Organization and actions of the noradrenergic input to the hamster's superior colliculus

Abstract

Immunocytochemistry using antisera directed against dopamine‐hydroxylase (DBH) was used to determine the organization of the noradrenergic (NE) input to the hamster's superior colliculus (SC). Immunocytochemistry for DBH was combined with retrograde transport of fluorogold (FG) to determine the sources of NE input to SC. Microiontophoretic techniques were used together with extracellular single unit recording and receptive field mapping techniques to determine the manner in which NE influenced the responses of individual SC neurons. The hamster's SC contained numerous DBH‐positive fibers but no immunopositive cells. These fibers formed a plexus that was most dense in the lower stratum griseum superficiale SCS. The density of DBH‐positive fibers was very low in the stratum opticum SO and increased in density in the stratum griseum intermediale SGI and the other deep layers. When FG injections into the SC were combined with immunocytochemical detection of DBH, double‐labeled cells were observed in the contralateral locus ceruleus. DBH‐positive neurons were observed in several other portions of the mesencephalon and pons, but none of these were labelled with FG. The effects of NE iontophoresis were assessed for a total of 135 SC neurons. In 74% N = 100, NE reduced spontaneous and/or stimulus evoked activity. In 3% (N = 4 cells), NE increased activity, and in 23%; N = 31 cells it had no effect. These percentages were essentially the same for superficial layer visual cells and somatosensory neurons in the deep laminae. The effect of NE iontophoresis upon signal to noise ratios was assessed for 46 visual and 56 somatosensory neurons. For 54% (N = 25) of the visual cells and 16% N = 9 of the somatosensory cells, NE iontophoresis decreased signal to noise ratios. For 13% N = 6 of the visual cells and 21% N = 12 of the somatosensory cells, NE iontophoresis increased signal to noise ratios. The effects of NE on the responsivity of SC neurons were antagonized by propranolol 86% of the 21 cells tested, sotalol 67% of the six cells tested, and atenolol effective in the single cell tested. All these agents are β‐adrenergic antagonists. The single β‐adrenergic antagonist that we evaluated, corynanthine, potentiated the effects of NE on the responsivity of the two SC neurons that we tested.