Parham K, Willott J F
Northern Illinois University, DeKalb 60115.
Behav Neurosci. 1990 Dec;104(6):831-40. doi: 10.1037//0735-7044.104.6.831.
"Nonspecific" electrolytic lesions (with respect to subdivision) of the mouse inferior colliculus (IC) resulted in the attenuation of acoustic startle response (ASR) amplitudes on the 1st post-operative day, but ASR amplitudes increased to above baseline levels 1 week later. Lesions of the IC central nucleus (CN) also attenuated ASR amplitudes on the 1st postsurgery day, but startle amplitudes recovered to baseline levels 1 week after surgery. Lesions of the IC lateral nucleus (LN) or dorsal cortex (DC) resulted in elevation of startle amplitudes above baseline 7 days after surgery and produced enhanced ASR amplitudes to repeated stimuli. Fourteen days after the surgery, lesion effects on startle amplitudes remained the same as those on Day 7 for each lesion condition. The present findings implicate the ICLN and the ICDC as inhibitory modulators of the ASR, but indicate only a minor role for the ICCN.
小鼠下丘(IC)的“非特异性”(就细分而言)电解损伤导致术后第1天听觉惊跳反应(ASR)幅度减弱,但1周后ASR幅度增加至基线水平以上。IC中央核(CN)损伤在术后第1天也减弱了ASR幅度,但惊跳幅度在术后1周恢复到基线水平。IC外侧核(LN)或背侧皮质(DC)损伤导致术后7天惊跳幅度高于基线水平,并对重复刺激产生增强的ASR幅度。术后14天,每种损伤情况下对惊跳幅度的损伤效应与第7天相同。本研究结果表明ICLN和ICDC是ASR的抑制性调节因子,但仅表明ICCN起次要作用。