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.
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.
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.
Molecular labeling, electrophysiology and calcium imaging have revealed a novel switching of neurotransmitter at the frog neuromuscular junction where motoneurons transiently release glutamate before acetylcholine at synapses on developing hindlimb muscles at the onset of metamorphosis.
Single synaptic vesicle imaging shows that kinetically distinct endocytic pathways are differentially regulated by calcium and temperature, and influence the fidelity of synaptic vesicle protein retrieval.
Activation of the subthalamic nucleus (STN) pauses or disrupts behavior, while STN inhibition reduces the disruptive effects of surprise, indicating that STN activation is both sufficient and necessary for behavioral inhibition.