Morphologic and neurochemical studies of embryonic brain development in murine trisomy 16.
Telencephalic and diencephalic/brainstem regions from embryonic trisomy-16 mice (Ts16) between gestational days 15-18 were analyzed for alterations of morphologic and neurochemical parameters and compared to phenotypically normal littermates. Mean trisomic wet weights from both regions were significantly diminished (greater than 20%) and total protein content was reduced. Ratios of the thickness of the ventricular (germinal) zone to the thickness of the whole cortex were increased, suggesting a delay in neuronal differentiation. Pre- and postsynaptic markers for GABAergic, cholinergic, catecholaminergic and serotonergic transmitter systems were compared. A significant impairment of the trisomic brain catecholaminergic and serotonergic system development was observed, based upon regional reductions in norepinephrine, dopamine and serotonin content. Choline acetyltransferase activity in the diencephalon/brainstem was reduced by 21-26% in contrast to normal levels within the cerebral hemispheres. Presynaptic GABAergic markers were not affected in the Ts16 embryos. It is concluded that although a genetic imbalance involving chromosome 16 in the mouse embryo produces a delay in neurogenesis, it has a more selective effect on the catecholaminergic, serotonergic and cholinergic systems than on GABAergic neurons.
D000596:Amino Acids / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000002:abnormalities / Q000196:embryology* / Q000378:metabolism; D002395:Catecholamines / Q000378:metabolism; D004298:Dopamine / Q000378:metabolism; D051379:Mice; D018377:Neurotransmitter Agents / Q000378:metabolism*; D012701:Serotonin / Q000378:metabolism; D014314:Trisomy; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D000596:Amino Acids; D002395:Catecholamines; D018377:Neurotransmitter Agents; D012701:Serotonin; D005680:gamma-Aminobutyric Acid; D004298:Dopamine