Autism causes neuropathological changes in varied anatomical loci. A coherent neural mechanism to explain the spectrum of autistic symptomatology has not been proposed because most anatomical researchers focus on point-to-point functional neural systems (e.g. auditory, social networks) rather than considering global chemical neural systems. Serotonergic neurons have a global innervation pattern. Their cell bodies are found in the midbrain but they project their axons throughout the neural axis beginning in the fetal brain. This global system is implicated in autism by animal models and by biochemical, imaging, pharmacological, and genetics studies. However, no anatomical studies of the 5-HT innervation of autistic donors have been reported. Our review presents immunocytochemical evidence of an increase in 5-HT axons in post-mortem brain tissue from autism donors aged 2.8 to 29 years relative to controls. This increase is observed in the principle ascending fiber bundles of the medial and lateral forebrain bundles, and in the innervation density of the amygdala and the piriform, superior temporal, and parahippocampal cortices. In autistic donors eight years of age and up, several types of dystrophic 5-HT axons were seen in the termination fields. One class of these dystrophic axons, the thick heavily stained axons, was not seen in the brains of patients with neurodegenerative diseases. These findings provide morphological evidence for the involvement of serotonin neurons in the early etiology of autism, and suggest a diet therapy may be effective to blunt serotonin’s trophic actions during early brain development in children.
An improved plasma clot culture system was developed for the culture of rat megakaryocyte colonies in vitro. Greater stimulation of megakaryocyte colony growth was provided when both serum and plasma were added to the culture medium than when plasma was added alone. Freeze-thawed extracts prepared from 900 x 10(6) platelets/ml saline and also 9 ng/ml of human platelet-derived growth factor (PDGF) caused maximum increases over the controls of 71% and 42%, respectively, in the numbers of megakaryocyte colonies. The increase in the numbers of megakaryocyte colonies induced by platelet extracts and by PDGF implied that substance(s) released by platelets might play an important role in the control of megakaryocytopoiesis.
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