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A new study shows that the transient manipulation of neural activity can sometimes have 'off-target' effects, making it challenging to determine the specific neural circuit that generates a particular behaviour.
The behavioural phenotype in a mouse model ofMECP2(methyl-CpG-binding protein 2) duplication syndrome can be rescued in adulthood by normalizing MeCP2 levels.
Parkinson disease-associated mutations in the gene encoding vacuolar protein sorting-associated protein 35 increase the turnover of dynamin-like protein 1 in the mitochondrial membrane of neurons, leading to mitochondrial fission and neuronal death.
In mice, an early ablation of myelinating oligodendrocytes can trigger a secondary, CD4+T cell-associated demyelination 30 weeks later, suggesting a possible mechanism for the onset of demyelinating diseases such as multiple sclerosis.
Training involving repeated long inter-trial intervals — spaced training — leads to more robust memory formation for many types of learning than does training involving short or no intervals. This Review examines the learning theories and the molecular and cellular mechanisms that may account for the effectiveness of spaced training.
CA2 has several characteristics that distinguishes it from CA1 and CA3. In this Review, Dudek and colleagues discuss an updated definition of the CA2 boundaries, and provide an overview of the unique synaptic properties and behavioural functions of this region.
Autoantibodies against neuromuscular junction targets are a well-established cause of myasthenic syndromes, and autoantibodies against CNS targets have also been associated with disease. In this Review, Vincent and colleagues discuss key examples of such autoantibodies, and the mechanisms by which they lead to neurological dysfunction.
Synaptic vesicle exocytosis is tightly regulated by a number of synaptic proteins, including complexin; however, several alternative models of complexin function have been presented. Trimbuch and Rosenmund propose that a better understanding of the properties of different domains of complexin may help to shed light on its function.
Impaired interneuron function is widely believed to contribute to schizophrenia pathophysiology. Hardingham and Do describe converging evidence suggesting that NMDA receptor (NMDAR) hypofunction and oxidative stress during development contribute to interneuron dysfunction and schizophrenia pathophysiology.
