TY - JOUR
T1 - Adaptive olfactory circuitry restores function despite severe olfactory bulb degeneration
AU - Licht, Tamar
AU - Yunerman, Michael
AU - Maor, Ido
AU - Lawabny, Naheel
AU - Oz Rokach, Renana
AU - Shiff, Idit
AU - Mizrahi, Adi
AU - Rokni, Dan
N1 - Publisher Copyright:
© 2023 The Authors
PY - 2023/11/20
Y1 - 2023/11/20
N2 - The olfactory bulb (OB) is a critical component of mammalian olfactory neuroanatomy. Beyond being the first and sole relay station for olfactory information to the rest of the brain, it also contains elaborate stereotypical circuitry that is considered essential for olfaction. Indeed, substantial lesions of the OB in rodents lead to anosmia. Here, we examined the circuitry that underlies olfaction in a mouse model with severe developmental degeneration of the OB. These mice could perform odor-guided tasks and even responded normally to innate olfactory cues. Despite the near total loss of the OB, piriform cortices in these mice responded to odors, and its neural activity sufficed to decode odor identity. We found that sensory neurons express the full repertoire of olfactory receptors, and their axons project primarily to the rudiments of the OB but also, ectopically, to olfactory cortical regions. Within the OB, the number of principal neurons was greatly reduced, and the morphology of their dendrites was abnormal, extending over large regions within the OB. Glomerular organization was totally lost in the severe cases of OB degeneration and altered in the more conserved OBs. This study shows that olfactory functionality can be preserved despite reduced and aberrant circuitry that is missing many of the elements believed to be essential for olfaction, and it may explain reported retention of olfaction in humans with degenerated OBs.
AB - The olfactory bulb (OB) is a critical component of mammalian olfactory neuroanatomy. Beyond being the first and sole relay station for olfactory information to the rest of the brain, it also contains elaborate stereotypical circuitry that is considered essential for olfaction. Indeed, substantial lesions of the OB in rodents lead to anosmia. Here, we examined the circuitry that underlies olfaction in a mouse model with severe developmental degeneration of the OB. These mice could perform odor-guided tasks and even responded normally to innate olfactory cues. Despite the near total loss of the OB, piriform cortices in these mice responded to odors, and its neural activity sufficed to decode odor identity. We found that sensory neurons express the full repertoire of olfactory receptors, and their axons project primarily to the rudiments of the OB but also, ectopically, to olfactory cortical regions. Within the OB, the number of principal neurons was greatly reduced, and the morphology of their dendrites was abnormal, extending over large regions within the OB. Glomerular organization was totally lost in the severe cases of OB degeneration and altered in the more conserved OBs. This study shows that olfactory functionality can be preserved despite reduced and aberrant circuitry that is missing many of the elements believed to be essential for olfaction, and it may explain reported retention of olfaction in humans with degenerated OBs.
KW - behavior
KW - neural representation
KW - odor
KW - olfactory epithelium
KW - piriform cortex
KW - smell
UR - http://www.scopus.com/inward/record.url?scp=85176399478&partnerID=8YFLogxK
U2 - 10.1016/j.cub.2023.09.061
DO - 10.1016/j.cub.2023.09.061
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C2 - 37858342
AN - SCOPUS:85176399478
SN - 0960-9822
VL - 33
SP - 4857-4868.e6
JO - Current Biology
JF - Current Biology
IS - 22
ER -