L'utilisation d'un miroir comme « substitut social » chez des oiseaux de laboratoire

WOS:000258353100005International audienceA mirror has been shown to reduce stereotypies in horses housed singly, presumably as it may provide some sort of ‘social stimulation’. We investigated here whether a mirror may have such a ‘quietening effect’ on birds kept in a laboratory, such as European starlings. We observed the reactions to a mirror of starlings of different sexes and with different social experiences. Females and pair-raised males seemed calmer, showing less movement and more comfort behaviour than socially and single-raised birds. The results are discussed in the light of the species' social organization and the effect of social experience. We conclude that a mirror might be a good way to reduce isolation-related stress in laboratory birds, but that sex and social experience of an individual have to be taken into account, as otherwise effects opposite to those wished for may be induced.La présence d'un miroir réduit les stéréotypies chez les chevaux isolés en box, probablement en apportant une « stimulation sociale ». Dans cette étude, nous examinons si un miroir peut avoir un tel effet « apaisant » sur des oiseaux de laboratoire tels que les étourneaux sansonnets. Les réactions d'oiseaux de sexe et d'expériences sociales différentes ont été observées. En présence d'un miroir, les femelles et les mâles élevés en paire semblent apaisés, expriment moins de mouvements et plus de comportements de confort que les oiseaux élevés isolément ou en groupes sociaux. Ces résultats sont discutés en regard de l'organisation sociale de l'espèce et de l'effet de l'expérience sociale précoce. Le miroir pourrait donc être un bon moyen pour réduire le stress lié à l'isolement chez des oiseaux de laboratoire, sachant que le sexe et l'expérience sociale des individus peuvent avoir des effets opposés

OPA1 mutations induce mitochondrial DNA instability and optic atrophy 'plus' phenotypes.

International audienceMutations in OPA1, a dynamin-related GTPase involved in mitochondrial fusion, cristae organization and control of apoptosis, have been linked to non-syndromic optic neuropathy transmitted as an autosomal-dominant trait (DOA). We here report on eight patients from six independent families showing that mutations in the OPA1 gene can also be responsible for a syndromic form of DOA associated with sensorineural deafness, ataxia, axonal sensory-motor polyneuropathy, chronic progressive external ophthalmoplegia and mitochondrial myopathy with cytochrome c oxidase negative and Ragged Red Fibres. Most remarkably, we demonstrate that these patients all harboured multiple deletions of mitochondrial DNA (mtDNA) in their skeletal muscle, thus revealing an unrecognized role of the OPA1 protein in mtDNA stability. The five OPA1 mutations associated with these DOA 'plus' phenotypes were all mis-sense point mutations affecting highly conserved amino acid positions and the nuclear genes previously known to induce mtDNA multiple deletions such as POLG1, PEO1 (Twinkle) and SLC25A4 (ANT1) were ruled out. Our results show that certain OPA1 mutations exert a dominant negative effect responsible for multi-systemic disease, closely related to classical mitochondrial cytopathies, by a mechanism involving mtDNA instability