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To investigate the possibility that cigarette smoking and other drug use are affected by menstrual phase in smokers with Late Luteal Phase Dysphoric Disorder (LLPDD), we examined daily diaries rating menstrual symptomatology, smoking, alcohol and nonprescription drug use, and caffeine intake in nine female smokers meeting criteria for LLPDD. Menstrual symptomatology peaked during the premenstrual phase. Smoking, alcohol, and nonprescription drug intake were increased during menses; caffeine intake was unaffected by phase. No systematic intrasubject correlation between symptomatology and smoking was detected. It was concluded that in women with LLPDD, smoking and alcohol and nonprescription drug intake appear to vary as a function of menstrual phase. The lack of intrasubject correlations between symptomatology and intake, and the failure of peak intake to coincide with peak symptomatology, however, indicate that these effects cannot be explained simply as "self-medication" of acute episodes of dysphoric mood.

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Molecular genetics is helping define the contribution of genetic involvement in behavioral disorders. At this time, however, a severely limiting factor for DNA linkage studies of these disorders remains the definition of the phenotype. An example of this is found in the group of studies examining linkage of schizophrenia to the 5q location. Although various broad clinical interpretations of the schizophrenia phenotype were used to test for linkage, all but one study reported findings negative for linkage of schizophrenia to the 5q area. We offer a strategy based on family studies using segregation data of behavioral subtypes. We apply this strategy using molecular genetic technology to our study of psychopathology in patients. This approach offers the possibility of a clearer definition of the phenotype and is suggested for use in both linkage and association studies of neuropsychiatric disorders.

A comprehensive developmental study of serum LH, FSH and androgen concentrations was carried out in male mice of two inbred strains. Gonadotropic hormone (GTH) levels rose 10-15 days prior to the pubertal increase in serum androgen with FSH preceding LH in this regard. In both strains GTH titer rose to a peak at 30 or 35 days and then steadily declined to adult levels which were strain-specific. Serum androgen was detected at low, relatively steady levels until the pubertal increase between 30 and 50 days postpartum. The results are interpreted as supporting the hypothesis that a shift in feedback sensitivity, occurring at about 20 days of age, may be involved in the onset of puberty in the male mouse.

It has been suggested that the Y chromosome of DBA/1Bg mice makes an incremental contribution to their aggressive behavior and to that of the C57BL/10 female X DBA/1 male F1 hybrids. To test this hypothesis, a congenic stock of C57BL/10 with the DBA/1 Y chromosome was developed by the backcross system of breeding; the stock is designated C57BL/10-Y1. There were no significant differences in aggressive behavior between the congenic C57BL/10 and C57BL/10-Y1. However, the hybrid B10D1 F1 and D1B10-Y1 F1 had identical aggression scores, and both of these were more aggressive than the hybrid D1B10 F1. These findings support the hypothesis that there is an interaction between DBA/1 Y chromosomes and autosomes in the development of intermale aggression of these mice.