Prominent inhibitory pathway is frequency-dependent disynaptic inhibition (FDDI) between L5 Pyr and Martinotti cells. MC inhibition is facilitating, MC axons extend up to layer 1. Target oblique, apical and tuft dendrites of neighboring PCs.
whole-cell recording from TTL5 PCs and L5 MCs. FDDI modulated by Ih in Py dendrites. PCs that receive both disynaptic inhibition and monosynaptic excitation from neighboring PCs transition from net depolarization to hyperpolarization based on frequency of excitation
By activating pre-synaptic MC and PC simultaneously, the resulting EPSPs sum linearly on average. This is because PCs target basal tree and MCs target apical tree, so no shunting. If the apical trunk is directly excited then there is stronger inhibition at the soma. The further away the trunk electrode is the larger this effect.
Only a few MCs are likely to mediate the FDDI effect. They shut down one by hyperpolarizing and saw big reduction in inhibition in post-synaptic PC. Possible that hyperpolarizing could shut down multiple (thus underestimating number of MCs) due to electrical coupling.
MCs can synchronize the activity of PCs. Activating 8-9 PCs with bursts can saturate the MC effect on PCs.
Basically, this fits in with the gist that PC bursting is a communication protocol, and MC inhibition is part of the inhibitory feed-back loop that interacts with burst-based signaling. PC bursts seem to arise when the apical tree is activated - typically because of a NMDA and VGCC calcium spike in apical tuft/trunk. This bursting will activate MC cells which feedback onto the apical tree, and then reduces bursting likelihood. Unclear if this could be a multiplicative mechanism via shunting the apical tree, or if its just additive.
Martinotti cells are SOM cells!
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