Pain Hypersensitivity is Associated with Increased Amygdala Volume and c-Fos Immunoreactivity in Anophthalmic Mice.

Touj, Sara; Tokunaga, Ryota; Aïn, Syrina Al; Bronchti, Gilles; Piché, Mathieu

doi:10.1016/j.neuroscience.2019.08.035

Cited by 16 publications

(28 citation statements)

References 70 publications

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“…These mice have orbits but neither eyes nor optic nerves. Other brain defects are described in detail in a previous report (Touj et al., 2019). In a previous study from our laboratory, a cross‐breeding was performed between the ZRDCT strain and the C57Bl/j6 strain (Masse et al., 2014).…”

Section: Methodsmentioning

confidence: 82%

“…The ZRDBA mouse strain is obtained by crossbreeding a sighted DBA‐6 mouse and a ZRDCT anophthalmic mouse (Touj et al., 2019). The ZRDCT mouse strain was first described by Chase (Chase, 1942, 1944; Chase & Chase, 1941).…”

Section: Methodsmentioning

confidence: 99%

“…The approach with the ZRDBA mouse obtained by cross‐breeding ZRDCT mice with DBA‐6 mice avoids this problem. In the ZRDBA strain, half of the offspring are heterozygous and sighted, while the other half are homozygous and anophthalmic (Touj et al., 2019).…”

Section: Introductionmentioning

confidence: 99%

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Structural brain plasticity induced by early blindness

Touj

Gallino

Chakravarty

et al. 2020

Eur J of Neuroscience

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It is well established that early blindness results in behavioural adaptations. While the functional effects of visual deprivation have been well researched, anatomical studies are scarce. The aim of this study was to investigate whole brain structural plasticity in a mouse model of congenital blindness. Volumetric analyses were conducted on high‐resolution MRI images and histological sections from the same brains. These morphometric measurements were compared between anophthalmic and sighted ZRDBA mice obtained by breeding ZRDCT and DBA mice. Results from MRI analyses using the Multiple Automatically Generated Templates (MAGeT) method showed smaller volume for the primary visual cortex and superior colliculi in anophthalmic compared with sighted mice. Deformation‐based morphometry revealed smaller volumes within the dorsal lateral geniculate nuclei and the lateral secondary visual cortex and larger volumes within olfactory areas, piriform cortex, orbital areas and the amygdala, in anophthalmic compared with sighted mice. Histological analyses revealed a larger volume for the amygdala and smaller volume for the superior colliculi, primary visual cortex and medial secondary visual cortex, in anophthalmic compared with sighted mice. The absence of superficial visual layers of the superior colliculus and the thinner cortical layer IV of the primary and secondary visual cortices may explain the smaller volume of these areas, although this was observed in a limited sample. The present study shows large‐scale brain plasticity in a mouse model of congenital blindness. In addition, the congruence of MRI and histological findings support the use of MRI to investigate structural brain plasticity in the mouse.

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Section: Methodsmentioning

confidence: 82%

Section: Methodsmentioning

confidence: 99%

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Structural brain plasticity induced by early blindness

Touj

Gallino

Chakravarty

et al. 2020

Eur J of Neuroscience

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“…Moreover, the visual cortex eceives feedback projections from auditory and somatosensory cortex as well as from motor and multisensory cortices [22,[52][53][54][55][56]. However, Trpm1 −/− mice did not show hypersensitivity to sensory stimuli, which is observed in visually impaired animals as well as in human patients [20][21][22][23][24][25][26][27][28][29], at least for thermal perception and auditory responses (Fig. 1B-D).…”

Section: Discussionmentioning

confidence: 87%

“…1A) in contrast to mGluR6 −/− mice [19]. It has been reported that the absence of vision in human and animals enhances auditory, haptic, and pain sensitivities [20][21][22][23][24][25][26][27][28][29], and causes structural changes in the visually deprived cortex and in other areas [23,30,31]. We examined sensory responses in Trpm1 −/− mice, but we did not nd any signi cance difference between Trpm1 −/− mice and wild type for the hot plate test, the acoustic startle response, and prepulse inhibition (Fig.…”

Section: Resultsmentioning

confidence: 97%

Mice with Mutations in Trpm1, a Gene within the locus of 15q13.3 Microdeletion Syndrome, Display Pronounced Hyperactivity and Decreased Anxiety-Like Behavior.

