Neural Control of Movement - Copenhagen > Research > Motoneurones

Plateau potentials in motoneurones amplify synaptic inputs, and increases the gain at the final output stage

The dendritic membrane area accounts for around 97% of the total membrane area of the motoneurone. They receive synaptic contacts from around 20.000 presynaptic neurones. The classic view of the mammalian motor neurones, which emerged from the laboratories of Eccles, Granit and Rall in the 1950s and 1960s, was that the dendritic membrane is essentially passive and that the sum of the unitary synaptic potentials was electrotonically conducted to the initial segment where an action potential was elicited if the threshold was reached. However, electrophysiological and computational evidence indicate that the excitatory current from the synapses on the somato-dendritic membrane is not large enough to drive the motoneurones to the firing frequencies actually attained under normal motor activity.

In the 1980s we discovered plateau potentials in motoneurones which were dependent on a monoaminergig innervation of the motoneurones to facilitate the voltage-dependent persistent inward currents (PICs) which were causing the plateaux. It was then proposed that that this paradox of a too weak synaptic excitation could be explained if the PICs present in the dendrites of motoneurones served to amplify synaptic excitation.

We have demonstrated that dendritic PICs cause a large amplification of synaptic excitation – and thus increase in firing frequency and contraction strength. Moreover the frequency reduction by synaptic inhibition is greatly enhanced at higher firing frequencies, when the current through the recording electrode has activated the dendritic PICs, as is the case when the current-to-frequency slope suddenly becomes steeper – “secondary range”. We also demonstrated that synaptic inhibition is several times more effective in reducing the firing caused by synaptic excitation than firing evoked by current injection through the recording microelectrode. That would be explained if motoneuronal discharge by synaptic excitation – but not by current injection in the soma – is always supported by dendritic PICs. We conclude that dendritic PICs contribute dynamically to the transformation of synaptic input into a motoneuronal frequency code.

Plateau potentials in motoneurones:

1) are caused by voltage-dependent persistent inward currents Cav1.3 (and INap)
2) depends on a facilitation by the serotonin- innervation of motoneurons (5 HT2 A&C) (and
other metabotropic receptors as well)
3) acts as an amplifier of synaptic excitation (by 5-10 x) during motor activity (“flight and
fight”)

Research group members:
Hans Hultborn (Coordinator)
Veronika Bonnevie
Claire Meehan
Katinka Stecina
Natalya Sukiasyan
Jacob Wienecke