Neuroscience 2000 Abstract
| Presentation Number: | 503.1 |
|---|---|
| Abstract Title: | The ultrastructural organization of the insulin knockout mouse brain. |
| Authors: |
Beju, D.*1
; Knox, D.1
; Schechter, R.1
1William K. Warren Medical Research Institute, Univ. of Oklahoma Health Sciences Center, Tulsa, OK |
| Primary Theme and Topics |
A. Development and Regeneration - 3. Neuronal specification and differentiation |
| Secondary Theme and Topics | A. Development and Regeneration<br />- 15. Hormones and development |
| Session: |
503. Neural differentiation: extracellular factors I Poster |
| Presentation Time: | Tuesday, November 7, 2000 1:00 PM-2:00 PM |
| Location: | Hall G-J |
| Keywords: | Insulin, Immunoreactivity, Hippocampus, Subcellular |
We have shown the synthesis of insulin by neurons in the brain in vivo and in vitro. Deltour et. al. showed insulin mRNA within the mouse brain (Proc.Natl.Acad. Sci. 90:527-531,1993). We demonstrated that neuron synthesized insulin [I((n)] promotes axonal growth and neurofilament distribution. The mouse expresses insulin I and II, codified by two genes. We studied the neuronal ultrastructure on the hippocampus and olfactory bulb in the 36 hrs old mouse in which the genes for insulin were knockout [I(-/-)] (Dr. J. Jami, INSERM, Paris, France). I(-/-) mice were diagnosed by the presence of glycosuria and negative pancreatic insulin immunoreaction (IMN). Control animals [I(+/+)] showed urine glucose of <10 mg/dl and positive pancreatic IMN. The neurons showed I(n) immunoreaction within the rough endoplasmic reticulum (RER), Golgi apparatus, soma, axons and dendrites. The neurons of the I(-/-) showed no I(n) immunoreaction. I(-/-) neuronal ultrastructure showed cell disorganization characterized by: swelling of the cytoplasm, mitochondria, Golgi apparatus and RER with detachment of the ribosome, and break down of the neurofilaments and microtubules. I(+/+) maintained the characteristic neural morphology. In addition, the pancreas of the I(-/-) mouse showed fewer number of β-cells and increased numbers of exocrine cells. We demonstrated: 1) that the I(+/+) mice has positive I(n) immunoreaction with the neurons, 2) that I(n) is present in the RER, 3) that I(-/-) mouse neurons showed negative I(n) immunoreaction and 4) a severe damage in the neurons of the I(-/-). Thus, we can hypothesize that insulin has a role in brain development and may act as a trophic factor.
Supported by William K. Warren Medical Research Institute.
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2000 Neuroscience Meeting Planner. New Orleans, LA: Society for Neuroscience, 2000. Online.
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