**6. Putative mechanisms mediating crossmodal plasticity**

A review of the literature indicates that a plethora of neuronal mechanisms such as stabilization of transient connections, unmasking of silent synapses, reinforcement/reweighing of subthreshold connections, structural changes such as axonal sprouting and dendritic arborization remodeling, are all putative mechanisms of crossmodal plasticity [59, 61, 108, 109]. Despite the wealth of data, these cellular and molecular mechanisms remain poorly understood. All these neural mechanisms may operate in subcortical, thalamocortical, as well as primary and associative cortical areas.

To offer some insight into the neural mechanisms underpinning crossmodal plasticity, we will mention a limited sample of studies. For example, concerning changes within the primary sensory areas, cross-modal synaptic plasticity is thought to involve LTP/LTD mechanisms [108]. Furthermore, the improved frequency selectivity and intensity discrimination of A1 neurons following visual deprivation in adult mice was attributed to a strengthening of thalamocortical synapses in A1, but not in V1 [107]. In addition, this deprivation was found to potentiate layer 4 to layer 2/3 synapses in A1 [110]. Such a selective effect suggests that the adult brain retains the capability for crossmodal changes, whereas this

**153**

**7. Conclusion**

of early-blind adults [117].

but less consistently in higher order species [61].

*Interplay between Primary Cortical Areas and Crossmodal Plasticity*

capability is absent or very limited within a sensory modality. This view seems to be corroborated by the observation that visual deprivation via lid suture that allows residual visual activity is sufficient to trigger a scaling-up of excitatory synapses in the S1 barrel fields. By contrast, this mild deprivation fails to trigger such a scaling up in V1 which requires a complete loss of visual activity [111]. Furthermore, dark rearing for 1 week in young rats (4-week-old) produces changes in synaptic function in S1 and A1. It was then hypothesized that the scaling-up of V1 synapses might allow recruitment of V1 for processing previously subthreshold inputs carrying tactile or auditory information, while scaling-down of S1 and A1 synapses may sharpen neuronal properties for enhanced perception thus constituting a basis for a sensory compensation [108, 111]. In these somatosensory and auditory cortical areas, decreased amplitudes of AMPA receptor-mediated excitatory transmission in layer 2/3 pyramidal neurons were observed, whereas opposite effects were recorded in the deprived visual cortex [112]. These changes were rapidly reversed after 2 days of light exposure. This study raises the question of whether the crossmodal plasticity induced in somatosensory cortex is due to the altered cortical processing of tactile inputs engaging cortico-cortical pathways or to differences in tactile experience involving thalamocortical projections. In addition to these alterations in the strength of intracortical synapses, visual deprivation (dark exposure for 6–8 days) was found to produce a refinement of intra- and inter-laminar functional circuitry in A1, in the adult mouse. Using *in vitro* whole-cell patch recordings in thalamocortical slices from auditory cortex, it was shown that this period of dark exposure can refine ascending and intralaminar excitatory and inhibitory circuits to layer 2/3 neurons [113], as well as interlaminar excitatory and inhibitory connections from layer 2/3 to layer 4 neurons [114]. Mathematical modeling of the data shows that the observed refinements increase the firing reliability of sound-evoked responses [113]. Visual deprivation in the rat was found to produce an increase in extracellular serotonin levels facilitating synaptic strengthening at layer 4 to layer 2/3 synapses in the barrel cortex [75]. Beyond this local effect, crossmodal plasticity may also engage large-scale modulatory mechanisms mediated, for instance, by the serotoninergic system to orchestrate cortical reorganization in relation with arousal and attention shift from the deprived to the intact sense [115, 116]. It is also worth mentioning that a positive correlation was depicted between behavioral performances in auditory and tactile tasks, and both the myelination of intracortical neurons and gray matter concentration measured in the occipital cortical areas

Even though crossmodal plasticity was demonstrated in early and late deprived subjects, the age of sensory loss onset seems to play a crucial role in the mechanisms involved [118]. In the case of congenitally or early sensory loss, primary cortical areas may retune their functional specificity based on the maintenance, during the developmental period, of intermodal projecting axons that would have otherwise been pruned. By contrast, in the case of late deprivation, crossmodal plasticity may rely on the remodeling and strengthening of pre-existing inputs in the deprived or spared cortical areas. Species-specificity also accounts for crossmodal plasticity, as primary-to primary areas connectivity changes have been show to occur in rodent,

Collectively, the reported studies on crossmodal interplay and plasticity in primary cortical areas after sensory loss challenge the view that multisensory integration and plasticity only exists in high-order cortical areas. Future studies should

*DOI: http://dx.doi.org/10.5772/intechopen.95450*

#### *Interplay between Primary Cortical Areas and Crossmodal Plasticity DOI: http://dx.doi.org/10.5772/intechopen.95450*

*Connectivity and Functional Specialization in the Brain*

while improving sensory guided behavior.

