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Biomedical subjects

J C Justafre

Publications and source records attributed to J C Justafre.

4 recordsLinked to original sources
PubMed1985

Passive transfer studies in demyelinating neuropathy with IgM monoclonal antibodies to myelin-associated glycoprotein.

Serum or IgM fraction from two patients with a demyelinating neuropathy and IgM monoclonal antibodies to myelin-associated glycoprotein were injected in three different animal species. There were no clinical, electrophysiological or morphological signs of demyelination in either chronic or acute passive transfer experiments. These results suggest that the pathogenesis of this human demyelinating neuropathy may be more complex than has been assumed.

Animals↗
PubMed1982

On the role of brain alpha-adrenergic systems in the production of paradoxical sleep.

In order to reinvestigate the role of brain alpha-adrenergic systems in the regulation of paradoxical sleep (PS), we recorded chronically implanted rats under the effect of various neuroactive substances. The functions describing the evolution of PS during sleep were calculated. The following substances were studied at different doses, alone and in various combinations: clonidine, phenoxybenzamine, chlorpromazine, yohimbine, piperoxane and desipramine. Chlorpromazine, yohimbine, piperoxane and desipramine were also studied after pretreatment with alpha-methylparatyrosine. The results are discussed in terms of the known pharmacological properties of these compounds, and indicate that brain alpha-adrenergic systems, probably mainly noradrenergic systems, are positively involved in the maintenance of PS. However, the activity of these systems is controlled by powerful regulatory mechanisms: inhibitory control of transmitter release at the effector site, collateral inhibition within the locus coeruleus and control of transmitter release at the site of collateral inhibition.

Animals↗
PubMed1981

[Decrease of paradoxical sleep in the rat under tricyclic antidepressant: the role of collateral inhibition (author's transl)].

The present study investigated the mechanisms of the action of a tricyclic antidepressant, desmethylimipramine, upon paradoxical sleep in the rat in acute administration. Desmethylimipramine induces an increase in paradoxical sleep latency, as well as a decrease of its total duration; these two modifications are dose-dependent. Different mechanisms may be evoked: inhibition of catecholamine synthesis, inhibition of locus coeruleus by adrenergic collaterals, or an anticholinergic effect. The results show that inhibition of synthesis is not quantitatively sufficient to induce the observed effects. It appears more probable that this decrease in paradoxical sleep results from a collateral inhibition, with the possible participation of an anticholinergic effect. The contributions of these different factors are discussed.

Animals↗