Brain stem pathways, cortical modulation, and habituation of the acoustic startle response

Abstract

Rats with bilateral lesions in the inferior colliculi, superior colliculi, anterior (mesencephalic) reticular formation, or posterior (pontine) reticular formation, in addition to sham-operated animals, were studied to determine the effects of damage to these sites on short-term (within sessions) or long-term (across days) habituation of the acoustic startle response. Lesions placed in posterior reticular formation reduced short-term habituation, while damage to other structures had little effect. Damage to the inferior colliculi, anterior reticular formation, and posterior reticular formation reduced or abolished long-term habituation. In addition, damage to the inferior colliculi abolished the acoustic startle response for 2 to 3 days postoperatively, but full recovery of the response was evident by 4-days postoperative recovery. Startle response amplitude was related to the anterior-posterior placement of reticular formation lesions. More posteriorly placed lesions reduced or abolished the startle response. These results suggest that the reticular formation may underlie short-term habituation of the acoustic startle response and that the normal pathway of this response involves information relayed to reticular formation via the inferior colliculi. However, parallel pathways from lower auditory relay appear to exist since complete recovery of the acoustic startle occurs within 4 days following removal of the inferior colliculi. Rats with lesions in the frontal poles, dorsal hippocampus and overlying parietal cortex, parietal cortex alone, or auditory cortex were studied to determine the effects of damage to these areas on short-term or long-term habituation of the acoustic startle response. With the exception of parietal cortical control lesions, all subjects showed some impairment of long-term habituation following cortical damage. Short-term habituation was unaffected by any of the lesions. The results are compared to previous reports of the effects of damage to cortex and the brain stem.