Transcriptional expression changes during compensatory plasticity in the terminal ganglion of the adult cricket Gryllus bimaculatus

Background Damage to the adult central nervous system often leads to long-term disruptions in function due to the limited capacity for neurological recovery. The central nervous system of the Mediterranean field cricket, Gryllus bimaculatus, shows an unusual capacity for compensatory plasticity, most obviously in the auditory system and the cercal escape system. In both systems, unilateral sensory disruption leads the central circuitry to compensate by forming and/or strengthening connections with the contralateral sensory organ. While this compensatory plasticity in the auditory system relies on robust dendritic sprouting and novel synapse formation, the compensatory plasticity in the cercal escape circuitry shows little obvious dendritic sprouting and instead may rely on shifts in excitatory and inhibitory synaptic strength. Results In order to better understand what types of molecular pathways might underlie this compensatory shift in the cercal system, we used a multiple k-mer approach to assemble a terminal ganglion transcriptome that included ganglia collected one, three, and 7 days after unilateral cercal ablation in adult, male animals. We performed differential expression analysis using EdgeR and DESeq2 and examined Gene Ontologies to identify candidates potentially involved in this plasticity. Enriched GO terms included those related to the ubiquitin-proteosome protein degradation system, chromatin-mediated transcriptional pathways, and the GTPase-related signaling system. Conclusion Further exploration of these GO terms will provide a clearer picture of the processes involved in compensatory recovery of the cercal escape system in the cricket and can be compared and contrasted with the distinct pathways that have been identified upon deafferentation of the auditory system in this same animal.

Optimal plasticity for memory maintenance during ongoing synaptic change

Synaptic connections in many brain circuits fluctuate, exhibiting substantial turnover and remodelling over hours to days. Surprisingly, experiments show that most of this flux in connectivity persists in the absence of learning or known plasticity signals. How can neural circuits retain learned information despite a large proportion of ongoing and potentially disruptive synaptic changes? We address this question from first principles by analysing how much compensatory plasticity would be required to optimally counteract ongoing fluctuations, regardless of whether fluctuations are random or systematic. Remarkably, we find that the answer is largely independent of plasticity mechanisms and circuit architectures: compensatory plasticity should be at most equal in magnitude to fluctuations, and often less, in direct agreement with previously unexplained experimental observations. Moreover, our analysis shows that a high proportion of learning-independent synaptic change is consistent with plasticity mechanisms that accurately compute error gradients.

Cortical and Subcortical Circuits for Cross-Modal Plasticity Induced by Loss of Vision

Cortical areas are highly interconnected both via cortical and subcortical pathways, and primary sensory cortices are not isolated from this general structure. In primary sensory cortical areas, these pre-existing functional connections serve to provide contextual information for sensory processing and can mediate adaptation when a sensory modality is lost. Cross-modal plasticity in broad terms refers to widespread plasticity across the brain in response to losing a sensory modality, and largely involves two distinct changes: cross-modal recruitment and compensatory plasticity. The former involves recruitment of the deprived sensory area, which includes the deprived primary sensory cortex, for processing the remaining senses. Compensatory plasticity refers to plasticity in the remaining sensory areas, including the spared primary sensory cortices, to enhance the processing of its own sensory inputs. Here, we will summarize potential cellular plasticity mechanisms involved in cross-modal recruitment and compensatory plasticity, and review cortical and subcortical circuits to the primary sensory cortices which can mediate cross-modal plasticity upon loss of vision.

Compensatory Plasticity in the Deaf Brain: Effects on Perception of Music

When one sense is unavailable, sensory responsibilities shift and processing of the remaining modalities becomes enhanced to compensate for missing information. This shift, referred to as compensatory plasticity, results in a unique sensory experience for individuals who are deaf, including the manner in which music is perceived. This paper evaluates the neural, behavioural and cognitive evidence for compensatory plasticity following auditory deprivation and considers how this manifests in a unique experience of music that emphasizes visual and vibrotactile modalities.

Compensatory Plasticity in the Deaf Brain: Effects on Perception of Music

When one sense is unavailable, sensory responsibilities shift and processing of the remaining modalities becomes enhanced to compensate for missing information. This shift, referred to as compensatory plasticity, results in a unique sensory experience for individuals who are deaf, including the manner in which music is perceived. This paper evaluates the neural, behavioural and cognitive evidence for compensatory plasticity following auditory deprivation and considers how this manifests in a unique experience of music that emphasizes visual and vibrotactile modalities.

