Sensory deprivation triggers phenotypic adjustment of dopaminergic interneurons in the mouse olfactory bulb

Abstract

abstractOlfactory sensory activity is a main factor factor controlling intergration and survival of neurons in the olfactory bulb. However, its impact on specific neuronal subtypes is unclear. Using reversible unilateral naris closure in concert with longitudinal in vivo imaging we show here that newborn GABAergic interneurons undergo significant cell death under sensory deprivation. In contrast, dopaminergic OB neurons survive under deprivation, but react with a reversible downregulation of tyrosine hydroxylase expression.long abstractNeurogenesis persists in the mammalian subventricular zone after birth, producing various populations of olfactory bulb (OB) interneurons. These include GABAergic and mixed dopaminergic/GABAergic double neurotransmitter neurons for the glomerular layer. While olfactory sensory activity is one of the main factors controlling newborn neuron integration, its effect on specific neuronal subtypes is far less clear. Here we use a reversible unilateral deprivation paradigm in combination with longitudinal in vivo imaging to characterize the behavior of newborn glomerular neurons. We find that a substantial fraction of purely GABAergic neurons die after four weeks of sensory deprivation. Tyrosine Hydroxylase (TH) positive dopaminergic/ GABAergic neurons show no signifficant cell death under deprivation, but react with an important decrease in TH expression levels. Importantly, this effect reverses after naris reopening, pointing to a specific adaptation of this neuron population to the level of sensory activity. We conclude that sensory deprivation induces adjustments in the excitation/inhibition balance of the OB implicating cell death and adaptation of neurotransmitter use in specific neuron types.