Presynaptic adhesion molecule PTPσ in the hippocampus regulates postsynaptic NMDA receptor function and behavioral novelty recognition through mechanisms independent of their trans-synaptic binding partners.

By facilitating glutamate and BDNF release, presynaptic NMDA receptors may control information transfer from the dentate gyrus to the CA3 area of the hippocampus.

The essential role of presynaptic NMDA receptors for granule cell GABAergic output elucidates the function of reciprocal spines in recurrent and possibly lateral inhibition of mitral cells during olfactory processsing.

LAR-RPTPs are not essential for synapse formation, but they are important determinants of synapse properties as they contribute to regulate postsynaptic NMDA receptor function.

Individual neurons can adjust the strength of their synapses by using spontaneous calcium influx through NMDA receptors to trigger the release of additional calcium from intracellular stores, which can in turn be used to regulate protein synthesis.

Electrophysiology experiments with genetic and pharmacological manipulations identify a role for astrocyte GluN2C NMDA receptors in maintaining the broad range of presynaptic strengths, which is suggested by numerical simulations to enhance the expression of synaptic plasticity.

A novel form of hippocampal synaptic plasticity is expressed by a change in channel function of GluA3-containing AMPA-receptors.

Optogenetic and electrophysiological experiments show how a behaviorally relevant 'feedback' pathway from auditory cortex controls neural activity in the inferior colliculus, an auditory midbrain region important for processing complex time-varying sounds such as speech.

Random fluctuations in neuronal firing may enable a single brain region, the medial entorhinal cortex, to perform distinct roles in cognition (by generating gamma waves) and spatial navigation (by producing a grid cell map).

An activity-dependent mechanism sculpts subcellular segregation of sensory inputs.