The function of presynaptic terminals is regulated by intracellular Cl -, the levels of which modify vesicular endocytosis and transmitter refilling and mediate the effects of presynaptic ligand-gated Cl- channels. Nevertheless, the concentration of Cl- in a central nerve terminal is unknown, and it is unclear whether terminals can regulate Cl - independently of the soma. Using perforated-patch recording in a mammalian synapse, we found that terminals accumulate Cl- up to 21mM, between four and five times higher than in their parent cell bodies. Changing [Cl-] did not alter vesicular glutamate content in intact terminals, unlike in vitro experiments. Thus, glutamatergic terminals maintain an elevated Cl- concentration without compromising synaptic transmission.
- Calyx of held
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