Posttraining but not pretraining lesions of the hippocampus interfere with feature-negative discrimination of fear-potentiated startle.

Previous studies have suggested that the hippocampus may play an important role in some forms of inhibitory learning. The goal of the present study was to assess whether the hippocampus is also important for inhibition of fear acquired after serial feature-negative discrimination training. Rats were given aspiration lesions of the hippocampus either before or after training in which a target light was paired with shock when presented alone, but not paired with shock when presented in serial compound with a noise feature (light+/noise-->light-). Conditioned fear to the target stimulus and feature-target compound were measured with fear-potentiated startle. Pre-training lesion of the hippocampus did not disrupt feature-negative discrimination performance relative to sham-operated and cortical lesioned controls. In contrast, hippocampal lesions performed after training severely disrupted performance. Specifically, rats with hippocampal lesions failed to inhibit fear when the noise feature was presented in compound with the target. However, these rats could reacquire the feature-negative discrimination. These observations suggest that the hippocampus may normally be involved in retention or retrieval of serial feature-negative discrimination; however, in its absence feature-negative discrimination can still be acquired.

A critical period for reduced brain vulnerability to developmental injury. II. Volumetric study of the neocortex and thalamus in cats.

Groups of young adult cats with a left hemineodecortication at postnatal (P) ages (in days) 5-15 (P10), 30 (P30) 60 (P60), 90 (P90), 120 (P120) and in adulthood, were used to measure the volume of the thalamus, bilaterally, and of the remaining neocortex (right hemisphere). The same subjects were employed for the behavioral studies reported in the preceding paper. There was a bilateral, age-dependent, thalamic volume decrease. Ipsilateral to the resection, the thalamic shrinkage was the largest for the adult-lesioned cats (by 56.7%) and it was the smallest for the P30 group (43.4%), with a tendency towards a greater atrophy as the age at lesion increased. A similar pattern of atrophy was seen for the contralateral thalamus but the volume reduction was much less pronounced such that it was significant only for the four older age-at-lesion groups (ranging from 18.2% to 11.2% for the P120 and P90 groups respectively). Once again, the shrinkage was the smallest for the P30 group (5.3%). The remaining neocortex also shrunk in these animals, but the volume decrease was significant only for the adult-lesioned (17.8%) and the P120 group (15.4%), while the P30 group had practically no shrinkage (2.4%). The frontal cortex had no atrophy or it was minimal but the shrinkage gradually increased caudally such that all lesioned groups had some size reduction of the occipital cortex. The present results, together with the main conclusion of the preceding paper, indicate that there is a critical maturation period (CMP) of reduced forebrain vulnerability to neocortical injury which, in cats, tends to end between 30 to 60 days postnatally. The implications for developmental brain damage in other higher mammal species as well as the possible morphological ontogenetical underpinnings of this period are discussed.