We will study at the cellular level the mechanisms responsible for the onset of sensory discharges in the carotid nerve. Some of these mechanisms are not entirely understood. Mainly two projects will be undertaken: a) Establishing whether or not there are sensory synapses in these receptors. To do this we will use carotid body (c.b.) slices of cats or rabbits and the mouse c.b. for intracellular recording and stimulation of glomus cells and nerve endings under visual observation. Preliminary experiments indicate that glomus cells are depolarized by acid and cholinergic substances and hyperpolarized by CN. We will employ also voltage clamping to determine current flows and current noise in the cells at rest and during stimulation. Intracellular recordings from nerve endings have shown numerous """"""""spontaneous"""""""" depolarizing potentials. During stimulation their frequency increases and this leads to nerve ending depolarization. S.d.p.'s may be produced by chemicals released from the cells. We will study then the pharmacology and ionic effects on their development and the effect of nerve ending stimulation on cell potentials. b) Trophic or inductive effects of the periphery (glomus cells) on sensory axons will be studied by implanting the c.b. in different areas and reinnervating it with foreign nerves. Also, intracellular recording from ganglion cells connected to chemo- or other receptors should indicate if neuronal spikes change after innervating foreign peripheral structures. Tissue culture will determine if chemoreception occurs before or after nerve processes make contact with glomus cells. These studies should indicate if sensory nerves are predetermined for a given task or whether they are conditioned for the job by influences from peripheral elements. The activity of denervated or foreign reinnervated glomus cells will be studied with intracellular recording since some cell functions are lost after denervation. Thus, experiments proposed in a and b should resolve whether there are peripheral receptor synapses and to what extent peripheral or preneural elements influence the function of sensory axons. Also, the extent of trophic influences of axons on the cells.

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Research Project (R01)
Project #
5R01NS005666-21
Application #
3393412
Study Section
Neurology B Subcommittee 1 (NEUB)
Project Start
1978-01-01
Project End
1985-12-31
Budget Start
1985-01-01
Budget End
1985-12-31
Support Year
21
Fiscal Year
1985
Total Cost
Indirect Cost
Name
University of Utah
Department
Type
Schools of Medicine
DUNS #
City
Salt Lake City
State
UT
Country
United States
Zip Code
84112