Research Articles: "Doc2b is a high-affi nity Ca 2+ sensor for spontaneous neurotransmitter release" by A. J. Groffen et al. (26 March, p. 1614). Several author affi liations were not footnoted properly; three corrected affi liations follow.

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Electroconvulsive seizure threshold in the mouse was found to be lowered by reserpine alld also by D-dcpriJ'ation (REM-deprivatiol/). D-deprivation plus reserpine produced a greater lowerillg thall either alone. High positive correlations between the two effects across animals (mice more "sensitive" to reserpine were more sensitive to D-deprivation) suggests that the same or closely related mechanisms are involved.The aim of this study was to investigate the effect on the electroshock convulsion threshold (cr) of a number of conditions and agents which produce altered sleep patterns. Cohen & Dement (l96S) have shown in the rat that four days of D-deprivation-preventing the animal from having D-periods (REM-periods)-produced a small but significant reduction in convulsion threshold. This study was indended to replicate these results in another species and then to study conditions other than D-deprivation which we have shown to affect D-pressure. D-pressure refers to the tendency to have D-periods, apparently augmented after D-deprivation. Dpressure, need for D, REM tendency, or some similar concept is used in almost every sleep laboratory in spite of our ignorance of the basic neural mechanisms involved. Increased D-pressure is usually measured by increased D-time or D-time per cent, decreased D-Iatency, or increased REM-density-i.e., number of eye movements per unit of time during D-periods. D-pressure appears to be reduced by certain antidepressant drugs (Hartmann, 1968a) and by EST (Cohen & Dement, 1966). In our experience it is increased by reserpine which has been shown by others to reduce CT (Bianchi & Camillo, 19S6; Chen & Bonner, 19S6). Thus we have suggested that depression is closely related to D-pressure (Hartmann, 1968a, b).We hypothesized that D-deprivation and reserpine, agents which increase D-pressure, would reduce CT in mice and would do so by the same mechanism, so that animals more susceptible to the effect of one agent would also be more susceptible to the effects of the other. Specific hypotheses were as follows: (I) D-tlcprivation will reduce IT; (2) reserpine will retluce CT; (3) reserpine plus D-deprivation will produce a greater reduction in CT than either the deprivation or reserpine alone; or (4) there will be a positive correlation across animals between the effects of reserpine and the effects of D-deprivation. METHOD A total of 60 young adult male Webster Swiss mice were employed. Groups of 10 to 20 mice were run in each experiment. Each animal was used as its own control, i.e., each had usually at least three baseline convulsion-threshold terminations at least 48 h apart and at least one experimental session for whatever condition was being studied. Convulsion threshold for each animal was then compared under baseline and experimental conditions. Separate experiments indicated that placebo injections had no effect on cr, and individual vs group housing had no effect onCT.er was determined by the method of Schwartzbaum et al (l9S8) with electrodes attached to the ears of the mi...