Objective: Prenatal cigarette smoke exposure (PCSE) is associated with numerous neurodevelopmental abnormalities such as respiratory depression. Although it is clear that 5-HT2A receptors play an important role in the generation and regulation of respiratory rhythm, but the role of 5-HT2A receptors in the depression of respiratory rhythmic discharge activity (RRDA) of medullary slice of neonatal rats with prenatal cigarette smoke exposure is not well understood.
Methods: 1-(2, 5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI), a 5-HT2A receptor agonist, could excite RRDA of control group and experimental group, and the effects of DOI on control group was stronger than those on experimental group; ketanserine, a 5-HT2A receptor antagonist, had inhibitory effects on RRDA of the two groups, and the inhibitory effects on control group was stronger than those on experimental group. The western blotting and RT-qPCR technology were used to detect whether 5-HT2A receptors protein and 5-HT2A receptors mRNA would be changed or not.
Results: We found that the expression of 5-HT2A receptors protein were down-regulation, and the expression of 5-HT2A receptors mRNA had not changed. Conclusion: The possible mechanism of PCSE inhibition respiratory rhythmic discharge activity in the medullary slice of neonatal rats is the decrease of the function of 5-HT2A receptors and down-regulation of protein expression.
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