Ou X, Buckwalter G, McNeill T H, Walsh J P
Ethel Percy Andrus Gerontology Center, USC Program in Neuroscience, University of Southern California, Los Angeles 9089-0191, USA.
Synapse. 1997 Sep;27(1):57-68. doi: 10.1002/(SICI)1098-2396(199709)27:1<57::AID-SYN6>3.0.CO;2-C.
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.
衰老会破坏包括纹状体在内的许多中枢神经系统（CNS）结构中突触可塑性的表达。我们发现，在γ-氨基丁酸（GABA）A和GABA（B）受体被阻断后，兴奋性纹状体突触处的双脉冲可塑性存在年龄差异，这一特性与被激活的传入神经数量无关。高镁/低钙人工脑脊液（ACSF）降低了释放概率，从而降低了诱发的兴奋性突触后电位（EPSP）的大小。高镁/低钙ACSF还增加了双脉冲易化的表达，并消除了先前在正常ACSF中观察到的年龄差异。这些数据表明，双脉冲可塑性的年龄差异反映了兴奋性纹状体突触处释放概率的改变。为支持这一假设，我们在另一种被称为突触增强的突触前可塑性形式中也发现了年龄差异。对条件性强直刺激期间出现的突触抑制的检查还揭示了与年龄相关的突触抑制增加。这些数据表明，与年龄相关的易化变化可能部分归因于突触小泡的易释放池减少。树突结构（棘密度和树突长度）与短期突触可塑性相关，但这些关系取决于与年龄相关的方差（分层回归）。年龄组内的事后回归显示了棘密度与双脉冲可塑性之间的关系。未发现其他与年龄相关的相关性。这些发现意味着树突形态改变与突触可塑性变化之间存在年龄依赖性关联。
