R. Strong, Jr., D. Simberloff, L. G. Abele, A. B. Thistle, Eds. (Princeton Univ. Press, Princeton, NJ, 1984), pp. 151-180; J. Roughgarden, Y. Iwasa, C. Baxtr, Ecology 66, 54 (1985); J. H. Connell,J. Ecp. Mar. Biol. Ecol. 93, 11 (1985). 3. S. D. Gaines and J. Roughgarden, Proc. NatI. Acad. Sci. U.S.A. 82, 3707 (1985); S. D. Gaines et al., Oecologia (Berlin) 67, 267 (1985). 4. San Francisco, California, to Baja California, Mexi- co, and Peru to Tierra del Fuego. M. S. Foster and D. R. Schiel, "The ecology of giant kelp forests in California: A community profile" [U.S. Fish WddI. Serp. Biol. Rep. 85(7.2) (1985)]; P. K. Dayton, Annu. Rev. Ecol. Syst. 16, 215 (1985). 5. P. K. Dayton at al., Ecol. Monogr. 54, 253 (1984). 6. L. F. Lowry and J. S. Pearse, Mar. Biol. 23, 213 (1973); J. A. Estes and J. F. Palmisano, Science 185, 1058 (1974); D. 0. Duggins, Ecology 61, 447 (1980). 7. P. K. Dayton and M. J. Tegner, Science 224, 283 (1984). 8. G. A. Jackson and C. D. Winant, Cont. ShelfRes. 2, 75 (1983); G. A. Jackson, J. Phys. Oceangr. 14, 1300 (1984). 9. G. A. Jackson, in Biochemical and Photasynthetic Aspects of Energy Production, A. San Pietro, Ed. (Academic Press, New York, 1980), pp. 31-80. 10. B. B. Bernstein and N. Jung, Ecol. Monogr. 49, 335 (1979). 11. R. N. Bray, Fish. Bull. (Dublin) 78, 829 (1980). 12. Samples (200 liters each) were taken from April through June. Thereaftcr, samples were increased to 400 liters because of low abundances in some taxa. 13. R. K. Grosberg, Ecology 63, 894 (1982); S. D. Gaines and J. Roughgarden, unpublished data. 14. Late stage II nauplii eventually exhibit weak nega- tive phototaxis. 15. S. D. Gaines and J. Roughgarden, unpublished data. 16. Early stage barnacle nauplii may be the exception because laboratory studies suggest nauplii are more readily eaten by several invertbrates resident in the kelp canopy (for example, caprellid amphipods, my- sids). Their concentrations may also be affected by changes in phototaxis with development (14). 17. D. J. Miller and J. J. Geibe, Calif Fish Game BuU. 158 (1973). 18. T. W. Anderson, thesis, California State University, Fresno (1983). Sebastes atrovirens, the kelp rockfish, is a noteworthy exception that reaches peak juvenile abundance in autumn. It was relatively rare through- out the study. 19. M. M. Singer, thesis, San Jose State University, San Jose, California (1982); S. D. Gaines and J. Rough- garden, unpublished data. 20. The rockfish are concentrated primarily at the pe- rimeter of the bed (11), and yearly variation in fish density is probably more important than yearly variation in kelp canopy area per se. A more defini- tive test awaits years m which rockfish recruitment success is decoupled from yearly fluctuations in kelp canopy area. 21. The cause of the relation is under further study. It is unlikely, however, that the observed variation in rockfish density was a direct response to changes in kelp bed area since paralle annual fluctuations were seen throughout the central California coast includ- ing rockfish species that do not recruit to kelp beds (unpublished data from E. Hobson). Moreover, preliminary data from 1986 show that rockfish recruitment rates are low despite a large kelp canopy comparable to that of 1985. 22. The error bars pertain to observation error inherent in measuring recruitment rates from several quad- rats; the error does not represent the sample variance in recruitment from diffrcnt ycars in which the canopy area was the same. Therefore, the differences in confidence interval size are largely irrelevant to the assumption of homoscedasticity. 23. Unpublished data from E. Hobson for the Mendoci- no coast. Less extensive records and qualitative reports from the California Department of Fish and Game suggest comparable patterns for Monterey Bay. Counts are number of fish secn per minute of water column observation time dunng the peak abundance periods of July and August. Totals of 45, 67, and 277 minutes of observation are included for 1983, 1984, and 1985, respectively. This density estimate probably has a conservative bias at high fish densities. 24. We thank C. Baxter, S. Brown, M. Denny, and T. Hahn for comments and field assistance, the Depart- ment of Energy (EV10108) for primary financial support, and the National Science Foundation (OCE 85-14755) for supplemental funds. 