At the next stage of neural processing, a mixture of L- and M-cones jointly contact ON and OFF diffuse bipolar cells, which in turn contact ON and OFF parasol ganglion cells of the same polarity (e.g., Polyak,
1941; Boycott & Dowling,
1969; Mariani,
1981; Boycott & Wässle,
1991; Jacoby, Stafford, Kouyama, & Marshak,
1996; Jacoby, Wiechmann, Amara, Leighton, & Marshak,
2000). In the fovea, diffuse bipolar cells contact about five to 10 L- and M-cones through the bipolar cells' dendritic arborisations (Boycott & Wässle,
1991; Calkins, Tsukamato, & Sterling,
1996; Calkins & Sterling,
2007), so that the spectral sensitivities of diffuse bipolar centers will be a combination of the L- and M-cone spectral sensitivities. The diffuse bipolar cells and parasol ganglion cells form the substrate of the magnocellular pathway that projects to the cortex via the magnocellular layers of the LGN (Leventhal, Rodieck, & Dreher,
1981; Perry, Oehler, & Cowey,
1984; Rodieck, Binmoeller, & Dineen,
1985). The magnocellular pathway is thought to provide the physiological substrate of the psychophysical luminance or achromatic pathway (e.g., Livingstone & Hubel,
1987; Lee, Martin, & Valberg,
1988; Lee, Pokorny, Smith, Martin, & Valberg,
1990; Smith et al.,
1992), and thus to be responsible for psychophysical performance in our achromatic flicker cancellation task.