Contribution a l'étude du syndrome moteur provoqué chez la Souris par l'amino-dipropionitrile (souris tournantes)

Thuillier, J; Burger, A.

doi:10.1007/bf02159284

Cited by 26 publications

(9 citation statements)

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“…A closely related synthetic iminonitrile, p,P'-iminodipropionitrile (IDPN), elicits a permanent hyperkinetic syndrome (neurolathryism) in mice (Delay et al, 1952;Thuillier et al, 1953) and in rats (Hartmann and Stich, 1957;Selye, 1957). The most striking features of this syndrome, that is, excitation with fine tremors, choreiform head and neck movements and circling, have led to it being called the "ECC-syndrome" (Selye, 1957).…”

Section: Introductionmentioning

confidence: 98%

Regional neurochemical studies on the effect of β,β′ ‐iminodipropionitrile (IDPN) in the rat

Langlais

Huang

Gabay

1975

J of Neuroscience Research

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A permanent hyperkinetic syndrome, characterized by excitation, choreiform head and neck movements and circling, which has led to it being called collectively the "ECC-syndrome," is induced in rats by the daily IP administration of beta, beta'-iminodipropionitrile (IDPN), 300 mg/kg, for 7 days. The levels of the biogenic amines, norepinephrine (NE), dopamine (DA), serotonin (5-HT) and its metabolite 5-hydroxyindoleacetic acid (5-HIAA), were measured in the striatum, midbrain, medulla, cortex, and cerebellum on the day the syndrome appeared (day 7) and one week later (day 14). The biogenic amine most affected by IDPN administration was 5-HT. On day 7, striatal 5-HT levels increased and 5-HIAA levels decreased while in the medulla and midbrain, 5-HIAA levels increased. On day 14, significant reductions in both 5-HT, in the midbrain, striatum, and cortex, and 5-HIAA, in all regions except the cortex, were observed. NE was markedly increased in the medulla, midbrain, and striatum on day 7, whereas on day 14 it was found to be within the normal range in these same regions. With the exception of a slight, but significant, increase in the cortex on day 7, DA levels in all regions were found to be relatively unaffected by IDPN administration on both day 7 and day 14. In an attempt to detect degenerative changes which might be taking place in the brain and which might provide an explanation for the permanency of the behavioral disturbances, the uptake of [3H]-labeled NE, DA, and 5-HT into synaptosomal-rich preparations of striatum and the uptake of NE and 5-HT into the midbrain area were compared between normal and syndromized rats on both day 7 and day 14. Small changes were observed but they were not statistically significant. The alterations of 5-HT and 5-HIAA levels in several regions of the brain under the conditions examined may indicate that IDPN's neurotoxicity primarily affects 5-HT-containing neurones. The active membrane transporting system of the nerve endings studied, however, remained relatively intact. This latter finding eliminates the possibility that neuronal degeneration in these areas is responsible for the decreased 5-HT and 5-HIAA levels or is the pathology underlying the permanency of the syndrome. These results are evaluated in terms of a possible model for hyperkinetic disorders.

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Section: Introductionmentioning

confidence: 98%

Regional neurochemical studies on the effect of β,β′ ‐iminodipropionitrile (IDPN) in the rat

Langlais

Huang

Gabay

1975

J of Neuroscience Research

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“…Some, including 3,3ø-iminodipropionitrile andb-dimethylaminopropionitrile, show striking central and peripheral neurotoxic properties (Chou & Hartmann 1964& 1965Baker et al 1981;Griffin & Price 1981). Besides producing an axonopathy characterized by swollen axons filled with large tangles of neurofilaments (Hartmann et al 1958;Clark et al 1980) accompanied by a slowing down of the nerve conduction velocities (Höfinger et al 1982;Lowndes et al 1985;Ivens 1990;Gagnaire & Marignac 1999), 3,3ø-iminodipropionitrile also causes behavioural abnormalities such as hyperexcitability, retropulsion, head bobbing and circling movements in mice and rats (Delay et al 1952;Thuillier et al 1953;Hartmann & Stick 1957;Selye 1957). Moreover, 3,3ø-iminodipropionitrile induces degeneration of the vestibular sensory hair cells (Llorens et al Author for correspondence: François Gagnaire, Department of Pollutants and Health, National Institute for Research and Safety, Avenue de Bourgogne, B. P. Nae 27, 54501 Vandoeuvre Cedex, France (fax π33 3 83 50 20 96, e-mail gagnaire/inrs.fr).…”

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confidence: 99%

The Ototoxic Effects Induced in Rats by Treatment for 12 Weeks with 2‐Butenenitrile, 3‐Butenenitrile and cis‐2‐Pentenenitrile

Gagnaire¹,

Marignac²,

Ban³

et al. 2001

Pharmacology & Toxicology

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Brainstem auditory and visual evoked-potentials were studied in male Sprague-Dawley rats during subchronic oral treatment with three unsaturated aliphatic nitriles. The rats were given, by gastric intubation, doses of 10, 20 and 40 mg ¡ kg ª1 3-butenenitrile (allyl cyanide) and 25, 50 and 100 mg ¡ kg ª1 of either cis/trans-2-butenenitrile (crotononitrile) or cis-2-pentenenitrile once a day, 5 days per week for 12 weeks. Oral administration of the three unsaturated nitriles produced deafness and absence of reaction when the animals were subject to droptest. Rats in the high dosage groups exhibited a complete disappearance of the five waves of the auditory evoked-potentials. There was a decrease in the amplitudes of the 2nd component of the auditory evoked-potentials. Those changes were not reversible at the 8th week of the recovery period. A dose-dependent effect on inner and outer hair cells was observed in the organ of Corti. The basal part of the cochlea was the most affected. Though no measurements were made of systemic exposure, a tentative ranking of decreasing ototoxicity of these three unsaturated nitriles might be proposed based on the electrophysiological deficiencies and histological losses observed: 3-butenenitrile Ͼcis-2-pentenenitrile Ͼcis/trans-2-butenenitrile. Moreover, rats treated with those nitriles showed a corneal opacity as well as a decrease in the amplitude and lengthening of the peak latencies of the visual evoked-potentials. These latter changes were reversible by the end of the 8th week of the recovery period and appeared to be related to the opacity of the cornea.

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“…Mice in which hyperkinesia had been induced by 8?/-iminodipropionitrile after the method of Thuillier and Burger (1954) were treated with benzethidine, furethidine and pethidine and the effect on activity was recorded semiquantitatively using a jiggle cage.…”

Section: H)mentioning

confidence: 99%

Pharmacological Actions of Two New Pethidine Analogues

Lister¹

1960

British Journal of Pharmacology and Chemotherapy

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Contribution a l'étude du syndrome moteur provoqué chez la Souris par l'amino-dipropionitrile (souris tournantes)

Cited by 26 publications

References 1 publication

Regional neurochemical studies on the effect of β,β′ ‐iminodipropionitrile (IDPN) in the rat

Regional neurochemical studies on the effect of β,β′ ‐iminodipropionitrile (IDPN) in the rat

The Ototoxic Effects Induced in Rats by Treatment for 12 Weeks with 2‐Butenenitrile, 3‐Butenenitrile and cis‐2‐Pentenenitrile

Pharmacological Actions of Two New Pethidine Analogues

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