5-Hydroxytryptamine1B and alpha 2 adrenaline receptors in the brain of rats prenatally treated with methylazoxymethanol.

Methylazoxymethanol (MAM)-induced cerebral hypoplasia resulted in a significant increase in concentrations of 5-hydroxytryptamine (5-HT, serotonin) and norepinephrine in the frontal cortex, suggesting that these monoaminergic neurons were compressed due to smaller brain volumes. The serotonergic and noradrenergic presynaptic autoreceptors in rat brain are thought to be 5-HT1B receptors and alpha 2-adrenoceptors, respectively. If so, prenatal MAM treatment should increase the density of 5-HT1B and adrenaline alpha 2 receptors in the brain via the compression of noradrenergic and serotonergic axon terminals in the brains of rats with MAM-induced microencephaly. However, neither the densities nor the affinities of 5-HT1B and adrenaline alpha 2 receptors were changed in the MAM rats, suggesting that these presynaptic autoreceptors comprise only a small percentage of the total receptor population. Most 5-HT1B and adrenaline alpha 2 receptors were localized post-synaptically.