GABAergic neurons in rat nuclei of solitary tracts receive inhibitory-type synapses from amygdaloid efferents lacking detectable GABA-immunoreactivity.
Academic Article
Overview
abstract
Gamma-aminobutyric acid (GABA) is a prominent inhibitory transmitter in both the central nucleus of the amygdala (Ce) and the medial nuclei of the solitary tracts (mNTS). These regions are reciprocally connected by anatomical pathways mediating the coordinated visceral responses to emotional stress. To further determine whether GABA is present in the amygdaloid efferents or their targets in the mNTS, we combined peroxidase labeling of Phaseolus vulgaris leucoagglutinin (PHA-L) or biotinylated dextran amine (BDA) anterogradely transported from the Ce with immunogold-silver detection of antibodies against GABA in the rat mNTS. By light microscopy, peroxidase labeling for either PHA-L or BDA was seen in varicose processes, whereas immunogold-silver labeling for GABA was detected in perikarya and processes throughout the rostrocaudal mNTS. The intermediate mNTS at the level of the area postrema, a region receiving mainly cardiorespiratory and gastric visceral afferents, were examined by electron microscopy. In this region, anterograde labeling was observed exclusively in unmyelinated axons and axon terminals. These terminals lacked detectable GABA-immunoreactivity, but formed symmetric synapses that are associated with inhibition. The targets of the anterogradely labeled terminals were medium-sized dendrites both with and without GABA-labeling. These dendrites often also received convergent input from terminals that were intensely GABA-immunoreactive. We conclude that visceral activation accompanying emotional response to stress is likely to involve inhibition of GABAergic neurons in the mNTS by non-GABA-containing amygdaloid efferents. Furthermore, our results indicate that the inhibition of these GABAergic neurons may be further augmented by release of GABA from other converging terminals in the mNTS.
