Specific inhibition of natural killer (NK) activity against different alloantigens

Allogeneic lymphocyte cytotoxicity (ALC), i. e., rapid rejection of i. v. injected allogeneic lymphocytes in unprimed hosts, is an example of NK activity. Apparently anomalous rejection patterns, such as acceptance of F₁ hybrid cells by parental hosts and rejection of parental cells by F₁ hybrid hosts in many strain combinations, would fit the hypothesis that the effector cells in ALC recognize the absence of certain self-molecules (passwords) rather than the presence of nonself determinants. However, cold target inhibition studies showed that ALC displays allospecificity: when a mixture of radiolabeled AO and DA cells were injected i. v. into euthymic or athymic PVG rats, adding a surplus of cold DA cells reduced killing only of labeled DA cells and vice versa. Furthermore, semiallogeneic cold target cells were ineffective in inhibiting elimination of fully allogeneic cells, which supports the argument against a modification of the hypothesis that self-determinants inhibit a postbinding stage of lysis. Finally, (DA × AO)F₁ cells injected into (DA × PVG)F₁ hosts were rapidly rejected, despite the fact that donor and host shared expressed DA determinants. In sum, our results show that a hypothesis based on inhibition of killing by self-determinants can only be sustained with extensive modifications, and favor the alternative mechanism that the effector cells positively recognize the presence of allospecific determinants on the target cell surface.     

Effects of chorda tympani nerve anesthesia on taste responses in the NST

Human clinical and psychophysical observations suggest that the taste system is able to compensate for losses in peripheral nerve input, since patients do not commonly report decrements in whole mouth taste following chorda tympani nerve damage or anesthesia. Indeed, neurophysiological data from the rat nucleus of the solitary tract (NST) suggests that a release of inhibition (disinhibition) may occur centrally following chorda tympani nerve anesthesia. Our purpose was to study this possibility further. We recorded from 59 multi- and single- unit taste-responsive sites in the rat NST before, during and after recovery from chorda tympani nerve anesthesia. During anesthesia, average anterior tongue responses were eliminated but no compensatory increases in palatal or posterior tongue responses were observed. However, six individual sites displayed increased taste responsiveness during anesthesia. The average increase was 32.9%. Therefore, disinhibition of taste responses was observed, but infrequently and to a small degree in the NST At a subset of sites, chorda tympani-mediated responses decreased while greater superficial petrosal-mediated responses remained the same during anesthesia. Since this effect was accompanied by a decrease in spontaneous activity, we propose that taste compensation may result in part by a change in signal-to-noise ratio at a subset of sites.