Distribution of GAT1 GABA Transporter Levels in the Bötzinger Complex at the Early Stages of Postnatal Development in Rats with Prenatal Serotonin Deficiency

Abstract

Objective. To study the distribution of GAT1 GABA transporter in the Botzinger complex at different time points in early postnatal development in rats in normal conditions and after prenatal serotonin deficiency. Materials and methods. Studies were performed on Wistar laboratory rats. Decreases in endogenous serotonin levels in the embryonic period were produced by inhibition of tryptophan hydroxylase with para-chlorophenylalanine (PCPA). GAT1 transporter protein was detected using an immunohistochemical reaction with primary rabbit anti-GABA transporter 1 polyclonal antibodies (AbCam, UK). Brains were studied on postnatal days 5, 10, and 20. Results. At the early periods of postnatal development, the Botzinger complex of control animals showed oscillations in the GAT1 GABA transporter level. At one week of life, the GAT1 level was high, both in networks of processes and terminals and in synapses. During the second week of life, the GAT1 level decreased, and by the end of the third week it again increased, reaching the initial level. Serotonin deficiency during the prenatal period induced a significant increase in the GAT1 level in the neuropil of the Botzinger complex in the experimental animals at all time points of postnatal development. Conclusions. Prenatal serotonin deficiency led to a significant increase in the level of GAT1 GABA transporter in the early periods of postnatal development, which may lead to changes in GABA transmission and, as a result, disruption of the balance between inhibitory and excitatory effects in the respiratory nucleus.