Contrast adaptation and excitatory amino acid receptors in cat striate cortex

We have employed two paradigms to investigate the mechanisms of contrast gain control in cat striate cortex. In the first paradigm, optimal drifting gratings were presented in three consecutive periods. The contrast was near threshold in the first and third periods and accompanied by iontophoretic pulses of glutamate or glutamate receptor (GluR) agonists. The contrast was set to evoke a higher firing rate in the second period. Although both visual and iontophoretic conditions were identical in the first and third periods, responses to glutamate, N-methyl-D-aspartic acid (NMDA), and (IS,3R)-1-Aminocyclopentane-1,3-dicarboxylic acid (ACPD) were reduced following the adapting interval. (S)-alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) responses were not reduced. Administration of ionotropic GluR antagonists did not affect adaptation to the high-contrast grating. The metabotropic GluR antagonist (+/-)-alpha-Methyl-4-carboxyphenylglycine (MCPG), which acts at presynaptic glutamate autoreceptors, decreased the degree of adaptation exhibited by striate cells. In a second paradigm, contrast response functions (CRFs) were obtained at various adapting contrasts and least-squares fits to a hyperbolic ratio equation generated for each adapting level. Similar to previous reports, DL-2-amino-5-phosphonovaleric acid (APV) reduced the slope of the CRF and increased the responsiveness of the cells but did not affect the semisaturation constant, sigma, or the exponent of the CRF, n. Only MCPG significantly altered the distribution of sigma and n for 19 cells. The effect on sigma suggests that this drug can interfere with the cell's ability to shift its operating point to match the adapting contrast. These results suggest the involvement of a presynaptic mechanism for contrast adaptation. The decrease in neuronal responsiveness immediately following the high-contrast period may reflect an additional, postsynaptic effect in which there is a decrease in the NMDA-mediated component of the visual response.