Computational model reveals how the fast exchange of neurotransmitter receptors between synapses induces a competition leading to a transient form of heterosynaptic plasticity and shaping the induction of homosynaptic plasticity.
Inhibition enhances the spatial specificity of high calcium influx for cooperatively stimulated synapses, suggesting that inhibitory inputs may regulate both synapse-specific and heterosynaptic plasticity to support learning and memory.
The secretory and recycling components of neuronal dendrites, smooth endoplasmic reticulum and endosomes, were discovered to support synaptogenesis underlying a cellular mechanism of learning and memory in the developing brain.
Combination of in vitro and in vivo approaches reveal how learning suppresses the microRNA system to trigger de novo synthesis of plasticity proteins, a missing link in the current model of microRNA-mediated translation in persistent synaptic plasticity and memory.
Skeletal muscle cells constantly monitor their own activity and that of their partner neuron at synapses, enabling them to provide the neuron with feedback regarding neurotransmitter release.
The learning rate for novel spatial environments in model networks of place cells is determined by the product of the window for plasticity and the auto-correlation of place-cell activity.
Biologically plausible changes in the excitabilities of single neurons may suffice to selectively modulate sequential network dynamics, without modifying of recurrent connectivity.
Rats exposed to a single stressful event experience days-long constitutive activation of the kappa opioid receptor at inhibitory synapses in part of the brain’s reward system, which increases their drug-seeking behavior.
A single astrocyte can decode neuronal activity and, consequently, release distinct gliotransmitters that differentially regulate neurotransmission at single hippocampal synapses.
