Circuit mechanisms encoding odors and driving aging-associated behavioral declines in Caenorhabditis elegans.

Abstract:

:Chemosensory neurons extract information about chemical cues from the environment. How is the activity in these sensory neurons transformed into behavior? Using Caenorhabditis elegans, we map a novel sensory neuron circuit motif that encodes odor concentration. Primary neurons, AWC(ON) and AWA, directly detect the food odor benzaldehyde (BZ) and release insulin-like peptides and acetylcholine, respectively, which are required for odor-evoked responses in secondary neurons, ASEL and AWB. Consistently, both primary and secondary neurons are required for BZ attraction. Unexpectedly, this combinatorial code is altered in aged animals: odor-evoked activity in secondary, but not primary, olfactory neurons is reduced. Moreover, experimental manipulations increasing neurotransmission from primary neurons rescues aging-associated neuronal deficits. Finally, we correlate the odor responsiveness of aged animals with their lifespan. Together, these results show how odors are encoded by primary and secondary neurons and suggest reduced neurotransmission as a novel mechanism driving aging-associated sensory neural activity and behavioral declines.

journal_name

Elife

journal_title

eLife

authors

Leinwand SG,Yang CJ,Bazopoulou D,Chronis N,Srinivasan J,Chalasani SH

doi

10.7554/eLife.10181

subject

Has Abstract

pub_date

2015-09-22 00:00:00

pages

e10181

issn

2050-084X

journal_volume

4

pub_type

杂志文章

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