PubMed · 14005755
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E A WEINSTEIN, S L MARVIN, N J KELLER. 1962. Amnesia as a language pattern.. https://doi.org/10.1001/archpsyc.1962.01710220001001
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In a recent eye-movement study [Psychol. Sci. 11 (2000) 454], amnesic patients failed selectively to exhibit long-term effects of memory for the relations among the constituent elements of scenes. This failure could be due to a deficit specifically in long-term relational memory, as we have suggested; or in retention of relational information over any delay, whether involving perceptual processing and short-term maintenance or long-term memory, consistent with suggestions from recent studies of the hippocampus; or in on-line processing of relational information, as would occur in perceptual or feature binding. Here we show robust eye-movement effects of relations among elements of scenes in amnesia in a short-delay matching task, with the same materials and in the same amnesic patients in which long-delay conditions elicited failure. These findings document intact processing and short-term retention of relational information in amnesia, indicating that amnesia associated with hippocampal damage results in a relational memory deficit, specifically of long-term memory.
Inhibition of sodium-potassium adenosine 5'-triphosphatase ((Na(+), K(+))-ATPase) activity causes edema and cell death in the central nervous system, and impairment of learning and memory. Several sex steroid hormones have a protective effect against neuronal cell damage and the hypofunction of learning and memory. To examine the possible roles and mechanism of action of steroid hormones against amnesia induced by ouabain, an inhibitor of (Na(+), K(+))-ATPase, gonadectomized male mice were administrated ouabain (0.1 microg per mouse) intracisternally (i.cist.), and the learning and memory abilities of the mice were assessed by a step-through passive avoidance task. Subcutaneous (s.c.) administration of 17beta-estradiol (betaE2; 10 microg kg(-1)) or testosterone (TES; 1 mg kg(-1)) improved the memory impairment induced by ouabain, while administration of dihydrotestosterone (1 mg kg(-1)) or corticosterone (COR) (1 mg kg(-1)) did not. Treatment with the estradiol receptor antagonists, tamoxifen (TAM) (10 mg kg(-1); s.c. or 0.1 microg; i.cist.) and 4-hydroxytamoxifen (10 mg kg(-1); s.c.), or the androgen receptor antagonist, cyproterone (10 mg kg(-1); s.c. or 1 microg; i.cist.), did not influence the protective effect of betaE2 or TES on ouabain-induced amnesia. Moreover, we studied the effects of several free radical scavengers-17alpha-estradiol (10 microg kg(-1); s.c.), alpha-tocopherol (VE: 200 mg kg(-1); per os (p.o.), ascorbic acid (VC: 200 mg kg(-1); p.o.), or VE+VC (200 mg kg(-1) each; p.o.)-on ouabain-induced amnesia, and compared those effects with that of betaE2. The administration of free radical scavengers had no significant effect on memory impairment. These results indicate that betaE2 and TES ameliorate the amnesia induced by inhibition of (Na(+), K(+))-ATPase activity, and that the protective effect of betaE2 is caused by a non-genomic, rather than a genomic effect or a radical scavenging action. Additionally, the ameliorative effect of TES does not appear to involve free radical scavenging, but its aromatization to estrogen could contribute to the non-genomic action of betaE2.
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