Sensory experience induces rapid molecular and structural changes at the synapse that have long-lasting effects on neuronal networks. These processes occur in the central as well as in the peripheral nervous system and appear to be highly conserved among species. Memory formation and consolidation is probably one of the best studied examples of long-term circuit change that provide critical advantages for the animal’s survival. In the past decade several highly conserved developmental molecules (Notch, Reelin, Wnt, EphB) with essential roles in morphogenesis have been shown to be regulated by sensory stimuli and are involved in activity dependent changes at the synapse influencing learning and memory. Interestingly these molecules also appear to be profoundly affected in neurologic disorders such as Alzheimer’s disease, Down syndrome, stroke and spinal cord injury.
Understanding novel combinatorial arrangements of these signaling pathways in the setting of the mature brain will allow the development of efficient therapeutic strategies by potentiating brain plasticity and its regenerative capacity.
This Research Topic in Frontiers in Cellular Neuroscience will focus on new ideas in the study of developmental molecules that contribute to the strengthening and weakening of neuronal circuits. This topic will include but is not limited to studies using genetic manipulation of neural plasticity in animal model systems that are relevant to neurologic or psychiatric disorders, structural and functional defects in the adult organism, molecular and cellular mechanisms underlying plastic changes and innovative techniques to detect bio-molecular changes in the brain following experience.
Researchers are encouraged to submit original as well as review articles directed towards showcasing current efforts in the field. We hope this topic with facilitate communication and collaborations between researchers and will result in advancing our understanding of activity-dependent mechanisms underlying neuronal network based disorders.
Sensory experience induces rapid molecular and structural changes at the synapse that have long-lasting effects on neuronal networks. These processes occur in the central as well as in the peripheral nervous system and appear to be highly conserved among species. Memory formation and consolidation is probably one of the best studied examples of long-term circuit change that provide critical advantages for the animal’s survival. In the past decade several highly conserved developmental molecules (Notch, Reelin, Wnt, EphB) with essential roles in morphogenesis have been shown to be regulated by sensory stimuli and are involved in activity dependent changes at the synapse influencing learning and memory. Interestingly these molecules also appear to be profoundly affected in neurologic disorders such as Alzheimer’s disease, Down syndrome, stroke and spinal cord injury.
Understanding novel combinatorial arrangements of these signaling pathways in the setting of the mature brain will allow the development of efficient therapeutic strategies by potentiating brain plasticity and its regenerative capacity.
This Research Topic in Frontiers in Cellular Neuroscience will focus on new ideas in the study of developmental molecules that contribute to the strengthening and weakening of neuronal circuits. This topic will include but is not limited to studies using genetic manipulation of neural plasticity in animal model systems that are relevant to neurologic or psychiatric disorders, structural and functional defects in the adult organism, molecular and cellular mechanisms underlying plastic changes and innovative techniques to detect bio-molecular changes in the brain following experience.
Researchers are encouraged to submit original as well as review articles directed towards showcasing current efforts in the field. We hope this topic with facilitate communication and collaborations between researchers and will result in advancing our understanding of activity-dependent mechanisms underlying neuronal network based disorders.
