Unilateral hippocampal and inferotemporal cortex lesions in opposite hemispheres impair learning of single-pair visual discriminations as well as visuovisual conditional tasks in monkeys.

Monkeys with unilateral ablations of the inferotemporal (IT) cortex were not impaired on learning or retention of single-pair object discriminations or visuovisual conditional tasks. Addition of an excitotoxic hippocampal lesion to the hemisphere opposite to the IT ablation impaired retention and acquisition of single-pair object discriminations and visuovisual conditional tasks. Histology revealed no areas of bilaterally symmetrical damage. Previous experiments have shown that bilateral excitotoxic hippocampal lesions do not impair single-pair object discriminations although they do produce a substantial impairment on visuovisual conditional tasks. Bilateral IT ablations produce impairment on single-pair object discrimination tasks. It is argued that the hippocampus in the hemisphere with the IT ablation is deprived of feed-forward visual input and that this, in addition to the contralateral hippocampal lesion, accounts for the impairment on the visuovisual conditional tasks. It is also argued that feed-back projections from the hippocampus to the IT cortex influence the learning of single-pair object discriminations. This influence may be difficult to demonstrate by the addition of hippocampal lesions to IT lesions because of the substantial effect of the IT lesion alone. It may be difficult to demonstrate by bilateral hippocampal lesions alone since the effect may be below that which generates an observable impairment. Nonetheless, an effect may be seen when a hippocampal lesion is made in monkeys with some IT damage, as in this experiment, as well as by the general observation that large lesions of the temporal lobes produce larger perceptuo-mnemonic impairments than lesions confined to the hippocampus or temporal neocortex in monkeys and man.

Learning impairments in monkeys with combined but not separate excitotoxic lesions of the anterior and mediodorsal thalamic nuclei.

Clinical studies in humans and experiments in macaques suggest that damage to the anterior and the mediodorsal thalamus can induce a moderate amnesia, but a more dense impairment may result from substantial damage within the temporal lobes or their subcortical connections. Lesions of the anterior thalamus in macaques produce impairments which resemble those seen after lesions of the fornix-mamillary pathway, which carries projections from the hippocampus to the anterior thalamus, while lesions of the mediodorsal thalamus, which receives inputs from frontal and temporal cortex, produce moderate impairments on a wider range of memory tasks. In the present study, we have made bilateral excitotoxic lesions of either the anterior or the mediodorsal thalamus, or both, in marmoset monkeys. Monkeys with lesions of both thalamic nuclei were severely impaired on retention and new learning of examples of the visuospatial conditional task, a task which is specifically impaired by lesions of the fornix or hippocampus. They were not impaired on performance of a visuovisual conditional task on which monkeys with hippocampal lesions are impaired, nor were they impaired on any visual discrimination task, including the concurrent discrimination task on which monkeys with temporal neocortical ablations are impaired. Monkeys with separate lesions of either the anterior or the mediodorsal thalamus were not impaired on any of these tasks. These results suggest that the mediodorsal thalamus and the anterior thalamus are both involved in processing the output of the hippocampal-fornix-thalamic circuit. Dense amnesia may result from damage to circuits additional to the temporal lobe efferents to either the anterior or the mediodorsal nuclei.