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A-D Morphopathology of the abnormal cat. A General view of the cat. Note the asymmetrical eyes: the right eye situated deep in the orbit and the large left eye. B Isolated eyes of the abnormal cat removed from their orbits after the animal was killed. Note the buphtalmic eye covered with a thick cataract and its large size compared with the left eye. C Hematoxylin-eosin-stained cross sections of the retina of both eyes. Note the extensive loss of ganglion cells (dashed arrow) and nerve-fiber layer (solid arrow) of the right eye as compared with the mild loss of the retinal ganglion cells of the left eye. Magnification ×400. D Whole brain of a normal (left) and the abnormal (right) cat. The right occipital regions were removed in both cases. Note the small size and smooth surface of the abnormal cat's brain and the large lateral ventricle as compared with the normal brain
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Early blindness in humans and experimental visual deprivation in animal models are known to induce compensatory somatosensory and/or auditory activation of the visual cortex. An abnormal hydrocephalic cat with extreme malformation of the visual system, born in our breeding colony, rendered a good model system for investigating possible cross-modal...
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The aim of this study was (1) to provide behavioral evidence for multimodal feature integration in an object recognition task in humans and (2) to characterize the processing stages and the neural structures where multisensory interactions take place. Event-related potentials (ERPs) were recorded from 30 scalp electrodes while subjects performed a...
We performed a systematic study to check whether neurons in the area TE (the anterior part of inferotemporal cortex) in rhesus monkey, regarded as the last stage of the ventral visual pathway, could be modulated by auditory stimuli. Two fixating rhesus monkeys were presented with visual, auditory or combined audiovisual stimuli while neuronal respo...
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... Being congenitally blind, Spalax ehrenbergi is deprived of visual inputs, and thus compensates via the diversion of the visual modality to the auditory modality. Cross-modal neuroplasticity in animal models is induced, in most cases, by experimental procedures (Izraeli et al., 2002;Rauschecker and Kniepert, 1994;Toldi et al., 1994a;Toldi et al., 1994b;Yaka et al., 2000). By using the blind mole rat as a model animal, we take advantage of its natural and congenital sensory deficit-its blindness. ...
On the social scale, the blind mole rat (BMR; Spalax ehrenbergi) is an extreme. It is exceedingly solitary, territorial, and aggressive. BMRs reside underground, in self-excavated tunnels that they rarely leave. They possess specialized sensory systems for social communication and navigation, which allow them to cope with the harsh environmental conditions underground. This review aims to present the blind mole rat as an ideal, novel neuroethological model for studying aggressive and solitary behaviors. We discuss the BMR's unique behavioral phenotype, particularly in the context of 'anti-social' behaviors, and review the available literature regarding its specialized sensory adaptations to the social and physical habitat. To date, the neurobiology of the blind mole rat remains mostly unknown and holds a promising avenue for scientific discovery. Unraveling the neural basis of the BMR's behavior, in comparison to that of social rodents, can shed important light on the underlying mechanisms of psychiatric disorders in humans, in which similar behaviors are displayed.
... Cross-modal plasticity alters perceptual abilities. For example, several studies have shown that bilateral lid suture or enucleation impairs orientation and direction selectivity of V1 neurons, but enhances the processing of auditory and somatosensory inputs in V1 (Rauschecker et al., 1992;Rauschecker and Kniepert, 1994;Yaka et al., 2000;Izraeli et al., 2002). Similar cross-modal activation patterns after sensory deprivation have been observed in other primary sensory cortices (Goel et al., 2006;Hunt et al., 2006;Lee and Whitt, 2015;Meng et al., 2015). ...
