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.

Caenorhabditis elegans has bona fide dendritic spines, suggesting that the advantages of small model organisms, such as genetic manipulations and live-cell imaging, can be exploited to study dendritic spines.

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.

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.

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

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.