2012-10-23
Glutamatergic neural transmission is involved in both neural plasticity and neurodegeneration. This combination of roles could result in ambivalent effects in which excitotoxic neurodegeneration augments neural plasticity in parallel. Neural plasticity can be induced by exposure-based learning (EBL) that resembles timing properties of long-term potentiation (LTP) protocols (i.e., LTP-like learning). Even though it has not been demonstrated so far in animal models that perceptual effects of such stimulation protocols are mediated by typical LTP mechanisms, it has been shown that exposure-based learning exerts strong effects on cognitive brain functioning and is modulated by glutamatergic neural transmission. We reveal that exposure-based perceptual learning is more efficient in a human model of excitotoxic neurodegeneration than in healthy participants. Pre-manifest Huntington's disease gene mutation carriers showed faster increases in perceptual sensitivities than controls. This in turn changed attentional processing in extrastriate visual areas objectified using electroencephalogram data. The emergence of faster learning correlated positively with genetic disease load. Our results confirm an ambivalent action of increased glutamatergic transmission, implying that the process of excitotoxic neurodegeneration is associated with enhanced perceptual learning, which can be used to improve attentional and behavioral control via the alteration of perceptual sensitivities.
“A thought-provoking new study has found that symptom-free carriers of the neurodegenerative Huntington’s disease present a dramatic two-fold acceleration in perceptual learning.” (Cardoso-Leite et al., 2012).
“These results are spectacular in the face of the massive literature showing subtle cognitive impairments in pre-HD patients.” (Cardoso-Leite et al., 2012).
“Adapting the exposure-based learning procedure pioneered in the present study to animal models in future research could be a productive way to characterize the respective mechanisms subtending enhanced learning and excitotoxicity in Huntington’s disease.” (Cardoso-Leite et al., 2012).
Glutamatergic neural transmission is involved in both neural plasticity and neurodegeneration. This combination of roles could result in ambivalent effects in which excitotoxic neurodegeneration augments neural plasticity in parallel. Neural plasticity can be induced by exposure-based learning (EBL) that resembles timing properties of long-term potentiation (LTP) protocols (i.e., LTP-like learning). Even though it has not been demonstrated so far in animal models that perceptual effects of such stimulation protocols are mediated by typical LTP mechanisms, it has been shown that exposure-based learning exerts strong effects on cognitive brain functioning and is modulated by glutamatergic neural transmission. We reveal that exposure-based perceptual learning is more efficient in a human model of excitotoxic neurodegeneration than in healthy participants. Pre-manifest Huntington's disease gene mutation carriers showed faster increases in perceptual sensitivities than controls. This in turn changed attentional processing in extrastriate visual areas objectified using electroencephalogram data. The emergence of faster learning correlated positively with genetic disease load. Our results confirm an ambivalent action of increased glutamatergic transmission, implying that the process of excitotoxic neurodegeneration is associated with enhanced perceptual learning, which can be used to improve attentional and behavioral control via the alteration of perceptual sensitivities.
“A thought-provoking new study has found that symptom-free carriers of the neurodegenerative Huntington’s disease present a dramatic two-fold acceleration in perceptual learning.” (Cardoso-Leite et al., 2012).
“These results are spectacular in the face of the massive literature showing subtle cognitive impairments in pre-HD patients.” (Cardoso-Leite et al., 2012).
“Adapting the exposure-based learning procedure pioneered in the present study to animal models in future research could be a productive way to characterize the respective mechanisms subtending enhanced learning and excitotoxicity in Huntington’s disease.” (Cardoso-Leite et al., 2012).
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Last update: Oct 04, 2023
