Tag: homeostatic synaptic plasticity

Mechanisms that connect autism with homeostatic synaptic plasticity

It is well established that homeostatic signaling systems interface with the mechanisms of developmental and learning-related plasticity to achieve stable yet flexible neural function and animal behavior. Experimental evidence from organisms as diverse as Drosophila, mice and humans demonstrates that homeostatic signaling systems stabilize neural function through the modulation of synaptic transmission, ion channel abundance and neurotransmitter receptor trafficking. At a fundamental level, if homeostatic plasticity is compromised, then the nervous system will be less robust to perturbation. As such, it is widely speculated that defective or maladaptive homeostatic plasticity will be relevant to the cause or severity of autism. However, clear molecular or genetic links between autism and homeostatic plasticity have yet to be defined in any organism.

Exploring a genetic intersection of autism and homeostatic synaptic plasticity

It is well established that homeostatic signaling systems interface with the mechanisms of developmental and learning-related plasticity to achieve stable yet flexible neural function and animal behavior. Experimental evidence from organisms as diverse as Drosophila, mice and humans demonstrates that homeostatic signaling systems stabilize neural function through the modulation of synaptic transmission, ion channel abundance and neurotransmitter receptor trafficking[ref]Davis G.W. Annu. Rev. Neurosci. 29, 307-323 (2006) PubMed[/ref], [ref]Davis G.W. Neuron 80, 718-728 (2013) PubMed[/ref], [ref]Marder E. Proc. Natl. Acad. Sci. USA 108 Suppl 3, 15542-15548 (2011) PubMed[/ref], [ref]Turrigiano G. Annu. Rev. Neurosci. 34, 89-103 (2011) PubMed[/ref]. At a fundamental level, if homeostatic plasticity is compromised, the nervous system is likely to be more sensitive to perturbations. Graeme Davis and his colleagues speculate that impaired homeostatic plasticity could contribute to autism by making the developing nervous system vulnerable to perturbations of any origin, including genetic, environmental or immunological stresses.

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