Bracha V, Webster M L, Winters N K, Irwin K B, Bloedel J R
Division of Neurobiology, Barrow Neurological Institute, Phoenix, AZ 85013.
Exp Brain Res. 1994;100(3):453-68. doi: 10.1007/BF02738405.
Intracranial microinjections of the GABAA agonist muscimol were used to assess the involvement of the dentato-interposed cerebellar nuclear complex in the performance of the conditioned (CR) and unconditioned (UR) nictitating membrane responses in the rabbit. Specifically, the experiments test the hypothesis that the cerebellar nuclei are involved in the performance of both the CRs and URs. The experiments employed temporary nuclear lesions to disrupt the CRs in order to examine parallel effects on URs. Animals were conditioned in a standard delay conditioning paradigm. Injection sites at which the muscimol application disrupted execution of the CRs were identified in each rabbit. Once these sites were found, the effects of muscimol and saline injections were evaluated while alternating paired trials with unpaired trials in which only the unconditioned stimuli were applied. There are two main findings in the present study. First, the activation of the GABAA receptors in the dentato-interposed cerebellar nuclear region reduced the amplitude and increased the latency of the UR. This change in the UR closely paralleled the disruption of the CR. This observation is consistent with the notion that the cerebellum is involved in the regulation of defensive flexion reflexes. Second, cerebellar nuclear inactivation did not eliminate the tone-induced enhancement of the UR. This finding suggests the presence of cerebellum-independent circuits subserving the intermodal interaction between the conditioned and unconditioned stimuli.
通过向兔颅内微量注射γ-氨基丁酸A(GABAA)受体激动剂蝇蕈醇,来评估齿状核-间位小脑核复合体在兔条件性(CR)和非条件性(UR)瞬膜反应中的作用。具体而言,这些实验检验了小脑核参与CR和UR的假设。实验采用暂时性核损伤来破坏CR,以研究对UR的平行影响。动物在标准延迟条件反射范式下进行训练。在每只兔中确定蝇蕈醇注射部位,这些部位的注射会破坏CR的执行。一旦找到这些部位,在交替进行配对试验和仅施加非条件刺激的非配对试验时,评估蝇蕈醇和生理盐水注射的效果。本研究有两个主要发现。第一,齿状核-间位小脑核区域GABAA受体的激活降低了UR的幅度并增加了其潜伏期。UR的这种变化与CR的破坏密切平行。这一观察结果与小脑参与防御性屈曲反射调节的观点一致。第二,小脑核失活并未消除紧张性诱导的UR增强。这一发现表明存在独立于小脑的回路,其支持条件刺激和非条件刺激之间的多模式相互作用。