Gutowski M, Altmann L, Sveinsson K, Wiegand H
Department of Neurotoxicology, Medical Institute of Environmental Hygiene, Heinrich-Heine-Universität, Düsseldorf, Germany.
Toxicol Lett. 1998 May;95(3):195-203. doi: 10.1016/s0378-4274(98)00036-8.
The effects of low level lead exposure on synaptic plasticity in hippocampal regions CA1 and CA3 were determined in adult rats in vitro. In the CA3 region the NMDA (N-methyl-D-aspartate)-independent mossy fiber-CA3 synapse potentiation was not influenced by chronic pre- and postnatal lead exposure, while in the same rats, in the CA1 region the NMDA-dependent long-term potentiation was slightly reduced as compared to controls. Paired-pulse facilitation was neither impaired in CA1 nor in CA3 region in the lead-exposed rats. These findings suggest that NMDA-dependent forms of synaptic plasticity are more susceptible to chronic low level lead exposure than NMDA-independent forms of potentiation or paired-pulse facilitation.
在成年大鼠体外实验中,测定了低水平铅暴露对海马区CA1和CA3突触可塑性的影响。在CA3区,不依赖N-甲基-D-天冬氨酸(NMDA)的苔藓纤维-CA3突触增强不受出生前和出生后慢性铅暴露的影响,而在同一只大鼠的CA1区,与对照组相比,依赖NMDA的长时程增强略有降低。在铅暴露大鼠的CA1区和CA3区,双脉冲易化均未受损。这些发现表明,与不依赖NMDA的增强形式或双脉冲易化相比,依赖NMDA的突触可塑性形式对慢性低水平铅暴露更敏感。