Stefania Evangelisti1,2, Claudia Testa1,2, Chiara La Morgia1,3, Gilles Vandewalle4, Claudio Bianchini1,2, David Neil Manners1,2, Paola Fantazzini5,6, Michele Carbonelli3, Alfredo Sadun7,8, Caterina Tonon1,2, Valerio Carelli1,3, and Raffaele Lodi1,2
1Department of Biomedical and NeuroMotor Sciences, University of Bologna, Bologna, Italy, 2Functional MR Unit, Policlinico S.Orsola - Malpighi, Bologna, Italy, 3IRCCS Institute of Neurological Sciences of Bologna, Bologna, Italy, 4Sleep Research Group; GIGA-Research, Cyclotron Research Centre/In vivo imaging unit, University of Liège, Liège, Belgium, 5Department of Physics and Astronomy, University of Bologna, Bologna, Italy, 6Centro Enrico Fermi, Roma, Italy, 7Doheny Eye Institute, University of California, Los Angeles, CA, United States, 8Doheny Eye Centers of UCLA, Department of Ophthalmology, David Geffen School of Medicine at University of California, Los Angeles, CA, United States
Synopsis
We
combined light stimulation and fMRI to investigate the contribution of melanopsin-expressing
retinal ganglion cells (mRGCs) to visual and non-visual processes in Leber
Hereditary Optic Neuropathy (LHON) paradigm of retinal degeneration .
Monochromatic
visual simulation showed a stronger effect in LHON visual cortex for blue vs
red light with relatively long stimuli, supporting the hypothesis of a role for
melanopsin in visual processes.
When light was combined with a working memory
task, blue light modulation of cognitive brain response was maintained in LHON;
indeed the effect was stronger than in healthy subjects, probably because of the
higher mRGCs/RGCs ratio in LHON retinas.
Introduction
A
third photoreceptor type, different from rods and cones, exists in mammalian
retina: melanopsin-expressing retinal ganglion cells (mRGCs). Melanopsin plays
a key role in non-image-forming functions and is maximally sensitive to blue light
1,2.
MRGCs are thought to play a prominent role in mediating fMRI attentional brain
response during blue light stimulation
3,4 but definite proof is difficult
to obtain in healthy volunteers.
Leber
Hereditary Optic Neuropathy (LHON) is a mitochondrial genetic disease that
manifests with loss of central vision due to RGC degeneration and consequent
optic nerve atrophy
5,6. Despite the loss of RGCs, those expressing melanopsin
are relatively spared
7 such that patient show a relative increase in
mRGC photoreception compared to classical visual photoreception.
The
aim of this study was to assess mRGC contribution to visual and non-visual
processes in LHON paradigm of retinal degeneration by studying cerebral fMRI
activation patterns during light stimulation.
Methods
We
evaluated 13 patients with genetically confirmed diagnosis of LHON and 13 matched
healthy controls (HC, Tab.1).
All
participants underwent a brain MR-protocol (1.5T GE scanner) including visual and
visual-cognitive fMRI paradigms (TR=3s,
resolution=1.875x1.875x4mm) and volumetric T1-w acquisition (1mm3).
The
pure visual task consisted of a pseudorandom alternation of blue, red and dark periods
(Fig.1). The visual-cognitive task was an independent combination of light
stimulation and auditory 0/3-back task (Fig.2). Blue (480nm) and red (620nm) lights
were transmitted using a specific instrumental setup6. Light intensities
were set to produce the same photon flux at the eye (5x1013ph cm−2s−1)
at both wavelengths.
Paradigms
were presented using COGENT-2000 (MATLAB). Before acquisitions, participants
were asked to follow a regular sleep-wake rhythm for one week. Pupils were
chemically dilated before participants were blindfolded in the dark for 1 hour before
fMRI recordings.
Analyses
were performed with FSL. Pre-processing included motion correction, high-pass
filtering (100s), spatial smoothing (FWHM=5mm) and slice-timing correction.
