Pennartz C M, Ameerun R F, Groenewegen H J, Lopes da Silva F H
Graduate School of Neurosciences Amsterdam, University of Amsterdam, The Netherlands.
Eur J Neurosci. 1993 Feb 1;5(2):107-17. doi: 10.1111/j.1460-9568.1993.tb00475.x.
Extra- and intracellular recordings in slices were used to examine what types of synaptic plasticity can be found in the core of the nucleus accumbens, and how these forms of plasticity may be modulated by dopamine. Stimulus electrodes were placed at the rostral border of the nucleus accumbens in order to excite primarily infralimbic and prelimbic afferents, as was confirmed by injections of the retrograde tracer fluoro-gold. In extracellular recordings, tetanization induced long-term potentiation (LTP) of the population spike in 20 out of 53 slices. The presynaptic compound action potential did not change following LTP induction. For the intracellularly recorded excitatory postsynaptic potentiation, three types of synaptic plasticity were noted: long-term potentiation (16 out of 54 cells), decremental potentiation (eight cells) and long-term depression (LTD; six cells). No correlation was found between the occurrence of potentiation or depression and various parameters of the tetanic depolarization (e.g. peak voltage, integral under the curve). The N-methyl-D-aspartate receptor antagonist D(-)-2-amino-5-phosphonopentanoic acid (50 microM; D-AP5) reduced, but did not completely prevent, the induction of LTP. The incidence of LTD was not markedly affected by D-AP5. No difference in LTP was found when comparing slices bathed in dopamine (10 microM) and controls. Likewise, slices treated with a mixture of the D1 receptor antagonist Sch 23390 (1 microM) and the D2 antagonist S(-)-sulpiride (1 microM) generated a similar amount of LTP as controls. In conclusion, both LTP and LTD can be induced in a key structure of the limbic-innervated basal ganglia. LTP in the nucleus accumbens strongly depends on N-methyl-D-aspartate receptor activity, but is not significantly affected by dopamine.
采用脑片的细胞外和细胞内记录方法，研究伏隔核核心区存在何种类型的突触可塑性，以及这些可塑性形式如何受多巴胺调节。刺激电极置于伏隔核嘴侧边界，以主要激发内嗅和前嗅传入纤维，这一点通过注射逆行示踪剂氟金得以证实。在细胞外记录中，53个脑片中的20个在强直刺激后诱发出群体峰电位的长时程增强（LTP）。LTP诱导后，突触前复合动作电位未发生变化。对于细胞内记录的兴奋性突触后电位增强，观察到三种类型的突触可塑性：长时程增强（54个细胞中的16个）、递减性增强（8个细胞）和长时程抑制（LTD；6个细胞）。强直去极化的各种参数（如峰值电压、曲线下积分）与增强或抑制的发生之间未发现相关性。N-甲基-D-天冬氨酸受体拮抗剂D(-)-2-氨基-5-膦酰戊酸（50μM；D-AP5）可减少但不能完全阻止LTP的诱导。D-AP5对LTD的发生率没有明显影响。比较用多巴胺（10μM）处理的脑片和对照脑片，未发现LTP有差异。同样，用D1受体拮抗剂Sch 23390（1μM）和D2拮抗剂S(-)-舒必利（1μM）混合物处理的脑片产生的LTP量与对照相似。总之，在边缘系统支配的基底神经节的关键结构中可诱导出LTP和LTD。伏隔核中的LTP强烈依赖于N-甲基-D-天冬氨酸受体活性，但不受多巴胺的显著影响。
