Axonal CB1 Receptors Mediate Inhibitory Bouton Formation via cAMP Increase and PKA.

Experience-dependent formation and removal of inhibitory synapses are essential throughout life. For instance, GABAergic synapses are removed to facilitate learning, and strong excitatory activity is accompanied by the formation of inhibitory synapses to maintain coordination between excitation and inhibition. We recently discovered that active dendrites trigger the growth of inhibitory synapses via CB1 receptor-mediated endocannabinoid signaling, but the underlying mechanism remained unclear.

Single Synapse LTP: A Matter of Context?

The most commonly studied form of synaptic plasticity is long-term potentiation (LTP). Over the last 15 years, it has been possible to induce structural and functional LTP in dendritic spines using two-photon glutamate uncaging, allowing for studying the signaling mechanisms of LTP with single synapse resolution. In this review, we compare different stimulation methods to induce single synapse LTP and discuss how LTP is expressed.

Endocannabinoid Signaling Mediates Local Dendritic Coordination between Excitatory and Inhibitory Synapses.

Dendritic inhibitory synapses are most efficient in modulating excitatory inputs localized on the same dendrite, but it is unknown whether their location is random or regulated. Here, we show that the formation of inhibitory synapses can be directed by excitatory synaptic activity on the same dendrite. We stimulated dendritic spines close to a GABAergic axon crossing by pairing two-photon glutamate uncaging with postsynaptic depolarization in CA1 pyramidal cells.

Rapid Modulation of Axon Initial Segment Length Influences Repetitive Spike Firing.

Neurons implement a variety of plasticity mechanisms to alter their function over timescales ranging from seconds to days. One powerful means of controlling excitability is to directly modulate the site of spike initiation, the axon initial segment (AIS). However, all plastic structural AIS changes reported thus far have been slow, involving days of neuronal activity perturbation.