist at excitatory striatal synapses following block of gamma aminobutyric acid (GABA)(A) and GAB A(B) receptors, a property that was independent of the number of affer ents activated. High Mg2+/low Ca2+ artificial cerebral spinal fluid (A CSF) reduced release probability and consequently the size of the evok ed excitatory post-synaptic potential (EPSP). High Mg2+/low Ca2+ ACSF also increased the expression of paired-pulse facilitation and elimina ted the age difference seen previously in normal ACSF. These data sugg est that age differences in paired-pulse plasticity reflect an alterat ion in release probability at excitatory striatal synapses. In support of this hypothesis, we found age differences in another presynaptic f orm of plasticity referred to as synaptic augmentation. Examination of the synaptic depression that developed during the conditioning tetanu s also revealed an age-related increase in synaptic depression. These data indicate that age-related changes in facilitation may be due in p art to a reduction in the readily releasable pool of synaptic vesicles . Dendritic structure (spine density and dendritic length) was correla ted with short-term synaptic plasticity, but these relationships depen ded upon the variance associated with age (hierarchical regression). P ost-hoc within-age group regressions demonstrated relationship between spine density and paired-pulse plasticity. No other age-specific corr elations were found. These findings imply an age-dependent association between altered dendritic morphology and changes in synaptic plastici ty. (C) 1997 Wiley-Liss, Inc.