Electrophysiological and optical analysis of neurotransmitter release at central synapses reveals that glutamate signalling is not required for the long-term potentiation (LTP) of presynaptic function, and instead only promotes presynaptic long-term depression (LTD).
Building on previous work (Huang et al., 2016), we show that translational control by p-eIF2α is a defense mechanism that prevents persistent cocaine-induced synaptic synaptic potentiation underlying compulsive drug seeking.
Three-dimensional electron microscopy (3DEM) demonstrates the dependence on presynaptic mitochondria for vesicle mobilization as dendritic spines are silently added at P15 or synapses are silently enlarged in adults after long-term potentiation.
To establish a trade-off between the speed and accuracy of a decision, neurons in lateral intraparietal cortex combine evidence bearing on the decision with a signal that incorporates the cost of time into the decision-making process.
Oligomeric Amyloid-β and Tau, two proteins involved in Alzheimer's disease pathogenesis, require Amyloid Precursor Protein to enter neurons and exert their detrimental effect on synaptic plasticity and memory.