Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

Evoked transmitter release depends upon calcium influx into synaptic boutons, but mechanisms regulating bouton calcium levels and spontaneous transmitter release are obscure. To understand these processes better, we monitored calcium transients in axons and presynaptic terminals of pyramidal neurons in hippocampal slice cultures. Action potentials reliably evoke calcium transients in axons and boutons. Calcium-induced calcium release (CICR) from internal stores contributes to the transients in boutons and to paired-pulse facilitation of EPSPs. Store depletion activates store-operated calcium channels, influencing the frequency of spontaneous transmitter release. Boutons display spontaneous Ca2+ transients; blocking CICR reduces the frequency of these transients and of spontaneous miniature synaptic events. Thus, spontaneous transmitter release is largely calcium mediated, driven by Ca2+ release from internal stores. Bouton store release is important for short-term synaptic plasticity and may also contribute to long-term plasticity.

Type

Journal article

Journal

Neuron

Publication Date

01/2001

Volume

29

Pages

197 - 208

Keywords

Action Potentials, Animals, Axons, Calcium, Calcium Channels, Electric Stimulation, Excitatory Postsynaptic Potentials, Hippocampus, In Vitro Techniques, Lysine, Male, Neuronal Plasticity, Neurotransmitter Agents, Presynaptic Terminals, Pyramidal Cells, Rats, Rats, Wistar, Ryanodine, Synaptophysin, Tetrodotoxin