Effects of cholecystokinin on Y, X, and W cells in the dorsal lateral geniculate nucleus of rats.
The role of the cholecystokinergic input to the rat's dorsal lateral geniculate nucleus (dLGN) was studied by examining the effect of iontophoretically administered CCK-8S on the neuronal response to stimulation of the receptive field center. Peristimulus activity was recorded extracellularly from 108 neurons grouped according to the type of receptive field (OFF, ON, or ON-OFF) and classified with respect to their Y, X, or W properties by means of discriminant analysis. CCK affected the response to a center-sized spot of light in two thirds of the neurons investigated. The center response decreased in 50 of 73 CCK-sensitive neurons (69%), predominantly in Y OFF and X OFF center cells (17 of 19). In the remaining 23 cells the center response increased, most consistently (11 of 17) in W ON center cells. Center and surround responses were similarly influenced. Inhibitions and excitations induced by CCK-8S were reproducible, dose dependent, and receptor mediated. The CCKB antagonist PD 135158 reduced the CCK effects in 10 of 14 cells; the CCKA antagonist KL 1001 reduced the CCK effects in 17 of 36 cells. The CCK-induced inhibition was B-receptor specific in 4 of 8 cells, A-receptor specific in 2 of 8 cells, and partially mediated by each of the two types of receptor in the remaining 2 cells. Blocking by the CCKA antagonist was more frequently observed in W cells than in cells with Y or X characteristics. The data show that CCK modifies the activity of dLGN cells in a variable direction depending on the specific cell type (Y, X, W) and response pattern (OFF, ON). The effects of CCK are discussed in relation to proposed functions of the superior collicular input to the dLGN.[1]References
- Effects of cholecystokinin on Y, X, and W cells in the dorsal lateral geniculate nucleus of rats. Gabriel, S., Gabriel, H.J., Grützmann, R., Berlin, K., Davidowa, H. Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale. (1996) [Pubmed]
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