The conventional picture of how a nerve cell behaves is that signals are received at synapses in the dendrites. If they are sufficient, the cell body produces a spike that travels down the axon to the synapses with other neurons. There have been some odd mechanisms added to this picture like activity starting at the cell-axon junction. Now there is a really novel behavior found. This is reported in a paper by Bukalo, Campanac, Hoffman and Fields in PNAS, Synaptic plasticity by antidromic firing during hippocampal network oscillations.
Some cells in the hippocampus that are involved in memory can be driven backwards – signals past up the axon to the cell body and then on to the synapses in the dendrites. That is really different. The process appears to re-balance the sensitivity of groups of synapses. It happens during sleep’s sharp-wave ripple complexes.
It seems reasonable that when a system is driven in one direction for a whole day that it would be an advantage to reset the system back so that there was ‘headroom’ for another day’s activities. This would need to be done without losing the relative changes in synaptic sensitivity that had been gained during the day (in fact, consolidate them) – in other words, to preserve the memories and learning that had happened during the day.
Here is the abstract:
Learning and other cognitive tasks require integrating new experiences into context. In contrast to sensory-evoked synaptic plasticity, comparatively little is known of how synaptic plasticity may be regulated by intrinsic activity in the brain, much of which can involve nonclassical modes of neuronal firing and integration. Coherent high-frequency oscillations of electrical activity in CA1 hippocampal neurons [sharp-wave ripple complexes (SPW-Rs)] functionally couple neurons into transient ensembles. These oscillations occur during slow-wave sleep or at rest. Neurons that participate in SPW-Rs are distinguished from adjacent nonparticipating neurons by firing action potentials that are initiated ectopically in the distal region of axons and propagate antidromically to the cell body. This activity is facilitated by GABA-mediated depolarization of axons and electrotonic coupling. The possible effects of antidromic firing on synaptic strength are unknown. We find that facilitation of spontaneous SPW-Rs in hippocampal slices by increasing gap-junction coupling or by GABA-mediated axon depolarization resulted in a reduction of synaptic strength, and electrical stimulation of axons evoked a widespread, long-lasting synaptic depression. Unlike other forms of synaptic plasticity, this synaptic depression is not dependent upon synaptic input or glutamate receptor activation, but rather requires L-type calcium channel activation and functional gap junctions. Synaptic stimulation delivered after antidromic firing, which was otherwise too weak to induce synaptic potentiation, triggered a long-lasting increase in synaptic strength. Rescaling synaptic weights in subsets of neurons firing antidromically during SPW-Rs might contribute to memory consolidation by sharpening specificity of subsequent synaptic input and promoting incorporation of novel information.