The emergence of cross-modal learning capabilities requires the interaction of neural areas accounting for sensory and cognitive processing. Convergence of multiple sensory inputs is observed in low-level sensory cortices including primary somatosensory (S1), visual (V1), and auditory cortex (A1), as well as in high-level areas such as prefrontal cortex (PFC). Evidence shows that local neural activity and functional connectivity between sensory cortices participate in cross-modal processing. However, little is known about the functional interplay between neural areas underlying sensory and cognitive processing required for cross-modal learning capabilities across life. Here we review our current knowledge on the interdependence of low- and high-level cortices for the emergence of cross-modal processing in rodents. First, we summarize the mechanisms underlying the integration of multiple senses and how cross-modal processing in primary sensory cortices might be modified by top-down modulation of the PFC. Second, we examine the critical factors and developmental mechanisms that account for the interaction between neuronal networks involved in sensory and cognitive processing. Finally, we discuss the applicability and relevance of cross-modal processing for brain-inspired intelligent robotics. An in-depth understanding of the factors and mechanisms controlling cross-modal processing might inspire the refinement of robotic systems by better mimicking neural computations.
... In cats with prolonged binocular deprivation, anterior ectosylvian visual area, which is normally purely visual, becomes largely driven by auditory and somatosensory stimuli (Rauschecker and Korte, 1993). Primary visual cortex can be driven by auditory input, in naturally blind mole rats (Heil et al., 1991) and visually deprived cats (Yaka et al., 2000). Blind humans display activation of visual areas, including V1, during Braille reading (Sadato et al., 1996;Buchel et al., 1998), and comprehending ultra fast speech (Dietrich et al., 2013). ...
... Primary visual cortex can be driven by auditory input, in naturally blind mole rats (Heil et al., 1991) and visually deprived cats (Yaka et al., 2000). V1 can also be recruited by somatosensory cortex. ...
Ocular dominance plasticity (ODP) is a well-characterized example of experience-dependent plasticity. Multiple molecular mechanisms have been implicated in the studying of ODP. We have previously demonstrated a temporal correlation between long-term depression (LTD) and ocular dominance plasticity. It has also been shown that blockade of LTD abolishes ocular dominance shift during the critical period, suggesting that LTD is necessary for ocular dominance plasticity. Here I go on to explore if LTD is sufficient for ocular dominance plasticity by augmenting it in adulthood. By administering D-serine, an NMDAR co-agonist that selectively enhances LTD in adult visual cortex, I am able to enhance ocular dominance plasticity in adulthood, as evidenced by data collected from single-unit recordings. D-serine operates via an LTD-like mechanism as its effect could be abolished by GluR2 3Y peptide, a selective LTD blocker. I therefore argue that LTD plays a key regulatory role in both juvenile and adult ocular dominance plasticity. In addition, D-serine helps facilitate recovery of visual input in long-term monocularly deprived adult mice, suggestive of therapeutic potentials.
In addition, I have examined the functional consequences of monocular deprivation on the rest of primary visual cortex (V1) and cerebral cortex. This is achieved with help of in vivo imaging of intrinsic optic signals and calcium imaging. Within the visual cortex, monocular deprivation decreases the correlation between the contralateral monocular zone with the rest of V1. I have also observed transient changes in global functional connectivity correlating with the duration of lid suture during the critical period, in keeping with cross-modal plasticity. However, this change in functional connectivity is not observed in adulthood, suggesting a sensory period for cross-modal connectivity.
... The loss of visual inputs results in the activation of occipital areas by non-visual stimuli. This has been observed in blind humans (see [1] for Review), as well as in visually deprived mice [2][3][4], rats [5][6][7], hamsters [8], opossum [9,10], blind mole rat [11,12] and cats [13,14]. Both striate and extrastriate areas are activated in the early blind during a non-visual task, whereas only Zeiss Benelux). ...
