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

Electrophysiological study in human brain slices reveals that short-term synaptic plasticity from presynaptic pyramidal neuron to postsynaptic interneuron connections are target-cell specific based on their subclass interneuron identity.

Local elimination of acetylcholine synthesis in habenular neurons demonstrates a key role for vesicular synergy and neurotransmitter co-release in nicotine dependence.

Subtypes of dendrite-targeting somatostatin cells segregate into separate networks by specifically connecting with neurons in different layers, forming circuits that could independently control different input pathways to the neocortex.

In a fast brainstem relay controlling hearing sensitivity, descending synaptic control from midbrain provides the dominant source of excitation, due to a distinct form of synaptic plasticity.

In cerebellar interneurons, somatodendritic subthreshold synaptic activity travels down the axon and augments AP-dependent GABA release by a modulation of the intermediate states of voltage-dependent Ca⁺⁺ channels in the presynaptic boutons.

Genetic and electrophysiological experiments define how homeostatic signaling stabilizes both the gain and short-term dynamic properties of neurotransmitter release, ensuring that synaptic information transfer remains robust to external perturbation.

The analytic theory establishes the general principles of synaptic transmission, enables extraction of microscopic parameters of synaptic fusion machinery from experiments, and links molecular constituents to synaptic function.

Storage of long-term memory in Aplysia does not require stable synapses.

The probability of occupancy of individual synaptic release sites at rest sets an upper limit to synaptic output when increasing action potential related calcium entry.