Formation of GABA-Aα1 and GABA-B1 receptor-mediated inhibitory network in the ventrolateral part of the solitary tract nucleus during the early postnatal period under normal conditions and prenatal serotonin deficiency

Аннотация

Time course of formation of the inhibitory receptor network (GABA-Aα1 and GABA-B1) in the respiratory subnuclei (ventral and lateral) of the solitary tract (NTS) during the early postnatal period was studied on laboratory Wistar rats under normal conditions and prenatal serotonin deficiency. It was found that in normal rats the maturation of the inhibitory receptor networks in both NTS subnuclei occurs within the first three postnatal weeks. Some features of their formation were noticed. The dynamics of changes in intensity of GABA-Аα1 expression in the ventral and lateral subnuclei proceeds in a similar way. During the first postnatal week, GABA-Aα1 expression is low. In the neuropil, the network of GABA-Aα1-containing presynaptic terminals and synapses is poorly developed. Within the second week, the number of GABA-Aα1-expressing neurons increases in both subnuclei with a simultaneous rise in the density of the network of terminals and synaptic structures. By the end of the third week, the number of GABA-Aα1-expressing neurons decreases, but the network density continues to increase. GABA-B1 expression in the ventral and lateral subnuclei occurs also simultaneously, although with some distinctions. During the first postnatal week, intensity of GABA-B1 expression is weak. In the neuropil, few GABA-B1-containing terminals form a loose network with sporadic synaptic structures. During the second week, expression of the receptor increases, being particularly considerable in the ventral subnuclei. Simultaneously, the density of the presynaptic terminals increases. By the end of the third week, the number of GABA-B1-expressing neurons in the ventral subnuclei decreases, while in the lateral subnuclei remains almost intact and the network density increases. The data obtained show that prenatal serotonin deficiency leads to malformation and impaired maturation of the GABAergic inhibitory neuronal network in the ventrolateral part of NTS.