Related Experiment Video
Updated: Aug 24, 2026

Recording Synaptic Plasticity in Acute Hippocampal Slices Maintained in a Small-volume Recycling-, Perfusion-, and Submersion-type Chamber System
Published on: January 1, 2018
Presynaptic disruption of transmitter release by lead
1Department of Cellular and Molecular Physiology, College of Medicine, University of Cincinnati, P.O. Box 670576, Cincinnati, OH 45267-0576, USA. j.suszkiw@uc.edu
Abstract:
Low concentrations of inorganic lead ions (Pb2+) disrupt transmitter release by causing aberrant augmentation of spontaneous and suppression of evoked release. These effects result from high affinity interactions of Pb2+ with the voltage-gated calcium channels (VGCC) as well as Ca2+ binding proteins which regulate the synaptic vesicle mobilization, docking, and exocytosis processes. Augmentation of spontaneous release may involve stimulation of vesicle mobilization consequent to Pb2+ activation of CaMKII-dependent phosphorylation of synapsin I and/or stimulation of asynchronous exocytosis via direct Pb2+ activation of the putative exocytotic Ca2+-sensor protein synaptotagmin I. In addition, synergistic stimulation of PLC and DAG/Pb2+-dependent activation of PKC may enhance the secretagogue effects of Pb2+ by increasing metal sensitivity of exocytosis and/or modulating calcium channel activity. In contrast to intracellularly-mediated actions of Pb2+ resulting in augmentation of spontaneous release, the inhibition of evoked transmitter release by Pb2+ is largely attributable to extracellular block of the voltage-gated calcium channels.
More Related Videos
Related Concept Videos
Drugs Affecting Neurotransmitter Release or Uptake
Neurochemical Transmission: Sites of Drug Action
Excitatory and Inhibitory Effects of Neurotransmitters
Drugs Affecting Neurotransmitter Synthesis
Chemical Synapses
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
Chemical Synapses
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...