Electromagnetic field and TGF-β enhance the compensatory plasticity after sensory nerve injury in cockroach Periplaneta americana

Recovery of function after sensory nerves injury involves compensatory plasticity, which can be observed in invertebrates. The aim of the study was the evaluation of compensatory plasticity in the cockroach (Periplaneta americana) nervous system after the sensory nerve injury and assessment of the effect of electromagnetic field exposure (EMF, 50 Hz, 7 mT) and TGF-β on this process. The bioelectrical activities of nerves (pre-and post-synaptic parts of the sensory path) were recorded under wind stimulation of the cerci before and after right cercus ablation and in insects exposed to EMF and treated with TGF-β. Ablation of the right cercus caused an increase of activity of the left presynaptic part of the sensory path. Exposure to EMF and TGF-β induced an increase of activity in both parts of the sensory path. This suggests strengthening effects of EMF and TGF-β on the insect ability to recognize stimuli after one cercus ablation. Data from locomotor tests proved electrophysiological results. The takeover of the function of one cercus by the second one proves the existence of compensatory plasticity in the cockroach escape system, which makes it a good model for studying compensatory plasticity. We recommend further research on EMF as a useful factor in neurorehabilitation.

Transcriptional expression changes during compensatory plasticity in the central nervous system of the adult cricket

Damage to the adult central nervous system often leads to long-term disruptions in function due to the limited capacity for neurological recovery. The central nervous system of the Mediterranean field cricket, Gryllus bimaculatus, shows an unusual capacity for compensatory plasticity, most obviously in the auditory system and the cercal escape system. In both systems, unilateral sensory disruption leads the central circuitry to compensate by forming and/or strengthening connections with the contralateral sensory organ. While this compensatory plasticity relies on robust dendritic sprouting and novel synapse formation in the auditory system, the compensatory plasticity in the cercal escape circuitry shows little obvious dendritic sprouting and instead may rely on shifts in excitatory and inhibitory synaptic strength. In order to better understand what types of molecular pathways might underlie this compensatory shift in the cercal system, we used a multiple k-mer approach to assemble a terminal ganglion transcriptome that included ganglia collected one, three, and seven days after unilateral cercal ablation in adult, male animals. We performed differential expression analysis using EdgeR and DESeq2 and examined Gene Ontologies to identify candidates potentially involved in this plasticity. Enriched GO terms included those related to the ubiquitin-proteosome protein degradation system, chromatin-mediated transcriptional pathways, and the GTPase-related signaling system. Further exploration of these GO terms will provide a clearer picture of the processes involved in compensatory recovery of the cercal escape system in the cricket and can be compared and contrasted with the distinct pathways that have been identified upon deafferentation of the auditory system in this same animal.

Interplay between Primary Cortical Areas and Crossmodal Plasticity

Perceptual representations are built through multisensory interactions underpinned by dense anatomical and functional neural networks that interconnect primary and associative cortical areas. There is compelling evidence that primary sensory cortical areas do not work in segregation, but play a role in early processes of multisensory integration. In this chapter, we firstly review previous and recent literature showing how multimodal interactions between primary cortices may contribute to refining perceptual representations. Secondly, we discuss findings providing evidence that, following peripheral damage to a sensory system, multimodal integration may promote sensory substitution in deprived cortical areas and favor compensatory plasticity in the spared sensory cortices.

Electromagnetic field and TGF-β enhance the compensatory plasticity after sensory nerve injury in cockroach Periplaneta americana

Recovery of function after sensory nerves injury involves compensatory plasticity, which can be observed in invertebrates. The aim of the study was the evaluation of compensatory plasticity in the cockroach (Periplaneta americana) nervous system after the sensory nerve injury and assessment of the effect of electromagnetic field exposure (EMF, 50 Hz, 7 mT) and TGF-β on this process. The bioelectrical activities of nerves (pre-and post-synaptic parts of sensory path) were recorded under wind stimulation of the cerci before and after right cercus ablation and in insects exposed to EMF and treated with TGF-β. Ablation of the right cercus caused an increase of activity of the left presynaptic part of the sensory path. Exposure to EMF and TGF-β induced an increase of activity in both parts of sensory path. This suggests strengthening effects of EMF and TGF-β on the insect ability to recognize stimuli after one cercus ablation. Data from locomotor tests proved electrophysiological results. The takeover of the function of one cercus by the second one proves the existence of compensatory plasticity in the cockroach escape system, which makes it a good model for studying compensatory plasticity. We recommend further research on EMF as a useful factor in neurorehabilitation.