Journal of Neurocytology

, Volume 15, Issue 5, pp 645–655

Electron microscopy of glutamate decarboxylase (GAD) immunoreactivity in the inner plexiform layer of the rhesus monkey retina

Authors

  • Andrew P. Mariani
    • Laboratory of Neurophysiology, National Institute of Neurological and Communicative Disorders and StrokeNational Institutes of Health
  • Maria T. Caserta
    • Laboratory of Neurophysiology, National Institute of Neurological and Communicative Disorders and StrokeNational Institutes of Health
Article

DOI: 10.1007/BF01611863

Cite this article as:
Mariani, A.P. & Caserta, M.T. J Neurocytol (1986) 15: 645. doi:10.1007/BF01611863

Summary

With indirect immunofluorescence, glutamate decarboxylase (GAD), the GABA synthesizing enzyme, was localized to cell bodies in the inner half of the inner nuclear layer and a few in the outer tier of the ganglion cell layer in the rhesus monkey retina. In the inner plexiform layer there were three strongly GAD-immunoreactive laminae separated by two less immunoreactive laminae. Electron microscopy demonstrated that the GAD was contained in amacrine cells and these GAD-immunoreactive amacrines were primarily pre- and postsynaptic to biopolar cell axon terminals. The GAD-containing processes possessed small synaptic vesicles and formed synapses that could be characterized as symmetrical. Large, dense-cored vesicles were often found in the cell bodies and synaptic processes of the GAD-immunoreactive amacrine cells. As the vast majority of the synaptic input and output of the GAD-containing amacrine cells was to and from bipolar cells and the strongest GAD-immunoreactivity correlated with the endings of bipolar cells that connect with a single cone, the functional effects of GABA in the primate retina are likely to be found in the responses of single cone pathways in the inner plexiform layer.

Copyright information

© Chapman and Hall Ltd. 1986