Grantyn R, Kraszewski K, Melnick I, Taschenberger H, Warton S S
Developmental Neurobiology Group, Max Planck Institute for Psychiatry, Martinsried, Germany.
Perspect Dev Neurobiol. 1995;2(4):387-97.
This article deals with basic determinants of synaptic efficacy during development of glutamatergic and GABAergic synaptic transmission: location and number of release sites, release probability and single cell-activated (unitary) conductances. We hypothesize that both types of neuronal connections differ in major aspects of synaptogenesis. Disregarding the fact that various test models and cell types could render diverging results, it can be observed that glutamatergic terminals display a preference for dendrites, whereas GABAergic terminals select soma locations at initial stages of development. Glutamatergic synapses are characterised by receptor accumulation in the region of terminal apposition, whereas in GABAergic synapses receptor concentration is weak, if present at all. The expression of glutamate receptors (GluRs), but not GABAA receptors is under control of interneurons. Developmental changes in glutamatergic synaptic transmission have not yet been assessed by quantal analysis. For GABAergic synapses, first results are now available from a culture preparation of the rat superior colliculus. In general terms, functional maturation seemed to lag behind the formation of structurally differentiated release sites. Compound binomial analysis revealed that during in vitro development a considerable fraction of GABAergic terminals remained in a low efficacy release state (p < 0.2). A developmental increase in synaptic strength was reached by the appearance of singular highly effective release sites. Presynaptic maturation could be manipulated by long-term drug treatment. Addition of GluR antagonists significantly increased amplitudes and decreased the coefficients of variations of evoked inhibitory postsynaptic currents. Thus, the strength of inhibitory synaptic transmission could be influenced by the status of heteronymous synaptic input.
本文探讨谷氨酸能和γ-氨基丁酸能突触传递发育过程中突触效能的基本决定因素:释放位点的位置和数量、释放概率以及单细胞激活(单位)电导。我们假设这两种类型的神经元连接在突触形成的主要方面存在差异。尽管各种测试模型和细胞类型可能会产生不同的结果,但可以观察到,谷氨酸能终末在发育初期偏好树突,而γ-氨基丁酸能终末则选择胞体位置。谷氨酸能突触的特征是在终末附着区域有受体聚集,而γ-氨基丁酸能突触中,即使有受体浓度也很弱。谷氨酸受体(GluRs)的表达受中间神经元控制,而γ-氨基丁酸A受体则不受其控制。谷氨酸能突触传递的发育变化尚未通过量子分析进行评估。对于γ-氨基丁酸能突触,现在已经从大鼠上丘的培养制剂中获得了初步结果。一般来说,功能成熟似乎落后于结构上分化的释放位点的形成。复合二项式分析表明,在体外发育过程中,相当一部分γ-氨基丁酸能终末处于低效能释放状态(p < 0.2)。突触强度的发育性增加是通过单个高效释放位点的出现实现的。突触前成熟可以通过长期药物治疗来调控。添加谷氨酸受体拮抗剂可显著增加幅度并降低诱发的抑制性突触后电流的变异系数。因此,抑制性突触传递的强度可能受异源突触输入状态的影响。