**6. Putative mechanisms mediating crossmodal plasticity**

A review of the literature indicates that a plethora of neuronal mechanisms such as stabilization of transient connections, unmasking of silent synapses, reinforcement/reweighing of subthreshold connections, structural changes such as axonal sprouting and dendritic arborization remodeling, are all putative mechanisms of crossmodal plasticity [59, 61, 108, 109]. Despite the wealth of data, these cellular and molecular mechanisms remain poorly understood. All these neural mechanisms may operate in subcortical, thalamocortical, as well as primary and associative

To offer some insight into the neural mechanisms underpinning crossmodal plasticity, we will mention a limited sample of studies. For example, concerning changes within the primary sensory areas, cross-modal synaptic plasticity is thought to involve LTP/LTD mechanisms [108]. Furthermore, the improved frequency selectivity and intensity discrimination of A1 neurons following visual deprivation in adult mice was attributed to a strengthening of thalamocortical synapses in A1, but not in V1 [107]. In addition, this deprivation was found to potentiate layer 4 to layer 2/3 synapses in A1 [110]. Such a selective effect suggests that the adult brain retains the capability for crossmodal changes, whereas this

sensory modalities.

tactile change detection, while tactile frequency discrimination thresholds tended to be reduced [104]. Beyond noticeable interspecies differences in the potential of crossmodal reorganization [61], the aforementioned studies highlight that deprived auditory sensory cortical areas become re-engaged in the processing of remaining

The crossmodal plasticity concept has been extended by studies demonstrating that the loss of one sense induces substantial alteration in remaining sensory cortical areas leading to experience-dependent refinement of neuronal responses. The so-called compensatory plasticity is conceived as underlying higher than normal perceptual abilities. However, it is notable that the available experimental evidence of compensatory plasticity is scarce compared to that documenting crossmodal plasticity. Nonetheless, changes involving processing of visual signals have been described following somatosensory and auditory deprivation. In adult mice, partial somatosensory deprivation (bilateral removal of macro-whiskers) lasting 12 days induced a massive increase of V1 responses elicited by weak visual stimuli, which was accompanied by a marked improvement of spatial frequency and contrast tuning (40%) of V1 neurons, as revealed by intrinsic signal imaging [105]. It is noteworthy that visual acuity and contrast sensitivity determined in behavioral tasks in individual animals improved by 40% and 60%, respectively, i.e., similarly to what was observed in V1. In addition, auditory deprivation in adult mice induces salient changes in visually evoked responses in V1, with improvement of spatial frequency and contrast tuning [106]. Conversely, visual deprivation (one week of dark exposure) in adult mice leads to improved frequency selectivity as well as increased frequency tuning and intensity discrimination performance of A1 neurons [107]. Collectively, these studies show that compensatory plasticity can develop after short-term deprivation in adult sensory cortices and highlight the fact that deprivation of one sense rapidly refines sensory processing in remaining cortical areas,

**5. Compensatory plasticity in the remaining sensory cortices**

**152**

cortical areas.

capability is absent or very limited within a sensory modality. This view seems to be corroborated by the observation that visual deprivation via lid suture that allows residual visual activity is sufficient to trigger a scaling-up of excitatory synapses in the S1 barrel fields. By contrast, this mild deprivation fails to trigger such a scaling up in V1 which requires a complete loss of visual activity [111]. Furthermore, dark rearing for 1 week in young rats (4-week-old) produces changes in synaptic function in S1 and A1. It was then hypothesized that the scaling-up of V1 synapses might allow recruitment of V1 for processing previously subthreshold inputs carrying tactile or auditory information, while scaling-down of S1 and A1 synapses may sharpen neuronal properties for enhanced perception thus constituting a basis for a sensory compensation [108, 111]. In these somatosensory and auditory cortical areas, decreased amplitudes of AMPA receptor-mediated excitatory transmission in layer 2/3 pyramidal neurons were observed, whereas opposite effects were recorded in the deprived visual cortex [112]. These changes were rapidly reversed after 2 days of light exposure. This study raises the question of whether the crossmodal plasticity induced in somatosensory cortex is due to the altered cortical processing of tactile inputs engaging cortico-cortical pathways or to differences in tactile experience involving thalamocortical projections. In addition to these alterations in the strength of intracortical synapses, visual deprivation (dark exposure for 6–8 days) was found to produce a refinement of intra- and inter-laminar functional circuitry in A1, in the adult mouse. Using *in vitro* whole-cell patch recordings in thalamocortical slices from auditory cortex, it was shown that this period of dark exposure can refine ascending and intralaminar excitatory and inhibitory circuits to layer 2/3 neurons [113], as well as interlaminar excitatory and inhibitory connections from layer 2/3 to layer 4 neurons [114]. Mathematical modeling of the data shows that the observed refinements increase the firing reliability of sound-evoked responses [113]. Visual deprivation in the rat was found to produce an increase in extracellular serotonin levels facilitating synaptic strengthening at layer 4 to layer 2/3 synapses in the barrel cortex [75]. Beyond this local effect, crossmodal plasticity may also engage large-scale modulatory mechanisms mediated, for instance, by the serotoninergic system to orchestrate cortical reorganization in relation with arousal and attention shift from the deprived to the intact sense [115, 116]. It is also worth mentioning that a positive correlation was depicted between behavioral performances in auditory and tactile tasks, and both the myelination of intracortical neurons and gray matter concentration measured in the occipital cortical areas of early-blind adults [117].

Even though crossmodal plasticity was demonstrated in early and late deprived subjects, the age of sensory loss onset seems to play a crucial role in the mechanisms involved [118]. In the case of congenitally or early sensory loss, primary cortical areas may retune their functional specificity based on the maintenance, during the developmental period, of intermodal projecting axons that would have otherwise been pruned. By contrast, in the case of late deprivation, crossmodal plasticity may rely on the remodeling and strengthening of pre-existing inputs in the deprived or spared cortical areas. Species-specificity also accounts for crossmodal plasticity, as primary-to primary areas connectivity changes have been show to occur in rodent, but less consistently in higher order species [61].
