At distal synapses onto hippocampal CA1 pyramidal neurons, synaptic plasticity is dependent on dendritically initiated sodium spikes, thus establishing a new role for voltage-gated sodium channels in the dendrites that may have important implications for how learning rules are implemented.

Dopaminergic cells uniquely receive input from a roughly equal mixture of synapses on dendritic spines and synapses formed directly on dendrites.

In the hippocampus, dendritic Na ⁺ spikes are required for signals from the entorhinal cortex to drive action potentials in CA2-but not CA1 or CA3-pyramidal neurons.

Spines with multiple excitatory contacts are potential sites for competition between thalamic and cortical axons, which is regulated by the astrocytes through the secreted synaptogenic protein hevin.

A novel mechanism of local plasticity in the distal dendrites of hippocampal granule cells.

Extrasynaptic GABA_A receptors that emerge at puberty trigger adolescent synaptic pruning; pruning is prevented and cognition is impaired if the receptors are absent.

Neurons use a non-canonical secretory network to deliver select proteins to postsynaptic sites in dendrites.

In mouse models of Huntington's disease, striatal spiny projection neurons up-regulate dendritic potassium channels, which impairs their normal function, but a zinc finger gene therapy can reverse this deficit.

A protein called RNF10 relays messages from synapses to neuron cell nuclei, and is responsible for long-lasting modifications of dendritic spines as observed after activation of synaptic glutamate receptors.

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.