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Bloch and Bonvallet (1960a), however, emphasize the importance of the level of anesthesia in these experiments. They show that, "le puissant controle inhibiteur bulbaire ne peut etre mis en evidence qu'apres suppression ou depression de Tinfluence predominante des formations activatrices mesencephaliques, dont Tactivite a son tour ne peut etre observee, a l'etat pour qu'apres suppression des decharges inhibitrices retroactives corticifuges [1960a, p. 4 5 ] . " They also go on to point out that the sensitivity to anesthesia is maximal at the cortical level and minimal at the bulbar level.

Lang, Tuovinen, and Valleala (1964) investigated the effect of direct stimulation of the amygdala upon electrodermal activity in lightly anesthetized cats. Stimulation of the amygdala, of sufficient intensity to cause an afterdischarge, brought about an increase in SPL which matched in time the duration of the afterdischarge. Stimulation of the amygdala, of an intensity which was insufficient to cause an afterdischarge, resulted in a phasic SPR. Lang et al. (1964) suggest that the discharge of the amygdala does not produce a change in SPL directly, but that the brain stem reticular formation acts as a transmitting structure, a view which would accord with the position of Bloch and Bonvallet outlined in the previous section.

5 . Mode l of th e skin . ( F r o m Edelberg , 1 9 6 8 . ) with a more consistent body of data, some of which has already been presented, suggesting that there is a lumen negative potential in the sweat duct. The importance of the 1968 model is that it suggests that it is necessary to take into account current pathways within the skin as explanatory mechanisms for some response phenomena. In the model (Fig. 5 ) th e batterie s S an d Å represen t potential s acros s swea t glan d membrane s an d epiderma l membrane s respectively .

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