1. The large, alpha type retinal ganglion cells (M-cells) that project
to the magnocellular layers of the lateral geniculate nucleus (LGN) a
re thought to be preferentially damaged in glaucoma. To test this hypo
thesis, we employed microelectrode recording techniques to analyze the
response properties of individual LGN neurons in both the parvo- and
magnocellular layers of nine monkeys with experimental glaucoma. 2. Th
e intraocular pressure of one eye of each monkey was elevated by laser
trabeculoplasty. The electrophysiological experiments were conducted
following survival periods of 20-52 months. 3. We found a reduction in
the encounter rate for neurons in LGN laminae innervated by the treat
ed eyes that varied as a function of eccentricity. However, in a given
animal the relative reduction in retinal inputs was the same for both
the parvo- and magnocellular layers. Quantitative investigations of o
rientation bias and spatial frequency tuning for individual cells demo
nstrated that the surviving LGN neurons had normal response properties
, when receptive field eccentricity was taken into account. 4. Our res
ults indicate that (1) the visual losses in long-standing experimental
glaucoma are due to retinal ganglion cell loss rather than a reductio
n in the functional capacity of surviving neurons, and (2) the retinal
ganglion cells that project to the magnocellular LGN are not selectiv
ely damaged in long-standing experimental glaucoma. It appears that th
e larger members of all functional ganglion cell classes are more susc
eptible to glaucomatous damage than their respective smaller members.