Sanchez-Vives M V, McCormick D A
Section of Neurobiology, Yale University School of Medicine, New Haven, Connecticut 06510, USA.
J Neurosci. 1997 Nov 15;17(22):8880-93. doi: 10.1523/JNEUROSCI.17-22-08880.1997.
The properties of the inhibitory influence of neurons in the perigeniculate (PGN) nucleus on thalamocortical cells were examined with intracellular recordings in the ferret geniculate slice maintained in vitro. Activation of PGN neurons with the local application of glutamate caused IPSPs in thalamocortical neurons that were mediated by both GABAA and GABAB receptors, as well as the activation of spindle waves. With low intensity stimulation of the PGN, local application of bicuculline to the dorsal lateral geniculate nucleus (LGNd) strongly inhibited evoked and spindle-associated IPSPs, indicating that these are largely mediated by GABAA receptors. The generation of GABAB receptor-mediated IPSPs in thalamocortical cells that were large enough to generate rebound low threshold Ca2+ spikes required substantially increased activation of the PGN with glutamate. The activation of synchronous bicuculline-induced slowed oscillations in thalamocortical neurons required the block of GABAA receptors in the LGNd as well as in the PGN. These results indicate that bursts of action potentials in PGN neurons can result in the activation of both GABAA and GABAB receptors in thalamocortical neurons, with the strong activation of GABAB receptors requiring an intense, simultaneous discharge of a number of PGN neurons. Functionally, these results suggest that PGN neurons inhibit thalamocortical cells preferentially through the activation of GABAA receptors, although the strong activation of GABAB receptors may occur under pathological conditions and contribute to the generation of abnormal, synchronous slow oscillations.
利用体外培养的雪貂膝状切片进行细胞内记录,研究了膝周核(PGN)中神经元对丘脑皮质细胞的抑制性影响特性。通过局部应用谷氨酸激活PGN神经元,可在丘脑皮质神经元中诱发由GABAA和GABAB受体介导的抑制性突触后电位(IPSPs),以及纺锤波的激活。在对PGN进行低强度刺激时,向背外侧膝状核(LGNd)局部应用荷包牡丹碱可强烈抑制诱发的和与纺锤波相关的IPSPs,表明这些主要由GABAA受体介导。在丘脑皮质细胞中,由GABAB受体介导的IPSPs的产生,大到足以产生反弹低阈值Ca2+尖峰,需要用谷氨酸大幅增加对PGN的激活。同步荷包牡丹碱诱导的丘脑皮质神经元缓慢振荡的激活,需要阻断LGNd以及PGN中的GABAA受体。这些结果表明,PGN神经元的动作电位爆发可导致丘脑皮质神经元中GABAA和GABAB受体的激活,GABAB受体的强烈激活需要多个PGN神经元同时强烈放电。从功能上讲,这些结果表明,PGN神经元主要通过激活GABAA受体来抑制丘脑皮质细胞,尽管GABAB受体的强烈激活可能在病理条件下发生,并有助于产生异常的同步慢振荡。