Hori

Ikuta

Takao

et al. 2020

Preprint

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15q13.3 microdeletion syndrome is a genetic disorder caused by a deletion of a region containing seven genes on chromosome 15, MTMR10, FAN1, TRPM1, MIR211, KLF13, OTUD7A, and CHRNA7, and characterized by a wide spectrum of psychiatric disorders. The contribution of each gene in this syndrome has been studied using mutant mouse models, but the phenotypes of these mice do not account for human phenotypes and the results are still controversial. The behavior of Trpm1−/− mice with relation to 15q13.3 microdeletion syndrome has not been investigated due to the visual impairment in these mice, which may confound the results of behavior tests that involve vision. We have now applied a comprehensive behavioral test battery to examine the relationship of TRPM1 and 15q13.3 microdeletion syndrome by using Trpm1 null mutant mice. Our data indicate abnormal behavior of Trpm1−/− mice which may explain some phenotypes of 15q13.3 microdeletion syndrome, including reduction of anxiety behavior, abnormality of social interaction, attenuation in fear memory, and hyperactivity, which is the most prominent phenotype of Trpm1 mutant mice. While the ON visual transduction pathway is impared in Trpm1−/− mice, we did not detect compensatory high sensitivities for other sensory modalities. Although Trpm1−/− mice share the same pathway for visual impairment with mGluR6−/− mice, hyperlocomotion activity has not been reported in mGluR6−/− mice. These data suggest that the phenotype of Trpm1−/− mice extends beyond that expected from visual impairment alone. This is the first evidence to associate TRPM1 with impairment of cognitive function similar to that found in the phenotypes of 15q13.3 microdeletion syndrome.

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Enhanced maternal behaviors in a mouse model of congenital blindness

Bouguiyoud

Xie

Bronchti

et al. 2023

Developmental Psychobiology

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In mammals, mothering is one of the most important prosocial female behavior to promote survival, proper sensorimotor, and emotional development of the offspring. Different intrinsic and extrinsic factors can initiate and maintain these behaviors, such as hormonal, cerebral, and sensory changes. Infant cues also stimulate multisensory systems and orchestrate complex maternal responsiveness. To understand the maternal behavior driven by complex sensory interactions, it is necessary to comprehend the individual sensory systems by taking out other senses. An excellent model for investigating sensory regulation of maternal behavior is a murine model of congenital blindness, the ZRDBA mice, where both an anophthalmic and sighted mice are generated from the same litter. Therefore, this study aims to assess whether visual inputs are essential to driving maternal behaviors in mice. Maternal behaviors were assessed using three behavioral tests, including the pup retrieval test, the home cage maternal behavior test, and the maternal aggression test. Our results show that blind mothers (1) took less time to retrieve their offspring inside the nest, (2) spent more time nursing and licking their offspring in the second‐ and third‐week postpartum, and (3) exhibited faster aggressive behaviors when exposed to an intruder male, compared to the sighted counterparts. This study provides evidence that congenitally blind mothers show more motivation to retrieve the pups, care, and protection towards their pups than sighted ones, likely due to a phenomenon of sensory compensation.

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Pain Hypersensitivity is Associated with Increased Amygdala Volume and c-Fos Immunoreactivity in Anophthalmic Mice.

Cited by 16 publications

References 70 publications

Structural brain plasticity induced by early blindness

Structural brain plasticity induced by early blindness

Mice with Mutations in Trpm1, a Gene within the locus of 15q13.3 Microdeletion Syndrome, Display Pronounced Hyperactivity and Decreased Anxiety-Like Behavior.

Enhanced maternal behaviors in a mouse model of congenital blindness

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