In blind individuals, visually deprived occipital areas are activated by non-visual stimuli. The extent of this cross-modal activation depends on the age at onset of blindness. Cross-modal inputs have access to several anatomical pathways to reactivate deprived visual areas. Ectopic cross-modal subcortical connections have been shown in anophthalmic animals but not in animals deprived of sight at a later age. Direct and indirect cross-modal cortical connections toward visual areas could also be involved, yet the number of neurons implicated is similar between blind mice and sighted controls. Changes at the axon terminal, dendritic spine or synaptic level are therefore expected upon loss of visual inputs. Here, the proteome of V1, V2M and V2L from P0-enucleated, anophthalmic and sighted mice, sharing a common genetic background (C57BL/6J x ZRDCT/An), was investigated by 2-D DIGE and Western analyses to identify molecular adaptations to enucleation and/or anophthalmia. Few proteins were differentially expressed in enucleated or anophthalmic mice in comparison to sighted mice. The loss of sight affected three pathways: metabolism, synaptic transmission and morphogenesis. Most changes were detected in V1, followed by V2M. Overall, cross-modal adaptations could be promoted in both models of early blindness but not through the exact same molecular strategy. A lower metabolic activity observed in visual areas of blind mice suggests that even if cross-modal inputs reactivate visual areas, they could remain suboptimally processed.
... 541 542 543 544 545 546 547 548 549 550 551 552 553 554 555 556 557 558 559 560 561 562 563 564 565 566 567 568 569 570 571 572 573 574 575 576 577 578 579 580 581 582 583 584 585 586 587 588 589 590 591 592 593 594 595 596 597 598 599 600 The absence of auditory activation of the primary visual cortex in the enucleated mice is surprizing considering that the visual cortex in intact and enucleated C57Bl/6J mice and ZRDCT/An mice receives similar extensive cortical auditory and somatosensory afferents (Charbonneau et al., 2012) as well as indirect corticocortical projections from the auditory cortex (Laramée et al., 2011). Moreover, auditory activation of the visual cortex was reported in enucleated hamsters (Izraeli et al., 2002), rats (Piché et al., 2007), opossum (Kahn and Krubitzer, 2002) and cats (Kahn and Krubitzer, 2002;Yaka et al., 2000Yaka et al., , 1999. In addition, significant somatosensory activity was shown in the visual cortex of enucleated rats (Toldi et al. 1988(Toldi et al. , 1994b and there is evidence for a significant somatosensory input to the dorsal lateral geniculate nucleus of similar extent in enucleated and eyeless mice (Asanuma and Stanfield, 1990). ...
Anophthalmia is a condition in which the eye does not develop from the early embryonic period. Early blindness induces cross-modal plastic modifications in the brain such as auditory and haptic activations of the visual cortex and also leads to a greater solicitation of the somatosensory and auditory cortices. The visual cortex is activated by auditory stimuli in anophthalmic mice and activity is known to alter the growth pattern of the cerebral cortex. The size of the primary visual, auditory and somatosensory cortices and of the corresponding specific sensory thalamic nuclei were measured in intact and enucleated C57Bl/6J mice and in ZRDCT anophthalmic mice (ZRDCT/An) to evaluate the contribution of cross-modal activity on the growth of the cerebral cortex. In addition, the size of these structures were compared in intact, enucleated and anophthalmic fourth generation backcrossed hybrid C57Bl/6J x ZRDCT/An mice to parse out the effects of mouse strains and of the different visual deprivations. The visual cortex was smaller in the anophthalmic ZRDCT/An than in the intact and enucleated C57Bl/6J mice. Also the auditory cortex was larger and the somatosensory cortex smaller in the ZRDCT/An than in the intact and enucleated C57Bl/6J mice. The size differences of sensory cortices between the enucleated and anophthalmic mice were no longer present in the hybrid mice, showing specific genetic differences between C57Bl/6J and ZRDCT mice. The post natal size increase of the visual cortex was less in the enucleated than in the anophthalmic and intact hybrid mice. This suggests differences in the activity of the visual cortex between enucleated and anophthalmic mice and that early in-utero spontaneous neural activity in the visual system contributes to the shaping of functional properties of cortical networks.
