Impairments in the sense of taste are debilitating, adversely affecting the quality of life and jeopardizing health. Specific and unequivocal impairments in taste responsiveness in rats result from gustatory nerve injury. This strongly suggests that information transmitted in the various nerves is to some extent differentially channeled through neural circuits in the brain that are involved with different taste functions. When the transected chorda tympani nerve (CT) or glossopharyngeal nerve (GL) regenerate to reinnervate their appropriate receptor fields, taste functions that are normally impaired by their respective transection entirely recover despite a reduction in the number of regenerated taste buds. For the GL, this includes the recovery of the spatially distinct pattern of neural activity in the nucleus of the solitary tract [NST] (as assessed by Fos-like immunoreactivity) stimulated by oral application of quinine. The purpose of the research here is to extend these findings in new and important ways to help clarify the peripheral organization of the gustatory system. A-response operant discrimination procedure will be modified so that it can be used to measure just-noticeable-differences (JNDs) in intensity in a rat models. This will provide animal researchers with a tool to quantitatively assess stimulus intensity processing in the suprathreshold range and provide a more challenging task to discern the consequences of taste nerve transection and regeneration. The capacity of the gustatory system to maintain function when input from taste receptor fields is channeled through atypical central gustatory circuits will also be tested. This will be accomplished by the use of sophisticated psychophysical procedures to behaviorally test rats that have cross- regenerated nerves in which the taste input of the anterior tongue is channeled through the GL or the taste input of the posterior tongue is channeled through the CT. Through the use of c-Fos immunohistochemistry, the extent to which the topography or quinine- induced neural activity in the NST and parabrachial nucleus is altered by cross regeneration of the CT and GL will be examined. These experiments will provide a useful functional framework to help guide the search for the neural circuits underlying taste-related behavior as well as begin to define the functional boundaries of neural plasticity in the gustatory system.

Agency
National Institute of Health (NIH)
Institute
National Institute on Deafness and Other Communication Disorders (NIDCD)
Type
Research Project (R01)
Project #
5R01DC001628-11
Application #
6719524
Study Section
Special Emphasis Panel (ZRG1-IFCN-2 (03))
Program Officer
Davis, Barry
Project Start
1993-12-01
Project End
2008-03-31
Budget Start
2004-04-01
Budget End
2005-03-31
Support Year
11
Fiscal Year
2004
Total Cost
$296,421
Indirect Cost
Name
University of Florida
Department
Psychology
Type
Schools of Arts and Sciences
DUNS #
969663814
City
Gainesville
State
FL
Country
United States
Zip Code
32611
Spector, Alan C; Schier, Lindsey A (2018) Behavioral evidence that select carbohydrate stimuli activate T1R-independent receptor mechanisms. Appetite 122:26-31
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King, Camille Tessitore; Garcea, Mircea; Spector, Alan C (2014) Restoration of quinine-stimulated Fos-immunoreactive neurons in the central nucleus of the amygdala and gustatory cortex following reinnervation or cross-reinnervation of the lingual taste nerves in rats. J Comp Neurol 522:2498-517
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King, Camille T; Garcea, Mircea; Stolzenberg, Danielle S et al. (2008) Experimentally cross-wired lingual taste nerves can restore normal unconditioned gaping behavior in response to quinine stimulation. Am J Physiol Regul Integr Comp Physiol 294:R738-47
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Jiang, Enshe; Blonde, Ginger; Garcea, Mircea et al. (2008) Greater superficial petrosal nerve transection in rats does not change unconditioned licking responses to putatively sweet taste stimuli. Chem Senses 33:709-23

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