Odor information is encoded in the activity of a population of glomeruli in the primary olfactory center. However, how this information is decoded in the brain remains elusive. Here, we address this question in Drosophila by combining neuronal imaging and tracking of innate behavioral responses. We find that the behavior is accurately predicted by a model summing normalized glomerular responses, in which each glomerulus contributes a specific, small amount to odor preference. This model is further supported by targeted manipulations of glomerular input, which biased the behavior. Additionally, we observe that relative odor preference changes and can even switch depending on the context, an effect correctly predicted by our normalization model. Our results indicate that olfactory information is decoded from the pooled activity of a glomerular repertoire and demonstrate the ability of the olfactory system to adapt to the statistics of its environment.
How cell-type-specific physiological properties shape neuronal functions in a circuit remains poorly understood. We addressed this issue in the Drosophila mushroom body (MB), a higher olfactory circuit, where neurons belonging to distinct glomeruli in the antennal lobe feed excitation to three types of intrinsic neurons, α/β, α'/β', and γ Kenyon cells (KCs). Two-photon optogenetics and intracellular recording revealed that whereas glomerular inputs add similarly in all KCs, spikes were generated most readily in α'/β' KCs. This cell type was also the most competent in recruiting GABAergic inhibition fed back by anterior paired lateral neuron, which responded to odors either locally within a lobe or globally across all lobes depending on the strength of stimuli. Notably, as predicted from these physiological properties, α'/β' KCs had the highest odor detection speed, sensitivity, and discriminability. This enhanced discrimination required proper GABAergic inhibition. These results link cell-type-specific mechanisms and functions in the MB circuit.
Synaptic depression is thought to underlie the loss of cortical responsiveness to an eye deprived of vision. Here, we establish a fundamental role for type 2 metabotropic glutamate receptors (mGluR2) in long-term depression (LTD) of synaptic transmission within primary visual cortex. Direct mGluR2 activation by (2S,2R,3R-2-(2,3-dicarboxycyclopropyl)glycine (DCG-IV) persistently depressed layer 2͞3 field potentials in slices of mouse binocular zone when stimulated concomitantly. Chemical LTD was independent of N-methyl-D-aspartate (NMDA) receptors but occluded conventional LTD by low-frequency stimulation, indicating shared downstream events. Antagonists or targeted disruption of mGluR2 conversely prevented LTD induction by electrical lowfrequency stimulation to layer 4. In contrast, Schaeffer collateral synapses did not exhibit chemical LTD, revealing hippocampal area CA1, naturally devoid of mGluR2, to be an inappropriate model for neocortical plasticity. Moreover, monocular deprivation remained effective in mice lacking mGluR2, and receptor expression levels were unchanged during the critical period in wild-type mice, indicating that experience-dependent plasticity is independent of LTD induction in visual cortex. Short-term depression that was unaffected by mGluR2 deletion may better reflect circuit refinement in vivo.
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