The traditional explanation of dense amnesia after medial temporal lesions
is that the amnesia is caused by damage to the hippocampus and related stru
ctures. An alternative View is that dense amnesia after medial temporal les
ions is caused by the interruption of afferents to the temporal cortex from
the basal forebrain. These afferents travel to the temporal cortex through
three pathways, namely the anterior temporal stem, the amygdala and the fo
rnix-fimbria, and all these three pathways are damaged in dense medial temp
oral amnesia. In four experiments using different memory tasks, we tested t
he effects on memory of sectioning some or all of these three pathways in m
acaque monkeys. In a test of scene-specific memory for objects, which is an
alogous in some ways to human episodic memory, section of fornix alone, or
section of amygdala and anterior temporal stem sparing the fornix, each pro
duced a significant but mild impairment. When fornix section was added to t
he section of anterior temporal stem and amygdala in this task, however, a
very severe impairment resulted. In an object recognition memory task (dela
yed matching-to-sample) a severe impairment was seen after section of anter
ior temporal stem and amygdala alone, with or without the addition of forni
x section; this impairment was significantly more severe than that which wa
s seen in the same task after amygdalectomy leaving the temporal stem intac
t, with or without fornix section. Animals with combined section of anterio
r temporal stem, amygdala and fornix were also impaired in object-reward as
sociation learning. However, the retention of pre-operatively acquired obje
ct-reward associations was at a high level. These results show that the pat
tern of impairments after section of anterior temporal stem, amygdala and f
ornix in the monkey, leaving hippocampus intact, resembles human dense amne
sia and is different from the effects of hippocampal lesions in the monkey.
(C) 2000 Elsevier Science Ltd. All rights reserved.