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pubmed:abstractText |
NMDA receptor (NMDAR)-dependent strengthening of neurotransmitter release has been widely observed, including in layer 5 (L5) pyramidal cells of the visual cortex, and is attributed to the axonal expression of NMDARs. However, we failed to detect NMDAR-mediated depolarizations or Ca(2+) entry in L5 pyramidal cell axons when focally stimulated with NMDAR agonists. This suggests that NMDARs are excluded from the axon. In contrast, local GABA(A) receptor activation alters axonal excitability, indicating that exclusion of ligand-gated ion channels from the axon is not absolute. Because NMDARs are restricted to the dendrite, NMDARs must signal to the axon by an indirect mechanism to alter release. Although subthreshold somatic depolarizations were found to spread electrotonically hundreds of micrometers through the axon, the resulting axonal potential was insufficient to open voltage-sensitive Ca(2+) channels. Therefore, if NMDAR-mediated facilitation of release is cell autonomous, it may depend on voltage signaling but apparently is independent of changes in basal Ca(2+). Alternatively, this facilitation may be even less direct, requiring a cascade of events that are merely triggered by NMDAR activation.
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