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1 Departments of Pharmacology and Pathology, Yale University School of Medicine, New Haven, Connecticut, and Department of Pharmacology, Harvard Medical School, Boston, Massachusetts
The reduction in endogenous stores of norepinephrine after denervation of the cat nictitating membrane (Smith et al., J. Pharmacol. Exp. Therap. 151: 87-94, 1966) was observed, in the present study, to have morphologic correlates in a diminution of catecholamine fluorescence, as determined microfluorometrically, and a reduction in the proportion of granular vesicles in electron micrographs of adrenergic nerve endings. The progression of fine structural changes during the process of degeneration of the nerve endings was described. The number of intact nerve endings remaining on electron-microscopic examination correlated well with the previously described (Smith et al., 1966) decrease in ability to retain exogenous H3- norepinephrine. Further evidence is thus presented for the hypothesis that the degeneration contraction of cat nictitating membrane is due to leakage of endogenous transmitter from degenerating nerve endings. Furthermore, morphologic support is provided for the explanation of denervation supersensitivity on the basis of inability of denervated tissue to retain exogenous norepinephrine. An observed lack of linear relationship between catecholamine fluorescence of nerve endings and endogenous norepinephrine content may be due to unequal sensitivity of the catecholarnine histochemical method to intra- and extravesicular norepinephrine.
Submitted on December 1, 1966