Presynaptic Ca2+ dynamics, Ca2+ buffers and synaptic efficacy

Area of Science:

• Neuroscience
• Synaptic transmission
• Calcium signaling

Background:

• Neurotransmitter release is initiated by calcium (Ca2+) influx at presynaptic terminals.
• Ca2+ dynamics, influenced by influx, diffusion, and buffering, dictate release probability.
• Synaptic facilitation, an increase in release during repetitive firing, is linked to elevated Ca2+ at release sites.

Purpose of the Study:

• To review theoretical and experimental evidence for proposed mechanisms of synaptic facilitation.
• To elucidate the role of Ca2+ dynamics in activity-dependent neurotransmitter release enhancement.

Main Methods:

• Review of existing theoretical models of Ca2+ dynamics and synaptic facilitation.
• Analysis of experimental data investigating Ca2+ buffering and release mechanisms.
• Comparison of proposed facilitation models: residual Ca2+ accumulation, multi-site binding, and partial buffer saturation.

Main Results:

• Activity-dependent increases in presynaptic Ca2+ concentration are the primary driver of synaptic facilitation.
• Evidence supports multiple contributing mechanisms, including residual Ca2+ and buffer saturation, depending on the synapse type.
• The interplay between Ca2+ sources, diffusion, and buffering critically shapes facilitation.

Conclusions:

• Understanding Ca2+ dynamics is crucial for comprehending synaptic plasticity and information processing.
• Synaptic facilitation arises from complex interactions within the presynaptic terminal, modulated by Ca2+ buffering and influx.
• Further research is needed to fully differentiate the contributions of various facilitation mechanisms across different neuronal synapses.