Schiene K, Staiger J F, Bruehl C, Witte O W
Neurologische Klinik, der Heinrich Heine Universität, Düsseldorf, Germany.
J Neurol Sci. 1999 Jan 1;162(1):6-13. doi: 10.1016/s0022-510x(98)00292-5.
It has been shown that cortical lesions are associated with an increase of excitability in surrounding brain regions, and with a downregulation of GABA(A) receptors. In the present study we investigated whether this increased excitability affects the cortical map of inputs represented in areas surrounding the lesioned brain area. Focal lesions with a diameter of 2-2.5 mm were induced photochemically in the hindlimb area at the border of the primary somatosensory cortex of the rat. One week after lesioning, the cortical representation of the B3 vibrissa was studied using 14C-deoxyglucose (DG) autoradiography. In all animals mechanical stimulation of the B3 vibrissa produced a column-shaped DG-labeling in the somatosensory cortex, corresponding to the B3-barrel with a maximum of the glucose uptake in layer IV. In control animals without cortical lesions (n=6), stimulation increased the glucose uptake rate by 50.8+/-10.5% in layer IV. In lesioned animals (n=6) maximum DG-uptake in layer IV (54.8+/-8.6%) did not differ significantly from that in controls. However, as compared to control animals, lesioned animals showed also increased glucose uptake within the activated column in layers II/II (51.+/-11.1%, lesioned animals; 31.8+/-11.2%, controls; P<0.05, lesioned vs. control) and V (47.5+/-5.8%, lesioned animals, 28.8+/-10.5%, controls; P<0.05, lesioned vs. control). The diameter of the metabolically activated B3-barrel area of layer IV was expanded from 461.8+/-77.6 microm in control animals to 785.5+/-103.6 microm; P<0.01) in lesioned animals. Lesioned animals also showed expansion of the activated area in layers II/III (890.4+/-134.8 microm, lesioned animals; 430.6+/-95.1 microm, controls; P<0.01) and layer V (1117.5+/-163.6 microm, lesioned animals; 648.7+/-114.1 microm, controls; P<0.01). The depth profile of the activation columns showed a maximum in layer IV in control animals, which was expanded towards layers II/III and layer V in lesioned animals. It is concluded that cortical lesions alter the representational area of neighboring afferent inputs through disinhibition or 'unmasking' of pre-existing silent or ineffectual intracortical synapses. The present observations raise the possibility that the brain supports recovery from lesions by decreasing GABAergic inhibition, thereby facilitating a remapping of the cortical representation in neighboring brain areas.
研究表明，皮质损伤与周围脑区兴奋性增加以及GABA(A)受体下调有关。在本研究中，我们调查了这种增加的兴奋性是否会影响损伤脑区周围区域所代表的输入的皮质图谱。通过光化学方法在大鼠初级体感皮层边界的后肢区域诱导直径为2 - 2.5毫米的局灶性损伤。损伤后一周，使用14C - 脱氧葡萄糖（DG）放射自显影术研究B3触须的皮质表征。在所有动物中，对B3触须的机械刺激在体感皮层产生柱状DG标记，对应于B3桶状结构，在IV层葡萄糖摄取量最高。在无皮质损伤的对照动物（n = 6）中，刺激使IV层葡萄糖摄取率增加了50.8±10.5%。在损伤动物（n = 6）中，IV层的最大DG摄取量（54.8±8.6%）与对照组无显著差异。然而，与对照动物相比，损伤动物在激活柱内的II/III层（损伤动物为51.±11.1%，对照动物为31.8±11.2%；P < 0.05，损伤组与对照组相比）和V层（损伤动物为47.5±5.8%，对照动物为28.8±10.5%；P < 0.05，损伤组与对照组相比）也显示出葡萄糖摄取增加。IV层代谢激活的B3桶状区域直径从对照动物的461.8±77.6微米扩大到损伤动物的785.5±103.6微米；P < 0.01）。损伤动物在II/III层（损伤动物为890.4±134.8微米，对照动物为430.6±95.1微米；P < 0.01）和V层（损伤动物为1117.5±163.6微米，对照动物为648.7±114.1微米；P < 0.
