I wouldn't be quite so pessimistic. We can capture a large part of neuronal variability using Hodgkin Huxley type models (like the one they use in the paper). Dendritic spikes have been hypothesized to be involved in computations for quite a while we just haven't had evidence in vivo. My take home from the paper is that the voltage dependent active properties of the dendritic tree act as an amplifier for synaptic events.
This doesn't fundamentally change how we think neurons work, it just fills in one of the major gaps in our understanding of how relatively few synaptic events could lead to a somatic action potential--something that is very hard to explain if dendrites only passively integrate incoming synaptic events. To give an example, there are connections in the brain between excitatory neurons and inhibitory neurons that are known to basically be 1:1 with virtually no failure rate, one spike in the excitatory neuron will evoke a spike in the inhibitory neuron pretty much every single time. Based on what we know about synaptic failure rates and the total number of synaptic events we think are required to generate and action potential, this phenomena is difficult to explain. Active dendritic properties as described in the paper provide a possible mechanism.
edit: I should say that dendritic spikes probably act as a kind of conditional amplifier for synaptic events. The conditions that come to mind are spatial and temporal proximity. This does complicate the idea that relief of the NMDA Mg2+ block is used to detect coincidence of somatic action potentials with presynaptic glutamate release, suggesting that the Mg2+ block may also be used to detect coincidence of a single synaptic event with other nearby synaptic events.
This doesn't fundamentally change how we think neurons work, it just fills in one of the major gaps in our understanding of how relatively few synaptic events could lead to a somatic action potential--something that is very hard to explain if dendrites only passively integrate incoming synaptic events. To give an example, there are connections in the brain between excitatory neurons and inhibitory neurons that are known to basically be 1:1 with virtually no failure rate, one spike in the excitatory neuron will evoke a spike in the inhibitory neuron pretty much every single time. Based on what we know about synaptic failure rates and the total number of synaptic events we think are required to generate and action potential, this phenomena is difficult to explain. Active dendritic properties as described in the paper provide a possible mechanism.
edit: I should say that dendritic spikes probably act as a kind of conditional amplifier for synaptic events. The conditions that come to mind are spatial and temporal proximity. This does complicate the idea that relief of the NMDA Mg2+ block is used to detect coincidence of somatic action potentials with presynaptic glutamate release, suggesting that the Mg2+ block may also be used to detect coincidence of a single synaptic event with other nearby synaptic events.