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Protons are a neurotransmitter that regulates synaptic plasticity in the lateral amygdala

Significance Synaptic transmission involves the release of neurotransmitters that activate receptors on postsynaptic cells. The results reveal that protons fulfill the criteria for a neurotransmitter and that they activate postsynaptic acid-sensing ion channels. This activity facilitates synaptic plasticity, a requirement for learning and memory in the amygdala. Stimulating presynaptic terminals can increase the proton concentration in synapses. Potential receptors for protons are acid-sensing ion channels (ASICs), Na+- and Ca2+-permeable channels that are activated by extracellular acidosis. Those observations suggest that protons might be a neurotransmitter. We found that presynaptic stimulation transiently reduced extracellular pH in the amygdala. The protons activated ASICs in lateral amygdala pyramidal neurons, generating excitatory postsynaptic currents. Moreover, both protons and ASICs were required for synaptic plasticity in lateral amygdala neurons. The results identify protons as a neurotransmitter, and they establish ASICs as the postsynaptic receptor. They also indicate that protons and ASICs are a neurotransmitter/receptor pair critical for amygdala-dependent learning and memory.