Scientific Understanding of Consciousness
Dendritic Branches— a Basic Unit for Synaptic Plasticity and Information Storage
Nature 520, 180–185 (09 April 2015)
Branch-specific dendritic Ca2+ spikes cause persistent synaptic plasticity
Skirball Institute, Department of Neuroscience and Physiology, New York University School of Medicine, New York, New York 10016, USA
The brain has an extraordinary capacity for memory storage, but how it stores new information without disrupting previously acquired memories remains unknown. Here we show that different motor learning tasks induce dendritic Ca2+ spikes on different apical tuft branches of individual layer V pyramidal neurons in the mouse motor cortex. These task-related, branch-specific Ca2+ spikes cause long-lasting potentiation of postsynaptic dendritic spines active at the time of spike generation. When somatostatin-expressing interneurons are inactivated, different motor tasks frequently induce Ca2+ spikes on the same branches. On those branches, spines potentiated during one task are depotentiated when they are active seconds before Ca2+ spikes induced by another task. Concomitantly, increased neuronal activity and performance improvement after learning one task are disrupted when another task is learned. These findings indicate that dendritic-branch-specific generation of Ca2+ spikes is crucial for establishing long-lasting synaptic plasticity, thereby facilitating information storage associated with different learning experiences.
One remarkable feature of the brain is to encode and store new information continuously without disrupting previously acquired memories. It is believed that experience-dependent changes in synaptic strength are crucial for information storage in the brain. However, it remains unclear whether and how synaptic plasticity induced by past experiences are maintained in the face of new experiences. To address this question, we examined the generation of dendritic Ca2+ spikes and their effect on synaptic plasticity in the primary motor cortex of mice performing different motor learning tasks.
Dendritic Ca2+ spikes trigger large Ca2+ influx into dendrites, and have been linked to activity-dependent increases or decreases of synaptic strength in brain slices. Recent studies have shown that NMDA (N-methyl-d-aspartate)-receptor-dependent dendritic Ca2+ spikes are generated in several brain regions and are involved in the integration and amplification of synaptic inputs. The function of Ca2+ spikes in regulating experience-dependent synaptic plasticity in the living brain remains undetermined. Here we show that different motor tasks induce dendritic Ca2+ spikes on different apical tuft branches of individual layer V (L5) pyramidal neurons in the mouse motor cortex. This spatial segregation of Ca2+ spikes is crucial for the induction and maintenance of synaptic potentiation related to different learning tasks. These findings underscore the important role of branch-specific dendritic Ca2+ spikes (BSDCS) in storing new information without disrupting existing memories in the brain.
To investigate the potential role of dendritic Ca2+ spikes in learning-dependent synaptic plasticity, we first examined Ca2+ spike generation in the motor cortex of mice using a treadmill training paradigm.
By performing Ca2+ imaging in the motor cortex of awake, behaving mice, we show that different motor learning experiences trigger NMDA-receptor-dependent Ca2+ spikes in non-overlapping apical tuft branches of L5 pyramidal neurons. This spatial segregation of Ca2+ spikes is crucial for the induction and maintenance of synaptic plasticity when several tasks are learned. These findings indicate that dendritic-branch-specific generation of Ca2+ spikes is a fundamental mechanism used in the brain to store different information with little or no interference.
Our studies in the motor cortex are consistent with a view that individual dendritic branches serve as a basic unit for synaptic plasticity and information storage. Recent studies have shown that NMDA-receptor-dependent Ca2+ spikes are involved in input integration and amplification in sensory cortices and hippocampus. As in the motor cortex, NMDA-receptor-dependent Ca2+ spikes in these brain regions may also have an important role in experience-dependent synaptic plasticity. Unlike the motor cortex, however, Ca2+ spikes in the barrel cortex occur in all apical tuft branches of an individual L5 pyramidal neuron. It would be interesting to investigate whether the lack of branch-specific generation of Ca2+ spikes in sensory cortices might compromise the maintenance of experience-dependent synaptic plasticity during sensory processing and perceptual learning. Furthermore, in addition to SST-expressing interneurons, the generation of branch-specific Ca2+ spikes and their effect on synaptic plasticity are probably regulated by other types of inhibitory neurons, ion channels and behavioural context. Future studies are needed to investigate these issues to understand better how information is encoded and stored in the brain.
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