Perseverative responding and hyperphagia following entorhinal lesions in cats.

Abstract

Cats with large bilateral lesions limited to entorhinal cortex were impaired on the reversal but not the original learning of position habits, displayed deficient passive-avoidance behavior, were hyperactive in the open field, and were hyperphagic for some days after the surgery. The lesions had no effect on the acquisition or the punishment extinction of a one-way activeavoidance response. Control experiments showed that effects of entorhinectomy on position-habit reversals and open-field activity were not secondary to hyperphagia. The pattern of behavioral deficits suggests that the entorhinal region participates in the suppression of appetitively reinforced responses but not in the suppression of aversively reinforced responses.

Localization of a “passive avoidance memory system”in the white rat

“…Despite differences in the relevant motive (the one underlying the response to be suppressed), the apparatus, and the retention measures, the results of the current study are generally in accord with earlier reports dealing with the effects of local brain damage on retention (and/or learning) of more conventional passive avoidance tasks. Correspondences were observed in connection with lesions to the frontal cortex (Kaada, Rasmussen, & Kveim, 1962), occipital cortex (Wilson & Vardaris, 1972), hippocampus (Kimura, 1958;Isaacson & Wickelgren, 1962;Wishart & Morgenson, 1970), septofornix area (deCastro & Hall, 1975;Thomas, 1972;Wishart & Morgenson, 1970), entorhinosubicular area (Entingh, 1971;Ross, Walsh, & Grossman, 1973), amygdala (Nagel & Kemble, 1976), medial hypothalamus (Kaada et al, 1962), medial forebrain bundle (Heybach & Coover, 1976;Kaada et al, 1962), anterior and/or medial thalamus (Gerbrandt, 1965;Kaada et al, 1962), interpeduncular nucleus (Wilson, Mitchell, & Van Hoesen, 1972), central tegmentum (Wilson ef al., 1972), dorsal mesencephalon (Uebman, Mayer, & Uebeskind, 1970), caudoputamen (Kirkby & Kimble, 1969;Mitcham & Thomas, 1972;Prado-Alcala, Grinberg-Zylberbaum, Arditti, Garcia, Prieto, & Brust-Carmona, 1975;Winocur, 1974), and substantia nigra (Mitcham & Thomas, 1972).…”

Long‐term synaptic alteration in the rat hippocampal CA3 field following an entorhinal cortex lesion

“…The role of the entorhinal cortex in providing the link between the neocortex and the hippocampus has long been recognized, yet relatively few studies have examined the behavioral consequences of entorhinal cortex 2,3 . We had described the importance of the entorhinal cortex in early neuropathological changes of Alzheimer's disease.…”

“…The role of the entorhinal cortex in providing the link between the neocortex and the hippocampus has long been recognized, yet relatively few studies have examined the behavioral consequences of entorhinal cortex. 2,3 We had described the importance of the entorhinal cortex in early neuropathological changes of Alzheimer's disease. Rats with excitotoxic lesion of entorhinal cortex showed impaired acquisition of both negative reinforcement operant learning and passive-and active-avoidance learning.…”

Bilateral entorhinal cortex lesions impair DRL performance in rats

“…1981; Ramirez, Fass, Karpiak, & Steward, 1987;Steward, Loesche, & Horton, 1977), impaired spatial alternation performance Olton et al, 1978;Ramirez, Fass, Kilfoil, et al, 1987;Ramirez & Stein, 1984), perseverative behavior (Entingh, 1971;Ramirez, Labbe, & Stein, 1988), and impaired Hebb-Williams maze performance (Stein & Will, 1983).…”