... For example, neurons in the primary auditory cortex of congenitally deaf cats and mice are driven by visual or somatosensory stimuli (Hunt et al., 2006;Rebillard et al., 1977). Furthermore, the neonatal loss of visual input, through various experimental manipulations like bilateral eyelid suturing and enucleation or in cases of congenital microphtalmia, leads to cell responsiveness in the visual cortex driven by other sensory modalities, such as audition and touch (Jiang et al., 1994;Rauschecker and Korte, 1993;Toldi et al., 1994Toldi et al., , 1996Yaka et al., 1999Yaka et al., , 2000. Similar results were obtained in hamsters, opossums, rats and mice Izraeli et al., 2002;Piché et al., 2007). ...
... Similar anatomical and electrophysiological findings have been reported in early postnatal and adult enucleated mice and rabbits414243. Enucleation at birth or congenital microphthalmia in kittens induces auditory activation of the visual cortex, principally area V1 [44, 45], which has also been shown in hamsters, opossums, and mice46474849. In very low-sighted mammals like the blind mole rat (Spalax ehrenbergi), the primary visual thalamic relay, the dorsal lateral geniculate nucleus (dLGN), receives direct atypical subcortical projections from the inferior colliculus (IC) which gets its auditory input from the cochlea [50]. ...
Early loss of a given sensory input in mammals causes anatomical and functional modifications in the brain via a process called cross-modal plasticity. In the past four decades, several animal models have illuminated our understanding of the biological substrates involved in cross-modal plasticity. Progressively, studies are now starting to emphasise on cell-specific mechanisms that may be responsible for this intermodal sensory plasticity. Inhibitory interneurons expressing γ-aminobutyric acid (GABA) play an important role in maintaining the appropriate dynamic range of cortical excitation, in critical periods of developmental plasticity, in receptive field refinement, and in treatment of sensory information reaching the cerebral cortex. The diverse interneuron population is very sensitive to sensory experience during development. GABAergic neurons are therefore well suited to act as a gate for mediating cross-modal plasticity. This paper attempts to highlight the links between early sensory deprivation, cortical GABAergic interneuron alterations, and cross-modal plasticity, discuss its implications, and further provide insights for future research in the field.
... Finally, studies of neural plasticity after brain damage or manipulation of sensory experience reveal the extent to which existing circuitry can adapt and compensate for changes in sensory input, providing rapid and functional accommodation of peripheral changes. In many studies it has been shown that deafferented primary sensory cortex is invaded by crossmodal inputs, creating multisensory cortex (Finney, Fine, & Dobkins, 2001;Hunt, Yamoah, & Krubitzer, 2006;Kahn & Krubitzer, 2002;Kujala et al., 1997;Neville, Schmidt, & Kutas, 1983;Piche et al., 2007;Sadato et al., 1996;Yaka, Yinon, & Wollberg, 2000). These findings create an opportunity to study the formation of multisensory cortex and may provide insight into how it has evolved. ...
... These capabilities appear to be correlated with the activation of their striate and extrastriate visual areas by somatosensory (Sadato et al., 1996Sadato et al., , 2004 Cohen et al., 1997) and auditory (Kujala et al., 1995; Gougoux et al., 2004 Gougoux et al., , 2005 Hertrich et al., 2009) stimuli. This non-visual activation of the occipital cortex has also been observed in visually deprived mice (Chabot et al., 2007; Larsen et al., 2009; Van Brussel et al., 2011), rats (Piche et al., 2007), hamsters (Izraeli et al., 2002), opossums (Kahn & Krubitzer, 2002; Karlen et al., 2006), cats (Yaka et al., 1999Yaka et al., , 2000 Sanchez-Vives et al., 2006) and blind mole rats (Heil et al., 1991; Bronchti et al., 2002). These results suggest underlying cross-modal plasticity following the loss of visual inputs in different species. ...
