Selective lifelong suppression of an odor processing channel in response to critical period experience
Sensory circuits undergo experience-dependent plasticity during early-life critical periods, attuning the nervous system to levels of key environmental stimuli. During a critical period in the Drosophila olfactory system, we found that exposure to ethyl butyrate (EB) induces glial phagocytosis of odorant receptor Or42a-positive olfactory sensory neuron (OSN) axon terminals which terminate in the…
Sensory circuits can undergo changes in response to experiences during early-life critical periods, fine-tuning the nervous system to environmental cues. In the Drosophila olfactory system, exposure to ethyl butyrate during a critical period leads to the phagocytosis of odorant receptor Or42a-positive olfactory sensory neuron (OSN) axon terminals by glial cells.
This study delves deeper into these findings, revealing the functional significance and circuit selectivity of this process. Utilizing two-photon Ca2+ imaging and a genetically-encoded voltage indicator, researchers discovered that Or42a OSN odor-evoked responses are permanently suppressed following critical period exposure to odors.
This implies that odor sensitivity in these OSNs undergoes long-term alterations due to critical period odor exposure. To further assess the selectivity of glial pruning for Or42a axon terminals, the study examined projection neurons (PNs) post-synaptic to these OSNs, as well as another group of OSNs, called Or43b OSNs, which are highly responsive to ethyl butyrate.
Results showed that within VM7, glial pruning selectively targets Or42a terminals, while Or43b OSNs experience modest pruning but retain their sensitivity to ethyl butyrate. To understand this discrepancy, the researchers turned to the Drosophila connectome, discovering significant differences in the scale of inhibitory connectivity to Or42a and Or43b OSNs.
However, the study found that suppressing GABA A receptor expression in both OSN types amplifies glial pruning. This research expands our comprehension of the critical period plasticity paradigm by demonstrating lifelong suppression of pruned Or42a OSNs and establishing the specificity of this phenomenon within and between sensory circuits.
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