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Contribution of neurogliaform cells to signal flow in the barrel cortex during whisking behaviour (Neurogliaform cells)
Start date: Mar 1, 2012, End date: Feb 28, 2014 PROJECT  FINISHED 

The barrel cortex is the part of rodent primary somatosensory cortex which is responsible for the tactile representation of whiskers. It is recognized as a key model system for understanding fundamental aspects of active sensory processing and more generally investigations into this cortical area have already provided a large amount of information about the basic architecture of cortical microcircuits.A considerable amount of information has been gathered about barrel cortex microcircuits from in vitro brain slice experiments, which forms a basis for understanding the differential roles of the various classes of excitatory and inhibitory neurons. However, we know much less about how these cells function in awake behaving animals. Recent improvements of the whole-cell patch-clamp recording technique make it possible to record from neurons in the cerebral cortex of anaesthetized and awake animalsNeurogliaform cells appear to play a unique role in cortical microcircuits. A single firing of a neurogliaform cell can activate both postsynaptic and presynaptic GABA-B and extrasynaptic GABA-A receptors residing outside the synaptic clefts. This gives to these cells the capacitiy of evoking long lasting inhibition of dendritic origin in the overwhelming majority of neighbouring neurons, besides the capacity of suppressing overall synaptic transmission in vicinity of them.My first research objective is to carry out dual in vivo whole-cell patch-clamp recordings from identified neurogliaform cells and from other neighbouring cells in layer 2/3 of barrel cortex of awake behaving animals and subsequently in order to investigate the consequences of synchronized activity of neighbouring neurogliaform cells on the operation of barrel cortex microcircuits, My second research objective is to manipulate them by optogenetical techinques through viral expression of channelrhodopsin 2 and halorhodopsin.
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