20 June 1986; accepted 9 October 1986 Mapping Human Brain Monoamine Oxidase A and B with 11C-Labeled Suiicide Inactivators and PET J. S. FOWLER, R. R. MACGREGOR, A. P. WOLF, C. D. ARNETr, S. L. DEWEY, D. SCHLYER, D. CHRISTMAN, J. LOGAN, M. SMITH, H. SACHS, S. M. AQUILONIUS, P. BJURLING, C. HALLDIN, P. HARTVIG, K. L. LEENDERS, H. LUNDQVIST, L. ORELAND, C.-G. STALNACKE, B. LANGSTROM The regional distributions of monoamine oxidase (MAO) types A and B have been identified in human brain in vivo with intravenously injected "C-labeled suicide enzyme inactivators, dorgyline and L-deprenyl, and positron emission tomography. The rapid brain uptake and retention of radioactivity for both "C tracers indicated irreversible trapping. The anatomical distribution of "C paralleled the distribution of MAO A and MAO B in human brain in autopsy material. The corpus striatum, thalamus, and brainstem contained high MAO activity. The magnitudes of uptake of both ["C]cdorgyline and L-[llC]deprenyl were markedly reduced in one subject treated with the antidepressant MAO inhibitor pheneizine. A comparison of the brain uptake and retention of the "C-labeled inactive (D-) and active (L-) enantiomers of deprenyl showed rapid clearance of the inactive enantiomer and retention of the active enantiomer within MAO B-rich brain structures, in agreement with the known stereoselectivity of MAO B for L-deprenyl. Prior treatment with unlabeled L-deprenyl prevented retention of L-[" C]deprenyl. Thus, suicide enzyme inactivators labeled with positron emitters can be used to quantitate the distribution and kinetic characteristics of MAO in human brain structures. M ONOAMINE OXIDASE (MAO) (E.C. 1.4.3.4) is responsible for the oxidative deamination of en- dogenous neurotransmitter amines as well as amines from exogenous sources. It exists in two forms, MAO A and MAO B, which are identified by their inhibitor sensitivity and by their substrate selectivity (1). Both forms may be important for neurotransmitter reg- ulation, and fluctuations in functional MAO 23 JANUARY I987 activity may be associated with human dis- eases such as Parkinson's disease, depres- sion, and certain psychiatric disorders (2). A number of MAO inhibitors are used as antidepressant drugs (3); L-deprenyl, an in- hibitor of MAO B, is used to treat Parkin- son"s disease (4), and brain MAO B plays a key role in 1-methyl-4-phenyl-1,2,3,6-tetra- hydropyridine (MPTP)-induced parkinson- ism (5). Speculation as to the relation of MAO activity to human disease has been based on the measurement of platelet MAO activity or on the analysis of postmortem human brain samples. However, platelet MAO is only MAO B (6), and, although the platelet enzyme is probably a genetic marker for serotonergic mechanisms in the brain (7), direct attempts to correlate platelet and brain MAO B have failed (8). Furthermore, even the process of isolation of MAO from its native environment within a tissue for measurement in vitro may change some properties of the enzyme (9, 10). A major milestone in the study of MAO has been the design and synthesis of the highly selective, mechanism-based inhibitors clorgyline (N-[3-(2,4-dichlorophenoxy)pro- pyl]-N-methyl-2-propynylamine) (11) and L-deprenyl [(-)-N,a-dimethyl-N-2-propyn- ylphenethylamine] (12), which irreversibly inhibit MAO A and MAO B, respectively, by binding covalently to the enzyme itself (13), a process frequently referred to as "suicide enzyme inactivation" (14). We have explored the feasibility of using "C-labeled clorgyline and L-deprenyl for mapping functional MAO in brain directly and noninvasively by using the covalent bond formation between labeled inhibitor and enzyme to label the enzyme in a selec- tive and irreversible manner. The regional J. S. Fowler, R. R. MacGregor, A. P. Wolf, C. D. Arnett, S. L. Dewey, D. Schlyer, D. Christman, J. Logan, M. Smith, H. Sachs, Brookhaven National Laboratory, Up- ton, NY 11973. S. M. Aquilonius, P. Bjurling, C. Halldin, P. Hartvig, K. L. Leenders, H. Lundgvist, L. Oreland, C.-G. StAlnacke, B. Ungstrom, University of Uppsala, Uppsala, Sweden. REPORTS 48I on February 1, 2016 Downloaded from on February 1, 2016 Downloaded from on February 1, 2016 Downloaded from on February 1, 2016 Downloaded from on February 1, 2016 Downloaded from