Neuroscience 2004 Abstract
| Presentation Number: | 1028.3 |
|---|---|
| Abstract Title: | MIGRATION AND DIFFERNTION DISORDER OF SEROTONERGIC NEURON IN THE EMBRYONAL THALIDOMIDE/VALPROIC ACID EXPOSED AUTISM MODEL RATS. |
| Authors: |
Konno, J.*1
; Narita, M.1
; Narita, N.1
1Dept Basic Med Sci, Univ Tsukuba, Tsukuba, Japan |
| Primary Theme and Topics |
Neurological and Psychiatric Conditions - Psychiatric Disorders -- Autism/related disorders |
| Session: |
1028. Autism-Related Disorders II Poster |
| Presentation Time: | Wednesday, October 27, 2004 3:00 PM-4:00 PM |
| Location: | San Diego Convention Center - Hall A-H, Board # EEE15 |
| Keywords: |
We have recently established an autism model rat by exposing embryonic day (E) 9 rat to known autism-inducible teratogen, thalidomide (THAL) or valproic acid (VPA). They showed;1)hyperserotonemia and significant increase of serotonin concentration in the hippocampus (Narita et.al.,Pediatr Res 2002),2)dramatic shift of the distribution of serotonergic neuron in the dorsal raphe nuclei, the origin of serotonergic neurons (Miyazaki et.al.,Int J Dev Neurosci, in press),3)behaviral defects in learning and memory examinations (Miyahara et. al., SFN meeting 2003). Since these phenotypes are, to some extent, relevant to human autistic phenotype, we hypothesized that disorganized serotonergic neuronal development commonly triggered by the teratogens in the model rats may play a key role in autism. We aimed to observe the effects of the E9-exposed teratogens on later serotonergic neuronal differentiation and migration. THAL, VPA, or vehicle was orally administered to pregnant rats on E9, and the embryos were dissected out on E15 or E18 to perform immunohistochemical study using anti-serotonin antibody. We found that the caudal cluster of raphe nuclei, which already appeared in the controls on E15, was not seen in the THAL or VPA-exposed embryos. The serotonin-positive cells in the rostral cluster of raphe nuclei were significantly smaller in size and the serotonergic neuronal projections were underdeveloped and sparse in the teratogen-exposed embryos compared to the control on E15. These results suggested that E9 THAL/VPA exposure identically results in retarded differentiation and migration of the serotonergic neurons in the raphe nuclei compared to the controls. We suspect that serotonergic dysfunction triggered by E9 exposure to teratogens is responsible for the biochemical, morphological, and behavioral changes found in the autism model rats, and that might be relevant to core pathogenesis of human autism.
Supported by Naoko Narita
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2004 Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience, 2004. Online.
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