Abstract

In brainstem-spinal cord preparations of neonatal control C3H and transgenic Tg8 mice where deletion of the gene encoding monoamine oxidase-A results in serotonin (5-hydroxytryptamine (HT)) excess, whole cell recordings of identified phrenic motoneurons (Phr Mns) were performed to study the modulation of their activity by 5-HT. In C3H mice, a dual effect was observed: (i) a facilitation via 5-HT 2A receptors and (ii) a decrease of the transmission of the central inspiratory drive via 5-HT 1B receptors. In Tg8 mice, the 5-HT 2A-mediated facilitation was present but the 5-HT 1B-mediated decrease was lacking. Therefore, the conservation of the 5-HT 2A response vs. the loss of the 5-HT 1B one suggest that the two types of receptors respond differently to 5-HT level changes.

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