The olfactory system provides a uniquely powerful environment in which to explore sensory plasticity in mammals, because the earliest central processing in the olfactory system takes place in the glomeruli of the olfactory bulb, a structure that is physically and optically accessible in vivo in animal models, and because recent advances in molecular genetic technology have produced excellent experimental tools for studies in this area. Using a combination of molecular genetic tools and in vivo optical imaging techniques, I have recently shown that the olfactory system exhibits rapid feedback presynaptic inhibition of transmitter release from the olfactory nerve. I hypothesize that the rapid plasticity of this circuit provides adaptive gain control for the primary sensory input from the nose, and thus plays a major role in the encoding of odorant concentration and the perception of odor intensity. Moreover, preliminary data suggest that this inhibitory circuitry may change over time to accommodate changes in the olfactory environment.
The first aim of these experiments is to test the hypothesis that this presynaptic modulation of primary sensory input to the olfactory bulb contributes to the encoding of odor concentration.
The second aim of these experiments is to use optical imaging techniques to test the hypothesis that changes in sensory environment induces plasticity in the representation of odors at the input to the olfactory bulb.
The final aim of these experiments is to use behavioral assays to test how this plasticity affects the perception of odor quality and intensity.

Public Health Relevance

Mammalian sensory systems constantly change to adapt to their environment and experience. While adaptation in some sensory organs is well understood, much less is knwn about how circuitry in the brain changes to handle different sensory situations. Basic research into this question is needed to better inform the treatment of patients with sensory problems and to enhance the development of artificial sensors.

Agency
National Institute of Health (NIH)
Institute
National Institute on Deafness and Other Communication Disorders (NIDCD)
Type
Research Transition Award (R00)
Project #
5R00DC009442-06
Application #
8288860
Study Section
Special Emphasis Panel (NSS)
Program Officer
Sullivan, Susan L
Project Start
2009-07-15
Project End
2014-03-31
Budget Start
2012-07-01
Budget End
2014-03-31
Support Year
6
Fiscal Year
2012
Total Cost
$172,138
Indirect Cost
$60,722
Name
Rutgers University
Department
Psychology
Type
Schools of Arts and Sciences
DUNS #
001912864
City
New Brunswick
State
NJ
Country
United States
Zip Code
08901
Kass, Marley D; Moberly, Andrew H; McGann, John P (2013) Spatiotemporal alterations in primary odorant representations in olfactory marker protein knockout mice. PLoS One 8:e61431
Kass, Marley D; Pottackal, Joseph; Turkel, Daniel J et al. (2013) Changes in the neural representation of odorants after olfactory deprivation in the adult mouse olfactory bulb. Chem Senses 38:77-89
Kass, Marley D; Moberly, Andrew H; Rosenthal, Michelle C et al. (2013) Odor-specific, olfactory marker protein-mediated sparsening of primary olfactory input to the brain after odor exposure. J Neurosci 33:6594-602
McGann, John P (2013) Presynaptic inhibition of olfactory sensory neurons: new mechanisms and potential functions. Chem Senses 38:459-74
Czarnecki, Lindsey A; Moberly, Andrew H; Turkel, Daniel J et al. (2012) Functional rehabilitation of cadmium-induced neurotoxicity despite persistent peripheral pathophysiology in the olfactory system. Toxicol Sci 126:534-44
Moberly, Andrew H; Czarnecki, Lindsey A; Pottackal, Joseph et al. (2012) Intranasal exposure to manganese disrupts neurotransmitter release from glutamatergic synapses in the central nervous system in vivo. Neurotoxicology 33:996-1004
Czarnecki, Lindsey A; Moberly, Andrew H; Rubinstein, Tom et al. (2011) In vivo visualization of olfactory pathophysiology induced by intranasal cadmium instillation in mice. Neurotoxicology 32:441-9