11/21/2023 0 Comments Dendrite axon synapse micrograph![]() ![]() Axo-axonic synapses are characterized by a presynaptic element or varicosity that contains neurotransmitter-filled synaptic vesicles and forms one or more electron-dense junctions with a similarly vesicle-filled axon terminal ( Figure 1d) ( Peters & Palay, 1996). Synapses on in the axon hillock or initial segment directly regulate action potential generation of the postsynaptic neuron ( Figure 1c). Axo-dendritic and axo-somatic synapses describe interactions in which an axon synapses on the dendrite ( Figure 1a) or cell body ( Figure 1b) of the post-synaptic neuron. The gold standard in elucidating neural circuits, electron microscopy (EM), provides nanometer scale resolution critical for discerning the morphological characteristics of axon terminals and postsynaptic targets ( Figure 1). Structurally defining axo-axonic synapses Here, we survey structural evidence for axo-axonic synapses, discuss how this configuration may impact circuit function, and describe how recent technological advances may aid in identifying and functionally assessing these non-canonical synapses. Such is the case for substantia nigra dopamine neurons, in which somatic action potential firing rates often fail to account for activity observed at the axon terminal (see Berke, 2018). Several studies now demonstrate that axon terminals synapsing on another axon terminal provide direct neural circuit routes for presynaptic modulation throughout the mammalian brain.Īmong other functions, the axo-axonic synapse allows for neurotransmitter release from the postsynaptic axon terminal that does not require action potential activity that is generated at the postsynaptic neuron’s axon hillock. Other sources of neurotransmitters exist to exert presynaptic regulatory action, including retrograde messengers sourced from postsynaptic membranes and astrocytic transmitters. Clearly most, if not all, axon terminals contain GPCR autoreceptors, which allows for autoregulatory negative feedback. Since then, a panoply of G-protein coupled receptors (GPCRs) and ionotropic heteroreceptors localized to axon terminals were identified to modulate neurotransmitter release ( Atwood et al., 2014). ![]() In 1961, Dudel & Kuffler discovered that the major inhibitory neurotransmitter GABA acts on the presynaptic terminal of a glutamatergic neuron to decrease the release probability of this major excitatory neurotransmitter. ![]()
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