Deficits for representational memory induced by septal and cortical lesions (singly and combined) in rats.

Abstract

A differentiation was made between dispositional memory and representational memory. A delayed-nonmatching-to-sample task in a T-maze operationalized this distinction. Experimental brain lesions in posterior septum and in prelimbic cortex resulted in amnesia for representational memories. The amnesia ameliorated as a function of continued reinforced postoperative testing. When lesions were placed in both structures in the same animals, amnesia for representational memories also occurred, and with further testing, the amnesia ameliorated as indicated by group data. However, examination of the behavioral performance and the lesions in individual animals revealed that when both lesions were adequate, choices remained at chance levels, results suggesting permanent amnesia for representational memories. That the lesion-induced amnesia was restricted to representational memory was indicated by the fact that the rats displayed no amnesia for dispositional memories regarding what to do in the maze. They did not act like naive animals, as they should if they had forgotten the dispositional memories necessary for successful T-maze performance.For almost a century (James, 1890), it has been customary for students of memory to divide hypothetical memory processes into two types. Squire (1982) described some of these classificatory divisions and remarked that the nervous system "honors" these distinctions. In the present article we describe some effects of brain lesions on one type of memory.At a simple, empirical level, this article distinguishes between dispositional memory and representational memory. A necessary (and commonly made) presumption is that memory is not a datum but is an inferred concept based on observable and learned discriminative responses, that is, a differential response (choice) between two or more cue stimuli. If the discrimination The authors are indebted to Mary G. Capozzi for assistance in preparing the manuscript and to Jean A. Conlon for assistance with the histological work.

Development of CDD‐0102 as a selective M1 agonist for the treatment of Alzheimer's disease

“…The paired-run alternation task assessed representational memory function, which is dependent on cues not available at the time of choice [Thomas and Spafford, 1984;Thomas and Gash, 1986]. 192 IgG-saporin produced consistent deficits in performance of the paired-run alternation task, with animals performing at essentially chance levels.…”

Effects of medial septal or unilateral hippocampal inactivations on reference and working spatial memory in rats

“…As shown by an extensive body of data, the hippocampal formation of rats is critically involved in spatial learning and memory. Animals with hippocampal damage have been repeatedly shown to be impaired in a wide variety of spatial tasks Morris et al, 1986;Okaichi, 1987;Poucet and Herrmann, 1990;Rasmussen et al, 1989;Save et al, 1992;Sutherland et al, 1983;Thomas and Spafford, 1984). Such evidence, together with the finding of a population of hippocampal neurons whose firing is highly correlated with the animal's spatial location (Muller et al, 1987;O'Keefe and Speakman, 1987), supports the notion that the hippocampus has some essential function in the processing of spatial information (O'Keefe and Nadel, 1978;Thinus-Blanc et al, 1991).…”

Performance factors in regard to impaired memory and tolerance induced by atropine sulfate

“…Atropine has been shown to cause disorientation, hallucinations, and delirium in humans (Weiner, 1980). SmalI, more or less discrete brain lesions in the posterior septum (Stanton et al, 1984;Thomas & Spafford, 1984)in prelimbic cortex (area 32) (Thomas & Spafford, 1984) in olfactory bulbs (Yu & Wong, 1980), in nucleus basalis magnocellularis (Ordy, Thomas, Dunlap, & Blosser, 1983), in mammillothalamic tracts (Thomas & Gash, 1984), and probably in other places, all impair representational memory. These observations suggest that the capability for representational memory is widespread in brain and not dependent on a single anatomieal system of now known cell groups and connections.…”