Plasticity in the functional connectivity and intrinsic properties of neurons is a fundamental feature of circuit function since it provides a mechanism for experience-dependent changes in cell-to-cell excitability. Whilst many studies have focused on the experience-dependent mechanisms of synaptic plasticity, there is not much known about experience-dependent intrinsic plasticity at the level of individual neurons. Here, I have performed whole-cell recordings from glutamic acid decarboxylase 2 (GAD2) and tyrosine hydroxylase (TH) positive interneurons, as well as from two types of principal neurons in the olfactory bulb, following extended exposure to specific odorants. In the olfactory bulb, GAD2+ glomerular interneurons are mostly involved in intraglomerular feed-forward and feedback inhibition, while TH+ cells participate in interglomerular lateral inhibitory circuits. Using a transgenic mouse line expressing YFP under the M72 olfactory receptor promoter, I chronically exposed mice to the monomolecular agonist of the M72 receptor 2’-hydroxyacetophenone and performed targeted recordings from M72 inhibitory and excitatory neurons in acute slices. Following odour exposure, the intrinsic properties of principal neurons remained unchanged, while we observed specific changes in the intrinsic properties of subtypes of interneurons. These findings suggest that while principal cells excitability remains stable during chronic exposure to a novel odour, interneurons are highly plastic. GAD2 plasticity occurs on a local level while TH+ neurons exhibit a global plasticity.
Using a model of the olfactory bulb, I showed that these two effects have very different consequences for local and global odour signalling in the olfactory bulb.