Miyata M, Kawakami Y
Department of Physiology, Tokyo Women's Medical College, Japan.
Neuroscience. 1995 Sep;68(1):47-55. doi: 10.1016/0306-4522(95)00078-w.
We have investigated the role of cortico-cortical inputs from the primary somatosensory cortex in the induction of long-lasting potentiation in the secondary somatosensory cortex. Long-lasting potentiation of evoked potentials in the feline secondary somatosensory cortex is induced by high frequency stimulation of the ventral posterolateral thalamic nucleus. The secondary somatosensory cortex receives two projections from the ventral posterolateral thalamic nucleus; a direct pathway from the ventral posterolateral thalamic nucleus and a cortico-cortical pathway via the primary somatosensory cortex. The present study was designed to examine dominance of these pathways in the induction of long-lasting potentiation in the secondary somatosensory cortex. Long-lasting potentiation was evaluated by changes in the amplitude of field potentials and current source densities elicited by ventral posterolateral thalamic nucleus test stimulation (0.1 Hz) following conditioning stimulation. The conditioning stimulation, consisting of 20 trains of 200 Hz bursts, was delivered to the ventral posterolateral thalamic nucleus or the primary somatosensory cortex. Field potentials in the secondary somatosensory cortex were simultaneously recorded at 16 points placed vertically at 150 microns intervals from the cortical surface and current source density was computed using these field potentials. First, we blocked inputs from the primary somatosensory cortex to the secondary somatosensory cortex by intracortical injection of lidocaine into the primary somatosensory cortex. The amplitudes of the field potentials recorded in the secondary somatosensory cortex diminished within 5 min after lidocaine injection. Current source density analysis showed a marked decrease in the sink currents in layers II/III (at depths of 450-600 microns).(ABSTRACT TRUNCATED AT 250 WORDS)
我们研究了来自初级体感皮层的皮质-皮质输入在次级体感皮层长时程增强诱导中的作用。猫次级体感皮层诱发电位的长时程增强是由高频刺激腹后外侧丘脑核诱导产生的。次级体感皮层从腹后外侧丘脑核接收两条投射;一条是来自腹后外侧丘脑核的直接通路,另一条是经由初级体感皮层的皮质-皮质通路。本研究旨在检验这些通路在次级体感皮层长时程增强诱导中的主导作用。通过在条件刺激后,由腹后外侧丘脑核测试刺激(0.1赫兹)诱发的场电位幅度和电流源密度的变化来评估长时程增强。条件刺激由20串、每串200赫兹的脉冲组成,施加于腹后外侧丘脑核或初级体感皮层。在次级体感皮层中,从皮质表面垂直以150微米间隔放置的16个点同时记录场电位,并使用这些场电位计算电流源密度。首先,我们通过向初级体感皮层内注射利多卡因来阻断从初级体感皮层到次级体感皮层的输入。利多卡因注射后5分钟内,次级体感皮层记录到的场电位幅度减小。电流源密度分析显示,II/III层(深度为450 - 600微米)的下沉电流显著降低。(摘要截断于250字)