Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 109, Issue 16, Pages 6259-6264Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1203843109
Keywords
calcium signaling; neurodegeneration; neurogenesis; relay circuit; tau
Categories
Funding
- UK National Institute for Health Research Biomedical Research Centre
- Medical Research Council UK
- Medical Research Council
- Alzheimer's Society
- Alzheimer's Research Trust
- Dunhill Medical Trust
- Scottish Universities Life Science Alliance
- European Commission [HEALTH-F2-2007-201159]
- National Institutes of Health [DA023214]
- Swedish Research Council
- Karolinska Institutet
- Marianne and Marcus Wallenberg Foundation
- Helmholtz Foundation
- European Research Council
- MRC [G1100540, G0400074, G0502157, G0900652, G0700718] Funding Source: UKRI
- Alzheimers Research UK [ART-EG2010A-1] Funding Source: researchfish
- Medical Research Council [G0400074, G0700718, G1100540, G0502157, G0900652] Funding Source: researchfish
- The Dunhill Medical Trust [R173/1110] Funding Source: researchfish
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Expanding the repertoire of molecularly diverse neurons in the human nervous system is paramount to characterizing the neuronal networks that underpin sensory processing. Defining neuronal identities is particularly timely in the human olfactory system, whose structural differences from nonprimate macrosmatic species have recently gained momentum. Here, we identify clusters of bipolar neurons in a previously unknown outer shell domain of the human olfactory tract, which express secretagogin, a cytosolic Ca2+ binding protein. These shell neurons are wired into the olfactory circuitry because they can receive mixed synaptic inputs. Unexpectedly, secretagogin is often coexpressed with polysialylated-neural cell adhesion molecule, beta-III-tubulin, and calretinin, suggesting that these neurons represent a cell pool that might have escaped terminal differentiation into the olfactory circuitry. We hypothesized that secretagogin-containing shell cells may be eliminated from the olfactory axis under neurodegenerative conditions. Indeed, the density, but not the morphological or neurochemical integrity, of secretagogin-positive neurons selectively decreases in the olfactory tract in Alzheimer's disease. In conclusion, secretagogin identifies a previously undescribed cell pool whose cytoarchitectonic arrangements and synaptic connectivity are poised to modulate olfactory processing in humans.
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