impulse (17). Our results cannot be attributed to the experimental procedure itself, since identically treated control animals that received immunoglobulins from nonmyasthenic humans showed none of the myasthenic features. Furthermore, dialysis performed during preparation of the immunoglobulin fraction would remove any residual anticholinesterase medication from the patients' serums.Our study differs from the many previous attempts to transfer myasthenia gravis to animals over the past three decades (6) in at least two important respects which contributed to the present positive results: (i) We exposed the test animals to the serum factor for a relatively prolonged time, in contrast to the minutes or hours previously attempted. (ii) We used more sensitive electrophysiological and radiometric methods to detect the myasthenic abnormalities rather than relying on clinical weakness or decremental responses, which are often absent.The nature of the myasthenia-producing serum factor has not yet been elucidated, but the 33 percent ammonium sulfate fraction used in these experiments contains the immunoglobulins as well as other serum proteins (18). Whether the antibody that binds to ACh receptor (3) is itself the transferable serum factor in myasthenic patients remains to be determined. Our experiments may provide the critical link between such an antibody and the pathogenesis of myasthenia gravis as a humorally mediated autoimmune disease.

Rats were made hyperphagic by 6-hydroxydopamine (6-OHDA) injected bilaterally into the ventral midbrain; then they were restricted to a 6 h/day feeding schedule and tested for appetite suppression with amphetamine and fenfluramine in randomized order. Amphetamine anorexia was diminished while fenfluramine anorexia was enhanced (both P less than 0.001). The opposite effect on fenfluramine anorexia shows that the effect of 6-OHDA on amphetamine anorexia was not due to hyperphagia masking the anorexia. Norepinephrine in the forebrain was 90% depleted, but DA and serotonin levels were within 9% of normal. These results demonstrate a new way to dissociate amphetamine and fenfluramine anorexia, as others have done with lateral hypothalamic lesions or DA depletion. The 6-OHDA injections, which were of a type that cause hyperphagia, apparently destroyed a substrate for amphetamine anorexia and also facilitated a substrate for fenfluramine anorexia.