Visual cortical areas are activated by auditory stimuli in blind mice. Direct heteromodal cortical connections have been shown between the primary auditory cortex (A1) and primary visual cortex (V1), and between A1 and secondary visual cortex (V2). Auditory afferents to V2 terminate in close proximity to neurons that project to V1, and potentially constitute an effective indirect pathway between A1 and V1. In this study, we injected a retrograde adenoviral vector that expresses enhanced green fluorescent protein under a synapsin promotor in V1 and biotinylated dextran amine as an anterograde tracer in A1 to determine: (i) whether A1 axon terminals establish synaptic contacts onto the lateral part of V2 (V2L) neurons that project to V1; and (ii) if this indirect cortical pathway is altered by a neonatal enucleation in mice. Complete dendritic arbors of layer V pyramidal neurons were reconstructed in 3D, and putative contacts between pre-synaptic auditory inputs and postsynaptic visual neurons were analysed using a laser-scanning confocal microscope. Putative synaptic contacts were classified as high-confidence and low-confidence contacts, and charted onto dendritic trees. As all reconstructed layer V pyramidal neurons received auditory inputs by these criteria, we conclude that V2L acts as an important relay between A1 and V1. Auditory inputs are preferentially located onto lower branch order dendrites in enucleated mice. Also, V2L neurons are subject to morphological reorganizations in both apical and basal dendrites after the loss of vision. The A1-V2L-V1 pathway could be involved in multisensory processing and contribute to the auditory activation of the occipital cortex in the blind rodent.
... Although cortical plasticity can involve either intramodal or cross-modal plasticity, interference with normal function seems more likely to occur as a result of ectopic, cross-modal invasion of the deafferented structure. For example, loss of visual input can lead to auditory activation of visual cortex (Yaka et al. 2000), and loss of auditory input can lead to cross-modal activation of the understimulated auditory cortex by somatosensory or visual inputs (Allman et al. 2009; Bavelier and Neville 2002; Fine et al. 2005; Finney et al. 2001; Hunt et al. 2006; Lomber et al. 2010; Neville 1990; Neville et al. 1983; Nishimura et al. 2000; Sharma et al. 2007; Sterr et al. 2003). Cross-modal plasticity is known to interfere with the effectiveness of subsequently implanted cochlear prostheses in humans (Lee et al. 2001; see Sharma et al. 2009 for review). ...
http://www.ncbi.nlm.nih.gov/pubmed/21273321
Sensory neocortex is capable of considerable plasticity after sensory deprivation or damage to input pathways, especially early in development. Although plasticity can often be restorative, sometimes novel, ectopic inputs invade the affected cortical area. Invading inputs from other sensory modalities may compromise the original function or even take over, imposing a new function and preventing recovery. Using ferrets whose retinal axons were rerouted into auditory thalamus at birth, we were able to examine the effect of varying the degree of ectopic, cross-modal input on reorganization of developing auditory cortex. In particular, we assayed whether the invading visual inputs and the existing auditory inputs competed for or shared postsynaptic targets and whether the convergence of input modalities would induce multisensory processing. We demonstrate that although the cross-modal inputs create new visual neurons in auditory cortex, some auditory processing remains. The degree of damage to auditory input to the medial geniculate nucleus was directly related to the proportion of visual neurons in auditory cortex, suggesting that the visual and residual auditory inputs compete for cortical territory. Visual neurons were not segregated from auditory neurons but shared target space even on individual target cells, substantially increasing the proportion of multisensory neurons. Thus spatial convergence of visual and auditory input modalities may be sufficient to expand multisensory representations. Together these findings argue that early, patterned visual activity does not drive segregation of visual and auditory afferents and suggest that auditory function might be compromised by converging visual inputs. These results indicate possible ways in which multisensory cortical areas may form during development and evolution. They also suggest that rehabilitative strategies designed to promote recovery of function after sensory deprivation or damage need to take into account that sensory cortex may become substantially more multisensory after alteration of its input during development.
