Elsevier

Experimental Neurology

Volume 9, Issue 6, June 1964, Pages 452-462
Experimental Neurology

A comparison of effects of orbitofrontal and hippocampal lesions upon discrimination learning and reversal in the cat

https://doi.org/10.1016/0014-4886(64)90053-6Get rights and content

Abstract

In contrast to normals and brain-damaged controls, cats with bilateral hippocampal or orbitofrontal lesions are severely impaired in their ability to reverse tactile discrimination problems. These lesions do not interfere with discrimination learning per se, and do not affect the cat's ability to learn new discrimination problems. Both effects are quantitatively and qualitatively similar. It takes either preparation more than twice as many trials than normal to master a reversal. The effect of removal of both structures in the same animal is not additive.

References (18)

  • C.M. Butter et al.

    Conditioning and extinction of a food rewarded response after selective ablations of the frontal cortex in Rhesus monkeys

    Exptl. Neurol.

    (1963)
  • H. Mahut et al.

    Spatial reversal deficit in monkeys with amygdalohippocampal ablations

    Exptl. Neurol.

    (1963)
  • W.R. Adey et al.

    An experimental study of hippocampal afferent pathways from prefrontal and cingulate areas in the monkey

    J. Anat.

    (1952)
  • J.V. Brady

    The paleocortex and behavioral motivation

  • C.F. Jacobson et al.

    An experimental analysis of the functions of the frontal association area in primates

    J. Nervous Mental Disease

    (1935)
  • D. Kimura

    Effects of selective hippocampal damage on avoidance behavior of the rat

    Can. J. Psychol.

    (1958)
  • P.E. Lichtenstein

    Studies of anxiety. II. The effects of lobotomy on a feeding inhibition in dogs

    J. Comp. Physiol. Psychol.

    (1950)
  • R.B. Loucks

    Efficacy of the rat's motor cortex is delayed alternation

    J. Comp. Neurol.

    (1931)
  • M. Mishkin

    Effects of small frontal lesions on delayed alternation in monkeys

    J. Neurophysiol.

    (1957)
There are more references available in the full text version of this article.

Cited by (0)

1

This investigation was carried out during the tenure of a USPH postdoctoral fellowship, the work being supported by a USPH grant (MH03372) to Professor R. W. Sperry. The author's present address is: Pharmacology Department, Albert Einstein College of Medicine, New York, N. Y.

View full text