Article
Bandage backfall: Labyrinthine and non-labyrinthine components

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Abstract

A cataleptic animal clings in a vertical position, unmoving, for abnormally long periods by supporting some of its weight on its hindlegs, grasping with the forepaws, flexing its forelimbs, and holding the head horizontal. When the head is snugly wrapped with a bandage, the head slowly falls backward, the neck hyperextends, the forelimbs extend and the grasp is released, resulting in the animal falling backward to the ground. It was earlier suggested that in cataleptic animals, the bandage inhibits vestibular and kinesthetic mechanisms of head support, yielding the backfall sequence [35]. However, preliminary experiments showed that labyrinthectomized rats made cataleptic by haloperidol fall backwards when placed in a vertical clinging position, even without a bandage, suggesting that in the rat the bandage-backfall reaction depends only on the vestibular system. In the present paper, this result is verified but, by additional experiments, the latter conclusion is shown to be incorrect. In labyrinthectomized rats made cataleptic by other means (lateral hypothalamic damage, or bulbocapnine), backfall from clinging did not occur unless a bandage was applied. Therefore, the bandage does indeed appear to inhibit the kinesthetic mechanisms that maintain head support in labyrinthectomized cataleptic rats. Haloperidol, particularly in high doses, greatly weakens postural support in labyrinthectomized rats (causing the animal to sag down and fall back when clinging), although the effect is not detectable in rats with labyrinths intact. However, labyrinthectomy reveals that the bandage can trigger an active dorsiflexion of the neck which in itself appears to inhibit clinging and righting. Bandage-induced dorsiflexion is present to a much lesser degree in intact animals, indicating that labyrinthine mechanisms inhibit the dorsiflexion reflex. Therefore, in the intact, cataleptic rat the bandage backfall reaction appears to be produced by the combined effects of a passive component (inhibition of kinesthetic support mechanisms), and an active component (elicitation of dorsiflexion of the neck).

References (45)

  • D. Troiani et al.

    Trigeminal contribution to the head righting reflex

    Physiol Behav

    (1981)
  • A. Van Harreveld et al.

    The clinging position of the bulbocapninized cat

    Exp Neurol

    (1961)
  • A. Van Harreveld et al.

    A propos de la nature de la catalepsie experimentale

    Arch Physiol Neerl

    (1935)
  • J. Brewster et al.

    Facilitation of maternal transport by Norway rat pups

    J Comp Physiol Psychol

    (1980)
  • A. Brodal et al.

    Retrograde cellular changes in the mesencephalic trigeminal nucleus in the cat following cerebellar lesions

    Acta Morphol Neerl Scand

    (1965)
  • B.M. Carpenter et al.

    Fiber projections from the spinal trigeminal nucleus in the cat

    J Comp Neurol

    (1961)
  • Y.-C. Chen

    Two components in the bandage-backfall reaction

  • H. De Jong

    Experimental Catatonia. A General Reaction-Form of the Central Nervous System and its Implication for Human Pathology

    (1945)
  • M. DeRyck et al.

    Morphine catalepsy as an adaptive reflex state in rats

    Behav Neurosci

    (1984)
  • R. Ewbank

    The behavior of animals in restraint

  • K.M. Horn et al.

    Behavioral assessment of sodium arsanilate induced vestibular dysfunction in rats

    Physiol Psychol

    (1981)
  • P.A.J. Jansen et al.

    Pimozide, a chemically novel, highly potent and orally long-acting neuroleptic drug. Part 1: The comparative pharmacology of pimozide, haloperidol and chlorpromazine

    Arzneimittelforsch

    (1968)
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