Cell assemblies are considered to be physiological as well as functional units in the brain. A repetitive and stereotypical sequential activation of many neurons was observed, but the mechanisms underlying it are not well understood. Feedforward networks, such as synfire chains, with the pools of excitatory neurons unidirectionally connected and facilitating signal transmission in a cascade-like fashion were proposed to model such sequential activity. When embedded in a recurrent network, these were shown to destabilise the whole network’s activity, challenging the suitability of the model. Here, we investigate a feedforward chain of excitatory pools enriched by inhibitory pools that provide disynaptic feedforward inhibition. We show that when embedded in a recurrent network of spiking neurons, such an augmented chain is capable of robust signal propagation. We then investigate the influence of overlapping two chains on the signal transmission as well as the stability of the host network. While shared excitatory pools turn out to be detrimental to global stability, inhibitory overlap implicitly realises the motif of lateral inhibition, which, if moderate, maintains the stability but if substantial, it silences the whole network activity including the signal. Addition of a disinhibitory pathway along the chain proves to rescue the signal transmission by transforming a strong inhibitory wave into a disinhibitory one, which specifically guards the excitatory pools from receiving excessive inhibition and thereby allowing them to remain responsive to the forthcoming activation. Disinhibitory circuits not only improve the signal transmission, but can also control it via a gating mechanism. We demonstrate that by manipulating a firing threshold of the disinhibitory neurons, the signal transmission can be enabled or completely blocked. This mechanism corresponds to cholinergic modulation, which was shown to be signalled by volume as well as phasic transmission and variably target classes of neurons. Furthermore, we show that modulation of the feedforward inhibition circuit can promote generating spontaneous replay at the absence of external inputs. This mechanism, however, tends to also cause global instabilities. Overall, these results underscore the importance of inhibitory neuron populations in controlling signal propagation in cell assemblies as well as global stability. Specific inhibitory circuits, when controlled by neuromodulatory systems, can robustly guide or block the signals and invoke replay. This mounts to evidence that the population of interneurons is diverse and can be best categorised by neurons’ specific circuit functions as well as their responsiveness to neuromodulators.

京都大学 / 新制・課程博士 / 博士(生命科学) / 甲第23340号 / 生博第458号 / 新制||生||61(附属図書館) / 京都大学大学院生命科学研究科高次生命科学専攻 / (主査)教授 松田 道行, 教授 見学 美根子, 教授 今吉 格 / 学位規則第4条第1項該当 / Doctor of Philosophy in Life Sciences / Kyoto University / DFAM

Mémoire numérisé par la Division de la gestion de documents et des archives de l'Université de Montréal.

Mémoire numérisé par la Division de la gestion de documents et des archives de l'Université de Montréal