In mammals, the vesicular glutamate transporter 1 acquired a proline-rich sequence that negatively regulates the spontaneous release of glutamate by reducing the exchange of synaptic vesicles along the axon.

Vglut2-based glutamatergic signaling in central noradrenergic neurons is dispensable for baseline breathing and hypercapnic, hypoxic chemosensory reflexes, which challenges the current understanding of central noradrenergic neurons in breathing control.

Whole endosome recording shows that chloride interacts with vesicular glutamate transporters as both allosteric activator and permeant ion, and although the mode of permeation differs, chloride and glutamate use a related conduction pathway.

Glutamate cotransmission from a subset of cortical GABAergic interneurons can promote network hyperexcitability.

In central synapses, the mobility and supply of synaptic vesicles are determined by two independent biological factors: the morphological and structural organization of nerve terminals and the molecular signature of vesicles.

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

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.

Neurite arbors of VGluT3-expressing amacrine cells (VG3-ACs) process visual information locally uniformly detecting object motion while varying in contrast preferences; and in spite of extensive overlap between arbors of neighboring cells population activity in the VG3-AC plexus encodes stimulus positions with subcellular precision.

Placing the PACAP/PAC1 signaling within glutamate/GABA cell type and subregional contexts in mouse brain reveals its conspicuous role for sensorimotor circuit interaction through modulating neuronal plasticity.

Glutamatergic brainstem neurons drive motor and respiratory deficits, and GABAergic basal ganglia neurons cause hypothermia and fatal epileptic events, in a model of mitochondrial disease.