Bert Sakmann

Cortical Microcircuits and Cortical Plasticity

Thursday, 3 July 2003
09:00 - 09:30 hrs CEST


The brain operates by small electrical signals and if we want to understand mechanistically brain functions like the recognition of a sensory stimulus, the initiation of a limb movement or the storage and retrieval of memories we must measure and understand the time and space dependent pattern of electrical signals in different parts of the cerebral cortex. Despite the immense progress made during the last century in elucidating the physiology of cortical functions a number of basic questions remain unanswered. In particular the gap in understanding the properties of large ensembles, consisting of thousands of neurons for example those of a cortical column on the one hand and the properties of cortical microcircuits consisting of a small number of morphologically defined neurons located within and between cortical layers on the other hand is still rather broad.
Is a cortical function represented solely by the pattern of action potentials (AP) or by both subthreshold postsynaptic potentials (PSP) and APs? Which are those cell connections that are modifiable during “plastic” changes in the functional architecture of the cortex induced, for example, by the use or disuse of the cortex? What are the cellular mechanisms underlying the changes in the efficacy of synaptic connections?
The results from experiments made by combining fast optical imaging of the rodent somatosensory cortex, intracellular voltage recording in vivo and in vitro and the reconstruction of small circuits of connected neurons suggest that sensory stimuli are represented mostly by a pattern of subthreshold PSPs which, however, vary widely between different cortical layers in their extent and which change rapidly in time. Changes in the functional architecture of the cortex which can be induced by the use and disuse of the somato-sensory system during postnatal development are based on changes in the arborisation of L2/3 pyramid axons as well as changes in synaptic efficacy of the connections between pyramidal cells in layer 2/3. Such changes are triggered by coincident, suprathreshold activity in pre- and postsynaptic neurons involving both axonal and back-propagating dendritic APs.

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