The neurons of axons constituting the corpus callosum are poorly understood in terms of their contribution to sensory processing in developing or mature cortex. We don't know whether they comprise a neurochemically unique or heterogeneous population of cells, or what neurochemical types of inputs they may receive. Conventional neurochemical techniques have been unsussessful in providing data on neurochemical, inputs and outputs of callosal cells. Since the loci of callosal somas are well-described in cat visual cortex and the ancillary anatomy and physiology developed to a high degree we propose to investigate the possible neurochemical identities of callosal neurons and some of their inputs using combined neurochemical/anatomical methods as follows: 1) Retrograde transcallosal transport of radiolabeled neurotransmitter candidates will be used to survery possible transmitters of callosal cells. This study is based on observations that microinjections of radioligands accumulated by specific classes of presynaptic terminals are used to localize the somas of cells giving rise to the terminal fields. Tritiatated candidates of acidic amino acids, choline, and conventional inhibitory substances, Gamma-aminobutyric acid (GABA) and glycine, will be injected at the Area 17/18 border in concentrations and rates biased for high-affinity transport. After appropriate transport time, the opposite hemicortex will be processed for light microscope autoradiography and examined for evidence of transcallosal transport. 2) A double-label technique will be used to investigate neurochemical inputs ot somas and dendritic arbors of callosal neurons. Callosal cells will be labeled in vivo by retrograde horseradish peroxidase (HRP) transport. Visual cortex containing the Area 17/18 border will be removed for preparation of in vitro brain slices which will be labeled by high affinity uptake of tritiated neurotransmitter candidates. Ligands of particular interest are GABA, acidic amino acids, norepinephrine and serotonin. Slices will be processed for light and electron microscope autoradiography, and callosal cells checked for evidence of synaptic input from labeled terminals. Such information will provide the beginnings of physiological/pharmacological assessments of collasal functions. In addition, these investigations will provide neurochemical markers that may be traced during postnatal callosal development.

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Research Project (R01)
Project #
7R01NS023330-01
Application #
3406668
Study Section
Neurology B Subcommittee 1 (NEUB)
Project Start
1985-08-01
Project End
1987-07-31
Budget Start
1985-08-01
Budget End
1986-07-31
Support Year
1
Fiscal Year
1985
Total Cost
Indirect Cost
Name
University of Tennessee Health Science Center
Department
Type
Overall Medical
DUNS #
941884009
City
Memphis
State
TN
Country
United States
Zip Code
38163