Upregulation of barrel GABAergic neurons is associated with cross-modal plasticity in olfactory deficit.
BACKGROUND
Loss of a sensory function is often followed by the hypersensitivity of other modalities in mammals, which secures them well-awareness to environmental changes. Cellular and molecular mechanisms underlying cross-modal sensory plasticity remain to be documented.


RESULTS
Multidisciplinary approaches, such as electrophysiology, behavioral task and immunohistochemistry, were used to examine the involvement of specific types of neurons in cross-modal plasticity. We have established a mouse model that olfactory deficit leads to a whisking upregulation, and studied how GABAergic neurons are involved in this cross-modal plasticity. In the meantime of inducing whisker tactile hypersensitivity, the olfactory injury recruits more GABAergic neurons and their fine processes in the barrel cortex, as well as upregulates their capacity of encoding action potentials. The hyperpolarization driven by inhibitory inputs strengthens the encoding ability of their target cells.


CONCLUSIONS
The upregulation of GABAergic neurons and the functional enhancement of neuronal networks may play an important role in cross-modal sensory plasticity. This finding provides the clues for developing therapeutic approaches to help sensory recovery and substitution.
Department of Physiology, Bengbu Medical College, Bengbu, Anhui, China.
Hong
H
Ni
Li
L
Huang
Na
N
Chen
Fengyu
F
Zhang
Dongbo
D
Liu
Ming
M
Ge
Sudong
S
Guan
Yan
Y
Zhu
Jin-Hui
JH
Wang
D000200:Action Potentials; D000818:Animals; D004195:Disease Models, Animal; D051379:Mice; D009474:Neurons / Q000378:metabolism*; D000857:Olfaction Disorders / Q000378:metabolism / Q000503:physiopathology*; D015854:Up-Regulation; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
D005680:gamma-Aminobutyric Acid