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Spine plasticity is the biological process by which neuronal activity leads to short- or long-term changes in the morphology, appearance or disappearance of dendritic spines – the specialized protrusions on a neuron’s dendrites that are the sites of excitatory synaptic input. Spine plasticity has been implicated in mediating synaptic plasticity.
The role of serotonin in prefrontal cortex development remains unexplored. Here, authors show that serotonin regulates maturation and stabilization of prefrontal excitatory synapses.
Benzodiazepines, used to treat anxiety and sleep disorders, may cause cognitive impairment. Shi et al. demonstrate that this is caused by interaction with the mitochondrial protein TSPO, which drives microglia to excessively remove synapses.
Synaptic dysfunction is a key feature of Alzheimer disease. In this Review, Padmanabhan, Kneynsberg and Götz examine insights provided by super-resolution microscopy into synaptic architecture and organization in Alzheimer disease, focusing on amyloid-β and tau, thought to be two key players in the pathophysiology of the disease.
Sleep plays an important role in learning and memory. Here the authors show that experience dependent elimination of spines is attenuated by REM sleep deprivation.
The binding of psychedelics to the BDNF receptor TrkB boosts plasticity in cultured neurons and underlies the antidepressant-like effects of these compounds in mice.
Certain lasting antidepressant effects of ketamine in a mouse model of depression depend on the restoration of dendritic spines in the prefrontal cortex.
