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Neuroimage. 2007 Mar;35(1):149-65. Epub 2007 Jan 17.

Modelling the role of excitatory and inhibitory neuronal activity in the generation of the BOLD signal.

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  • 1Cuban Neuroscience Center, Ave. 25, Esq. 158, No. 15202, Cubanacan, Playa, Ciudad Habana, P.O. Box 6412/6414, Cuba.


A biophysical model of the coupling between neuronal activity and the BOLD signal that allows for explicitly evaluating the role of both excitatory and inhibitory activity is formulated in this paper. The model is based on several physiological assumptions. Firstly, in addition to glycolysis, the "glycogen shunt" is assumed for excitatory synapses as a mechanism for energy production in the astrocytes. As a result, oxygen-to-glucose index (OGI) is not constant but varies with excitatory neuronal activity. In contrast, a constant OGI=6 (glycolysis) is assumed for inhibitory synapses. Finally we assume that cerebral blood flow is not directly controlled by energy usage, but it is only related to excitatory activity. Simulations' results show that increases in excitatory activity amplify the oscillations associated with the transient BOLD response, by increasing the initial dip, the maximum, and the post-stimulus undershoot of the signal. In contrast, increasing the inhibitory activity evoked an overall decrease of the BOLD signal along the whole time interval of the response. Simultaneous increase of both types of activity is then expected to reinforce the initial dip and the post-stimulus undershoot, while respective effects on the maximum tend to counteract each other. Two mechanisms for negative BOLD response (NBS) generation were predicted by the model: (i) when inhibition was present alone or together with low activation levels and (ii) when deactivation occurred independently of the accompanying inhibition level. Interestingly, NBS was associated with negative oxygen consumption changes only for the case of mechanism (ii).

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