A
general linear model was applied, modelling the effects of interest with
box-car functions convolved with a double-gamma HRF. Stick functions were added
to model light onsets/offsets. For the visual-cognitive paradigm, interactions
between light and task were investigated. Linear modulated regressors were also
added to the design. Functional images were registered to T1-w images (BBR) and
T1-w images were non-linearly (FNIRT) aligned to MNI.
Group
comparisons were performed with FLAME-1 mixed-effect analysis, with age, sex
and contemporaneous daylight length as nuisance regressors. Statistical maps
were corrected for multiple comparisons (cluster z=2.3, FWE p<0.05). Results
Visual
stimulation results were considered for different durations of light stimuli:
transient effects, 10s and 50s sustained effects (Fig.3).
At
light onset, the visual cortex was activated for both groups and both colors.
Regarding
occipital cortex modulation, with 10s sustained stimuli a significant LHON
group activation was lacking for red, while no group differences were present
with blue.
With
longer sustained effects (50s), visual cortex activations were present in both
groups with both colors, but without group differences for blue, while a lower
activation was found for red in LHON. The most straightforward result was that
brain response was higher with blue
vs red
in the occipital pole for LHON.
Regarding
the cognitive paradigm, all the participants got at least 75% of correct
answers, without group or light effects; brain activations, irrespectively of
light conditions, were in line with fMRI literature for n-back8 and analogous
between groups (data not shown). As for the interactions between light and task,
we found no light modulation effect on HC cognitive response, while a higher
brain activity was found in LHON when the task was performed under blue light
compared to red, mainly in middle and inferior frontal gyri, temporo-occipital
regions, insula, putamen, cerebellum, and, with lower significance, brainstem
(Fig.4).
Discussion and conclusions
With
purely visual simulation, a stronger effect in visual cortex for LHON with blue
vs red became clearer as the duration
of the stimuli got longer. Considering the sluggish and sustained response of
melanopsin, these support the hypothesis of a role for melanopsin in visual
processes
9.
The
blue light modulation of cognitive brain response we observed in LHON was in brain
regions that were consistent with previous results
3,4. We saw a
stronger effect in LHON probably due to the higher ratio of mRGCs to RGCs in
their retinas
7. These results showed that mRGCs’ function of
modulating brain activity during a working memory task was maintained in LHON.
In
conclusion, this first fMRI study in LHON patients demonstrates that mRGCs maintained
functionality, and also provides a good paradigm of retinal degeneration to study
human mRGCs in-vivo.
Acknowledgements
No acknowledgement found.References
- Provencio
I, Rodriguez IR, Jiang G et al. A novel human opsin in the inner retina,
Journal of Neurosciences 2000; 20: 600-605.
- Hankins
MW, Peirson SN, Foster RG. Melanopsin: an exciting photopigment, review, Trends
in neurosciences 2007; 31 (1): 27-36.
- Vandewalle
G, Schmidt C, Albouy G et al. Brain responses to violet, blue and green
monochromatic light exposures in humans: prominent role of blue light and the
brainstem, Plos One 2007; 2(11): e1247.
- Vandewalle
G, Maquet P, Dijk DJ. Light as a modulator of cognitive brain function, Trends
in cognitive sciences 2009; 13(10):429-438.
- Man PYW, Turnbull DM, Chinnery PF. Leber
hereditary optic neuropathy. J Med Genet, 39(3):162–9, 2002
- Carelli
V, Ross-Cisneros FN, Sadun AA. Mitochondrial dysfunction as a cause of optic
neuropathies. Prog Retin Eye Res, 23(1):53–89, 2004.
- La
Morgia C, Ross-Cisneros FN, Sadun AA et al. Melanopsin retinal ganglion cells
are resistant to neurodegeneration in mitochondrial optic neuropathies, Brain
2010; 133: 2426-2438
- Owen
AM, McMillan KM, Laird AR et al. N-back working memory paradigm: a
meta-analysis of normative functional neuroimaging studies. Hum Brain Mapp,
25(1):46–59, 2005
- Brown
TM, Gias C, Hatori M et al. Melanopsin contributions to irradiance coding in
the thalamo-cortical visual system. PLoS Biol, 8:e1000558, 2010