Dendritic inhibition: local coordination by excitation

The brain consists of billions of neurons that each form thousands of synaptic connections with each other. Synapses are essential building blocks and through continuous forming and shaping, synapses allow us to learn, adapt, adjust, and grow. This thesis focuses on investigating the local coordination of inhibition and excitation after plasticity of excitatory synapses. By forming these large number of synapses, highly complex neural networks are formed. Within these networks, our brains store information that enable us to learn and adapt to our everchanging lives. The information transfer from one neuron to another forms the basis of neuronal information processing. Neurons are capable of judging whether incoming information is important enough to forward. This occurs by the total strength of the incoming signals and those that promote information processing are called excitatory. Opposing these are inhibitory signals that lower the total signal. The balance between excitation and inhibition is essential to our health. For instance, it is known that a disturbance of this balance can result in autism, schizophrenia, or epilepsy. It is thus essential to understand how these signals are maintained and which factors contribute. In our work, we show that inhibition is regulated on an exceptionally small scale, within micrometers. By increasing the excitation locally, we show that an inhibitory synapse can be formed. We stimulated dendritic spines close to a GABAergic axon crossing by pairing two-photon glutamate uncaging with postsynaptic depolarization in CA1 pyramidal cells. We found that repeated spine stimulation promoted growth of a new GABAergic bouton onto the same dendrite. Our findings reveal a dendritic signaling mechanism to trigger growth of inhibitory boutons at dendritic locations with strong excitatory synaptic activity, which may serve to ensure inhibitory control over clustered excitatory inputs