Glutamate Decarboxylase-immunoreactive Boutons in Synaptic Contacts with Hypothalamic Dopaminergic Cells: a Light and Electron Microscopy Study Combining Immunocytochemistry and Radioautography

Double post-embedding immunolabeling of both tyrosine hydroxylase and glutamate decarboxylase on 1-micron semi-thin sections allowed the visualization of numerous endings that use gamma-aminobutyrate as a transmitter apposed to dopaminergic cell bodies in the periventricular-arcuate hypothalamic complex. Up to fifteen glutamate decarboxylase-positive contacts per tyrosine hydroxylase-positive cell profile could be observed. In some favourable planes of section glutamate decarboxylase-positive endings were also seen in close apposition to proximal dopaminergic dendrites. About 250 tyrosine hydroxylase-positive cell profiles, whose diameter approached the maximum diameter of the dopaminergic cells, were surveyed. An average of 7.4 glutamate decarboxylase-positive contacts were counted on these profiles. From these figures it was estimated that a dopaminergic cell body was contacted on average by 75-175 terminals that use gamma-aminobutyrate as a transmitter. At the electron-microscopic level, the nature of these contacts was investigated by a method combining radioautographic detection of cell bodies having taken up tritiated dopamine and pre-embedding immunostaining of glutamate decarboxylase containing endings. Glutamate decarboxylase-positive axon terminals were seen apposed to somatic and dendritic elements. On some favorable planes of section, they were found to be engaged in morphologically defined synaptic complexes of the symmetrical or asymmetrical type. A number of the postsynaptic perikarya were labelled by tritiated dopamine and, in agreement with the light microscopic observations, they were frequently seen in contact with more than one immunopositive ending. The present findings provide a morphological substratum for a direct gamma-aminobutyrate control of the tuberoinfundibular dopaminergic neurons. Such a control could account more particularly for the central, stimulatory effects of gamma-aminobutyrate on prolactin secretion.