Studies are proposed to examine further the transmitter-specific cell classes, afferent brainstem pathways, and synaptic circuitry of the cat superior colliculus and to study how these are altered by monocular deprivation.
Three aims are proposed for the current grant period.
The first aim i s to study further the synaptic connections and molecular properties of putative GABAergic neurons in the superior colliculus. We propose to: (1) determine whether one or more types of GABA labeled cell project to nuclei of the dorsal thalamus; (2) determine whether cells labeled by the anti-GABA are also labeled by peptide antibodies, including cholecystokinin, somatostatin, and substance P; (3) determine whether specific GABA cell classes are also labeled by antibodies to the calcium binding proteins parvalbumin and calbindin D; (4) examine the distribution of an antibody to the GABAa receptor complex and determine whether the receptor is associated with specific classes of GABA cell. Antibodies will be localized using double-label immunocytochemistry at the light and electron microscope levels and measured using computer-assisted quantitative image analysis.
The second aim i s to study the synaptic organization of norepinephrine (NE) inputs to the superior colliculus. We propose to: (1) determine the synaptic connections between fibers labeled by an antibody to dopamine- Beta-hydroxylase and specific sensory afferents and intrinsic neurons of SC using serial section reconstruction. (3) determine whether the density, distribution, or synaptic organization of NE fibers is altered by monocular deprivation (MD) as measured with an image analyzer.
The third aim i s to examine the synaptic organization of acetylcholine (ACh) pathways to the superior colliculus. We propose to: (1) examine the synaptic relationships of fibers labeled by an antibody to choline acetyltransferase (ChAT) using serial section reconstruction; (2) determine the distribution of an antibody to the AChR nicotinic receptor with the light and electron microscopes; (3) determine whether there are alterations in the distribution or density of ChAT labeled fibers or the AcHR nicotinic receptor produced by MD. These results will characterize in detail the transmitter-specific synaptic circuitry which underlies cellular physiology in the superior colliculus and determine how specific synapses and receptors are altered by developmental abnormalities.

Agency
National Institute of Health (NIH)
Institute
National Eye Institute (NEI)
Type
Research Project (R01)
Project #
5R01EY002973-11
Application #
3257287
Study Section
Visual Sciences B Study Section (VISB)
Project Start
1979-08-01
Project End
1991-12-31
Budget Start
1991-01-01
Budget End
1991-12-31
Support Year
11
Fiscal Year
1991
Total Cost
Indirect Cost
Name
University of Tennessee Health Science Center
Department
Type
Schools of Medicine
DUNS #
941884009
City
Memphis
State
TN
Country
United States
Zip Code
38163
Mize, R Ranney; Graham, Sean K; Cork, R John (2002) Expression of the L-type calcium channel in the developing mouse visual system by use of immunocytochemistry. Brain Res Dev Brain Res 136:185-95
Lo, Fu-Sun; Mize, R Ranney (2002) Properties of LTD and LTP of retinocollicular synaptic transmission in the developing rat superior colliculus. Eur J Neurosci 15:1421-32
Scheiner, C A; Kratz, K E; Guido, W et al. (2001) Prenatal and postnatal expression of nitric oxide in the developing kitten superior colliculus revealed with NADPH diaphorase histochemistry. Vis Neurosci 18:43-54
Lo, F S; Mize, R R (2000) Synaptic regulation of L-type Ca(2+) channel activity and long-term depression during refinement of the retinocollicular pathway in developing rodent superior colliculus. J Neurosci 20:RC58
Mize, R R; Butler, G D (2000) The NMDAR1 subunit of the N-methyl-D-aspartate receptor is localized at postsynaptic sites opposite both retinal and cortical terminals in the cat superior colliculus. Vis Neurosci 17:41-53
Wu, H H; Cork, R J; Huang, P L et al. (2000) Refinement of the ipsilateral retinocollicular projection is disrupted in double endothelial and neuronal nitric oxide synthase gene knockout mice. Brain Res Dev Brain Res 120:105-11
Mize, R R; Lo, F (2000) Nitric oxide, impulse activity, and neurotrophins in visual system development(1). Brain Res 886:15-32
Wu, H H; Cork, R J; Mize, R R (2000) Normal development of the ipsilateral retinocollicular pathway and its disruption in double endothelial and neuronal nitric oxide synthase gene knockout mice. J Comp Neurol 426:651-65
Cork, R J; Calhoun, T; Perrone, M et al. (2000) Postnatal development of nitric oxide synthase expression in the mouse superior colliculus. J Comp Neurol 427:581-92
Scheiner, C A; Cork, R J; Mize, R R (1999) Failure to disrupt development of cholinergic fiber patches in the superior colliculus in nitric oxide synthase deficient mice. Brain Res Dev Brain Res 118:217-20

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