April 2009
Volume 50, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2009
Light-Induced Melatonin Suppression in Mitochondrial Optic Neuropathies
Author Affiliations & Notes
  • C. La Morgia
    Department of Neurological Sciences, University of Bologna, Bologna, Italy
  • E. Sancisi
    Department of Neurological Sciences, University of Bologna, Bologna, Italy
  • A. Munarini
    Biomedical Centre Applied Research CRBA, S.Orsola-Malpighi University Hospital, Bologna, Italy
  • V. Mantovani
    Biomedical Centre Applied Research CRBA, S.Orsola-Malpighi University Hospital, Bologna, Italy
  • P. Barboni
    D'Azeglio Ophtalmologic Centre, Bologna, Italy
  • R. Liguori
    Department of Neurological Sciences, University of Bologna, Bologna, Italy
  • P. Montagna
    Department of Neurological Sciences, University of Bologna, Bologna, Italy
  • A. A. Sadun
    Doheny Eye Institute, University of Southern California, Keck School of Medicine, Los Angeles, California
  • V. Carelli
    Department of Neurological Sciences, University of Bologna, Bologna, Italy
  • Footnotes
    Commercial Relationships  C. La Morgia, None; E. Sancisi, None; A. Munarini, None; V. Mantovani, None; P. Barboni, None; R. Liguori, None; P. Montagna, None; A.A. Sadun, None; V. Carelli, None.
  • Footnotes
    Support  Telethon Grant GGP06233 to VC
Investigative Ophthalmology & Visual Science April 2009, Vol.50, 5663. doi:
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      C. La Morgia, E. Sancisi, A. Munarini, V. Mantovani, P. Barboni, R. Liguori, P. Montagna, A. A. Sadun, V. Carelli; Light-Induced Melatonin Suppression in Mitochondrial Optic Neuropathies. Invest. Ophthalmol. Vis. Sci. 2009;50(13):5663.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: : To test the integrity of the retino-hypothalamic tract (RHT), originating from the intrinsically photosensitive melanopsin-containing retinal ganglion cells (ipRGCs), in mitochondrial optic neuropathies (ON), which selectively affect retinal ganglion cells (RGCs). The non-rod/cone photoreceptors ipRGCs convey the detection of light irradiance to the brain through the RHT, photoentraining circadian rhythms and contributing to the pupillary light reflex (PLR).

Methods: : Melatonin suppression test (MST) was performed in five Leber hereditary optic neuropathy (LHON) and four dominant optic atrophy (DOA) patients, and in nine gender and age-matched controls. A baseline and suppression night tests with monochromatic (470 nm) blue light between 1:30 to 3:30 am were performed. Melatonin was assayed by radioimmunoassay on plasma samples collected hourly from 12:30 pm to 3:30 am. The suppression score was calculated comparing the suppression night melatonin to the baseline night and statistics was run by One-way analysis of variance. Clinical ON severity was determined by retinal nerve fiber layer thickness (RNFL) as evaluated with Optical Coherence Tomography (OCT). All subjects completed self-administered questionnaires (Pittsburgh sleep quality index, Morningness and eveningness, Epworth Sleepiness Scale, Life quality index SF-36, Zung Anxiety and Depression Scale).

Results: : A significant suppression of melatonin plasma levels by light was observed both in control subjects (67% ± 17%) and patients (LHON 65% ± 25% ; DOA 53% ± 33%). The suppression score was not statistically different among groups. All patients had severe optic atrophy and normal PLR. OCT evaluation documented an average RNFL of 52 µm ± 9 in LHON and 59,3µm ±5,8 in DOA (controls 97,3µm±8,4). Self-administered questionnaires showed statistical differences between controls and ON patients only for SF-36 A and C items.

Conclusions: : We demonstrate in both LHON and DOA a substantial preservation of the circuit sustaining the photic input to the circadian system (RHT), as documented by suppression of melatonin secretion by light and PLR preservation in these blind patients.

Keywords: melatonin • optic nerve • circadian rhythms 
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