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Significance How neuronal circuits maintain stable activity despite continuous environmental changes is one of the most intriguing questions in neuroscience. Previous studies proposed that deficits in homeostatic control systems may underlie common neurological symptoms in a variety of brain disorders. However, the key regulatory molecules that control homeostasis of central neural circuits remain obscure. We show here that basal activity of GABA B receptors is required for firing rate homeostasis in hippocampal networks. We identified the principal mechanisms by which GABA B receptors control homeostatic augmentation of synaptic strength to chronic neuronal silencing. We propose that deficits in GABA B receptor signaling, associated with epilepsy and psychiatric disorders, may lead to aberrant brain activity by erasing homeostatic plasticity.
Neurons, Mice, Mice, Inbred BALB C, Receptors, GABA-B, Animals, Homeostasis, Evoked Potentials, Hippocampus, Cells, Cultured
Neurons, Mice, Mice, Inbred BALB C, Receptors, GABA-B, Animals, Homeostasis, Evoked Potentials, Hippocampus, Cells, Cultured
citations This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | 50 | |
popularity This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network. | Top 10% | |
influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | Top 10% | |
impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network. | Top 10% |