THE ROLE OF GABA-MEDIATED INHIBITION IN THE RAT VENTRAL POSTERIOR MEDIAL THALAMUS .1. ASSESSMENT OF RECEPTIVE-FIELD CHANGES FOLLOWING THALAMIC RETICULAR NUCLEUS LESIONS

THE ROLE OF GABA-MEDIATED INHIBITION IN THE RAT VENTRAL POSTERIOR MEDIAL THALAMUS .1. ASSESSMENT OF RECEPTIVE-FIELD CHANGES FOLLOWING THALAMIC RETICULAR NUCLEUS LESIONS
复制标题

DOI:
10.1152/jn.1994.71.5.1702
复制
发表时间:
1994-05-01
影响因子:
2.5
通讯作者:
EBNER, FF
EBNER, FF
中科院分区:
医学3区
文献类型:
--
作者:
LEE, SM;FRIEDBERG, MH;EBNER, FF

文献摘要

被引文献

相似文献

1.采用单单位记录技术,对同侧丘脑网状核(TRN)进行选择性兴奋毒性损伤后,丘脑VPM神经元感受野(RF)特性的变化进行了定量评估。结果:1.正常动物97个VPM神经元和TRN损伤动物102个VPM神经元对控制性偏转对侧触须的反应曲线. TRN病变的组织学迹象是可检测的尼斯染色切片早在20小时后释放红藻氨酸到TRN。正常动物VPM神经元的平均RF大小为2.39 +/- 0.18须(平均值+/- SE)。在TRN损伤后即刻,VPM中RF的平均大小显著增大,并在TRN破坏后1个月仍保持扩大(7.64 ± 0.47须,P < 0.001).随后的病变三叉神经亚核interpolaris(SpVi)在TRN损伤的动物产生了显着减少RF大小的VPM神经元。TRN/ SpVi损伤动物的平均VPM RF大小为2.14 +/- 0.64个须。从TRN的抑制损失增加的平均响应概率和幅度的中心RF晶须分别为38%和34%。周围RF晶须的响应概率和幅度分别增加了64%和69%。TRN损伤后,VPM神经元对中心和周围RF须的平均反应潜伏期明显延长;随后TRN损伤病例中SpVi的损伤使VPM神经元的平均反应潜伏期降低到正常动物中所见的水平。在正常和TRN损伤的情况下,VPM神经元的RF显示出强烈的前-后(“行”)偏好。在VPM中,紧邻的前后胡须引起反应的可能性是紧邻的背腹胡须的两倍。VPM单位进行了测试,优先响应触须运动在四个方向(向上,向下,向后,向前)之一。在正常和TRN损伤的情况下,大多数神经元表现出方向选择性反应,主要是在向上的方向。因此,γ-氨基丁酸(GABA)介导的大鼠VPM抑制似乎并不负责VPM神经元的方向选择性。几乎所有的神经元在大鼠VPM TRN病变后显示的反应,持续的刺激(25.5%,在正常的TRN病变的情况下,88.2%)。显示持续(紧张性)反应的VPM单位保持了较高的自发活动率,平均而言,对2-3倍以上的胡须的反应比相位反应单位。结果表明,TRN的破坏使同侧VPM的RF大小平均增加3.2倍。我们的数据表明,这种增加的RF大小后看到的TRN的影响的损失是依赖于SpVi的存在。在TRN损伤的病例中,在SpVi破坏后,在VPM神经元中诱发反应的胡须的平均数量(即,仅由三叉神经主亚核介导的须相关输入与正常动物几乎相同(正常组为2.67 ± 0.31,TRN/SpVi损伤组为2.14 ± 0.64)。
1. Changes in the receptive field (RF) properties of thalamic VPM neurons were assessed quantitatively using single-unit recording techniques following a selective excitotoxic lesion of the ipsilateral thalamic reticular nucleus (TRN). The response profiles to controlled deflections of the contralateral vibrissae were obtained from 97 VPM neurons in normal and 102 VPM neurons in TRN-lesioned animals.2. Histological signs of TRN lesions were detectable in Nissl-stained sections as early as 20 h after the release of kainic acid into TRN.3. The average RF size of VPM neurons in normal animals was 2.39 +/- 0.18 whiskers (mean +/- SE). Immediately after the lesion of TRN, the average RF size in VPM was enlarged significantly and remained expanded for as long as 1 mo after the destruction of TRN (7.64 +/- 0.47 whiskers, P < 0.001).4. Subsequent lesions of trigeminal subnucleus interpolaris (SpVi) in TRN-lesioned animals produced a marked reduction in the RF size of VPM neurons. The average VPM RF size for TRN/ SpVi lesioned animals was 2.14 +/- 0.64 whiskers.5. The loss of inhibition from TRN increased the average response probability and magnitude to the center RF whisker by 38 and 34%, respectively. The response probability and magnitude of the surround RF whiskers increased by 64 and 69%, respectively. The average response latencies to the center and surround RF whiskers were significantly longer after the lesion of TRN; subsequent lesions of SpVi in TRN-lesioned cases reduced the average response latencies of VPM neurons to those seen in normal animals.6. The RF of VPM neurons in both normal and TRN lesioned cases displayed a strong anterior-posterior( ''row'') preference. Immediately adjacent anterior-posterior whiskers were twice as likely to elicit a response in VPM than immediately adjacent dorsal-ventral whiskers.7. VPM units were tested for a preferential response to whisker movement in one of four directions (up, down, backward, and forward). The majority of the neurons in both normal and TRN-lesioned cases showed direction-selective responses, mostly in the up direction. Thus gamma-aminobutyric acid (GABA)-mediated inhibition in rat VPM does not appear to be responsible for direction selectivity of VPM neurons.8. Virtually all neurons in rat VPM after TRN lesions displayed responses that were sustained for the duration of the stimulus (25.5% in normal vs. 88.2% in TRN-lesioned cases). VPM units showing sustained (tonic) responses maintained a high rate of spontaneous activity and, on average, responded to 2-3 times more whiskers than phasically responding units.9. The results show that the destruction of TRN increases the RF size in the ipsilateral VPM by an average of 3.2-fold. Our data indicate that this increase in the RF size seen after the loss of TRN influence is dependent upon the presence of SpVi. The average number of whiskers that evoked responses in VPM neurons after the destruction of SpVi in TRN-lesioned cases (i.e., whisker-related input mediated by trigeminal subnucleus principalis only) was nearly identical to that of normal animals (2.67 +/- 0.31 in normal and 2.14 +/- 0.64 in TRN/SpVi-lesioned cases).