GABABR silencing of nerve terminals. Academic Article uri icon

Overview

abstract

  • Control of neurotransmission efficacy is central to theories of how the brain computes and stores information. Presynaptic G-protein coupled receptors (GPCRs) are critical in this problem as they locally influence synaptic strength and can operate on a wide range of time scales. Among the mechanisms by which GPCRs impact neurotransmission is by inhibiting voltage-gated calcium (Ca2+) influx in the active zone. Here, using quantitative analysis of both single bouton Ca2+ influx and exocytosis, we uncovered an unexpected non-linear relationship between the magnitude of action potential driven Ca2+ influx and the concentration of external Ca2+ ([Ca2+]e). We find that this unexpected relationship is leveraged by GPCR signaling when operating at the nominal physiological set point for [Ca2+]e, 1.2 mM, to achieve complete silencing of nerve terminals. These data imply that the information throughput in neural circuits can be readily modulated in an all-or-none fashion at the single synapse level when operating at the physiological set point.

publication date

  • April 4, 2023

Research

keywords

  • Presynaptic Terminals
  • Synapses

Identity

PubMed Central ID

  • PMC10115440

Scopus Document Identifier

  • 85153121764

Digital Object Identifier (DOI)

  • 10.1371/journal.pcbi.1002456

PubMed ID

  • 37014052

Additional Document Info

volume

  • 12