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Synaptic plasticity is the biological process by which specific patterns of synaptic activity result in changes in synaptic strength and is thought to contribute to learning and memory. Both pre-synaptic and post-synaptic mechanisms can contribute to the expression of synaptic plasticity.
Excitatory synapses on somatostatin sensory neurons in the cortex are not fully characterised. Here the authors report that visual cortex somatostatin neurons are regulated by sensory experience by utilizing two distinct types of excitatory synapses.
Radulescu et al. show that homeostatic mechanisms that reduce cortical activity following overstimulation are dysregulated later in life, such that overstimulation results in synaptic strengthening, elevated activity and cognitive impairment.
In glioma, malignant synapses hijack mechanisms of synaptic plasticity to increase glutamate-dependent currents in tumour cells and the formation of neuron–glioma synapses, thereby promoting tumour proliferation and progression.
A study reports that in the mouse hippocampus, the induction of long-term potentiation is dependent on the structural functions of CaMKII and not its enzymatic activity.
In a recent study a phenomenological model was used to study the effects of activity-dependent myelination (ADM) on network activity and information transmission in the brain. The model explores how the conduction velocity of an axon — and thus the overall transmission delay — varies as a function of neural activity.
Dynamin mediates vesicle scission during endocytosis, and here is shown to exist with syndapin 1 in biomolecular condensates at the endocytic zone that enable its participation in ultrafast endocytosis.
