von Krosigk M, Monckton J E, Reiner P B, McCormick D A
Yale University School of Medicine, Section of Neurobiology, New Haven, CT 06510-8001, USA.
Neuroscience. 1999;91(1):7-20. doi: 10.1016/s0306-4522(98)00557-0.
The properties of postsynaptic potentials evoked by stimulation of cortical, retinal and GABAergic thalamic afferents were examined in vitro in thalamocortical neurons of the guinea-pig dorsal lateral geniculate nucleus. Brief trains of stimulation (2-10 stimuli) delivered to corticothalamic fibers led to a frequency-dependent increase in excitatory postsynaptic potential amplitude associated with an increase in activation of both N-methyl-D-aspartate and non-N-methyl-D-aspartate glutamate receptors. In addition, repetitive stimulation of corticothalamic fibers also gave rise to a slow excitatory postsynaptic potential that was blocked by local application of the glutamate metabotropic receptor antagonist alpha-methyl-4-carboxyphenylglycine. In contrast, repetitive stimulation of optic tract fibers resulted in monosynaptic excitatory postsynaptic potentials that did not potentiate and were not followed by the generation of a slow excitatory postsynaptic potential. Repetitive activation of the optic radiation also evoked both GABA(A) and GABA(B) receptor-mediated inhibitory postsynaptic potentials. These inhibitory postsynaptic potentials exhibited frequency-dependent depression during repetitive activation. The presence of frequency-dependent facilitation of corticothalamic excitatory postsynaptic potentials and frequency-dependent decrement of inhibitory postsynaptic potentials, as well as the ability of corticothalamic fibers to activate glutamate metabotropic receptors, suggests that sustained activation of corticothalamic afferents in vivo may result in postsynaptic responses in thalamocortical cells that are initially dominated by GABAergic inhibitory postsynaptic potentials followed by prominent monosynaptic excitatory postsynaptic potentials as well as a slow depolarization of the membrane potential.Therefore, the corticothalamic system may inhibit or enhance the excitability and responsiveness of thalamocortical neurons, based both on the spatial and temporal features of thalamocortical interactions.
在豚鼠背外侧膝状核的丘脑皮质神经元中,对刺激皮质、视网膜和GABA能丘脑传入纤维所诱发的突触后电位特性进行了体外研究。向皮质丘脑纤维施加短暂的刺激序列(2 - 10次刺激)会导致兴奋性突触后电位幅度呈频率依赖性增加,这与N - 甲基 - D - 天冬氨酸和非N - 甲基 - D - 天冬氨酸谷氨酸受体的激活增加相关。此外,重复刺激皮质丘脑纤维还会产生一种缓慢的兴奋性突触后电位,该电位可被局部应用谷氨酸代谢型受体拮抗剂α - 甲基 - 4 - 羧基苯甘氨酸所阻断。相比之下,重复刺激视束纤维会导致单突触兴奋性突触后电位,该电位不会增强且之后不会产生缓慢的兴奋性突触后电位。视辐射的重复激活也会诱发GABA(A)和GABA(B)受体介导的抑制性突触后电位。这些抑制性突触后电位在重复激活期间表现出频率依赖性抑制。皮质丘脑兴奋性突触后电位的频率依赖性易化、抑制性突触后电位的频率依赖性衰减以及皮质丘脑纤维激活谷氨酸代谢型受体的能力表明,体内皮质丘脑传入纤维的持续激活可能导致丘脑皮质细胞的突触后反应,最初由GABA能抑制性突触后电位主导,随后是明显的单突触兴奋性突触后电位以及膜电位的缓慢去极化。因此,基于丘脑皮质相互作用的空间和时间特征,皮质丘脑系统可能会抑制或增强丘脑皮质神经元的兴奋性和反应性。