Joost le Feber

The brain has been extensively studied from the cellular level, as well as from the cognitive level. However, it appears difficult to combine findings across these levels.

For example, the underlying neural basis of memory formation has been studied in detail at the single cell level, and many studies show that long-term potentiation and/or depression mechanisms, initiated by e.g. tetanic stimulation, cause changes in cortical connectivity. However, to bridge the gap to cognitive functions, such as learning or memory, we need to investigate the effects of such stimulation at the neural network level.

Comparably, common treatment against hyper excitability that occurs in epileptic brains is based on cellular mechanisms; anti-epileptic drugs (AEDs) usually aim to increase neuronal inhibition or decrease excitation. However, there are indications that networks may become hyper excitable when the level of ongoing activity is insufficient. If this is true, these commonly used AEDs may in certain situations even enlarge network excitability.

The major objective of this principal investigator track is to bridge the gap between intracellular and cognitive studies by investigating neurological phenomena at the network level.

Present projects focus on two general challenges at the network level:


Memory in cultured cortical networks


(Modulation of) Network excitability


Joost le Feber

Tim Witteveen

Timo Lauteslager

Wim Rutten

Richard van Wezel

Irina Stoyanova

Bettie Klomphaar

Marcel Weusthof


EEMCS Prints

Joost le Feber


The brain consists of billions of neurons that are as an ensemble capable of memorizing. It is widely assumed that memories are encoded in the connections between neurons. Thus, new experiences induce connectivity changes in the network, that encode for that memory. However, it remains one of the mysteries of the brain how older memories are protected when new ones are formed ... read more

Network Excitability

Characteristic of spontaneous activity in the sleeping neocortex are synchronous poly-neuronal bursts. These play an important role in the homeostatic regulation of network excitability. Long-term suppression of these bursts in the cortex leads to hyper excitability what is usually obseverd in the form of epileptic activity patterns. In contrast to the sleep state, the neocortex receives cholinergic input from other nuclei during the more active States (awake or REM sleep), during these states the bursts disappear. ... read more