- Email: [email protected]
Hindbrain abnormalities: a shared neuropathology across cognitive developmental disorders
1997 NBTS ABSTRACTS
were dose dependent. Thus, the NOAEL for methanol effects is below 200 ppm. (Supported by grant #90-9 from the Health Effects Institute and grant # ES06773 from NIEHS)
NBTS 21 GRAY*, KA.,G.kRICHfiRDSON,N.L. DAY,Department ofEpidemiology, University of Pittsburgh, Pittsburgh, PA. Prenatal mariiuana use & child depression at apt ten. Studies examining the consequences of prenatal marijuana use have focused predominantly on the children’s behavioral and cognitive development. However, research on other neurobehavioral development such as mental health outcome of children prenatally exposed is very limited. There are studies in the animal literature evaluating the neurobiology of prenatal exposure (Bonin, 1995; Rodriguez, 1991). For example, Rubio et al. (1995) studied the role of A 9-THC on the activation and sensitization of the hypothalamus-pituitary-adrenal (HPA) axis. These findings suggests that perinatal THC exposure modifies brain dcvclopment and function. This altered brain neuronal circuitry may result in impaired stressor rcsponsc. This study examines the relationship between prenatal marijuana use and child depression at 10 years of age with data from the 1O-year follow-up of the Maternal Health Practices and Child Development Project. Prenatal and current drug use, home environment, demographics and psychosocial characteristics wcrc asccrtaincd. The children complctcd the Children’s Depression Inventory (CDI), a self-report of depressive symptoms (Kovacs, 1982). The majority of women reported moderate substance use during the first trimester which declined by the third trimester. Stepwise multiple regressions were used to test trimester-specific effects of marijuana on the CD1 total score, while adjusting for home environment, so&demographics, maternal psychological characteristics, prenatal & current substance use, and mother & child’s IQ Prenatal marijuana exposure was significantly score. associated with increased CD1 scores for each trimester. Further ANCOVA analyses indicated a significant linear relationship. This study revealed an unreported long-term consequence of prenatal marijuana use on child depressive symptomatology. These findings add to the reports of effects of prenatal marijuana exposure on behavior (Fried, 1995) and cognitive development (Day, 1994) and may be a further marker of the teratogenic effects of exposure.
NBTS 22 Adams, J. and D. Annis. Dept of Psychology, Univ. of Massachusetts, Boston, MA. Hindbrain abnormalities: a shared neuropathology across cognitive developmental disorders.
245 A review of genetic mental retardation syndromes, certain brain malformation syndromes, and teratogen-induced syndromes involving cognitive dysfunction reveals a shared neuropathology in This paper hindbrain structures. will examine the neuropathological and neuropsychological characteristics of children with autism, Down, Fragile X, Turner, and Williams Syndrome, the Arnold Chiari malformation, isotretinoin, All and ethanol teratogenesis. share hindbrain abnormality and reduced intelligence: most share a profile of relative weaknesses in organizational, and attentional, visuospatial processing. The mediating role of hindbrain structures and projection pathways in these processes will be It will be argued that discussed. hindbrain abnormality can account for these cognitive deficits: deficits which are commonly attributed to frontal and/or cortical pathology when adult models are applied. Supported by NIH: ROl-HD29510.
NBTS 23 FUKUMURA*, M., G.D. CAPPON*, H.W. BROENING and C.V. VORHEES. Div. of Dev. Biol., Children’s Hosp. Res. Found. and Univ. of Cincinnati, Cincinnati, Ohio. Lack of aender difference in methamphetamine (MA)-induced caudate-putamen (CPU) dopamine and serotonin reductions in rats. In mice, it has been reported that MA-induced CPU DA reduction is greater in males than in females. We examined MA-induced neurotransmitter alterations in Sprague-Dawley CD rats (saline, MA 5, and MA 10 mg/kg, N=8/group; expressed as free base). The treatments were administered S.C. four times at 2 hr intervals. Body temperatures were measured every 30 min from the first MA administration until 3 hr after the final dose. If rectal temperatures 241.5X, subjects were placed on ice. Animals were sacrificed 3 days post-treatment. MA induced significant DA and 5-HT reductions in CPU but the magnitude of these reductions were not significantly different between the sexes. In the MA 5 mg/kg groups, CPU DA content was reduced by 44.8% and 51.2%, and CPU 5-HT content was reduced by 23.9% and 30.5% of controls for females and males, respectively. In the MA 10 mg/kg
were dose dependent. Thus, the NOAEL for methanol effects is below 200 ppm. (Supported by grant #90-9 from the Health Effects Institute and grant # ES06773 from NIEHS)
NBTS 21 GRAY*, KA.,G.kRICHfiRDSON,N.L. DAY,Department ofEpidemiology, University of Pittsburgh, Pittsburgh, PA. Prenatal mariiuana use & child depression at apt ten. Studies examining the consequences of prenatal marijuana use have focused predominantly on the children’s behavioral and cognitive development. However, research on other neurobehavioral development such as mental health outcome of children prenatally exposed is very limited. There are studies in the animal literature evaluating the neurobiology of prenatal exposure (Bonin, 1995; Rodriguez, 1991). For example, Rubio et al. (1995) studied the role of A 9-THC on the activation and sensitization of the hypothalamus-pituitary-adrenal (HPA) axis. These findings suggests that perinatal THC exposure modifies brain dcvclopment and function. This altered brain neuronal circuitry may result in impaired stressor rcsponsc. This study examines the relationship between prenatal marijuana use and child depression at 10 years of age with data from the 1O-year follow-up of the Maternal Health Practices and Child Development Project. Prenatal and current drug use, home environment, demographics and psychosocial characteristics wcrc asccrtaincd. The children complctcd the Children’s Depression Inventory (CDI), a self-report of depressive symptoms (Kovacs, 1982). The majority of women reported moderate substance use during the first trimester which declined by the third trimester. Stepwise multiple regressions were used to test trimester-specific effects of marijuana on the CD1 total score, while adjusting for home environment, so&demographics, maternal psychological characteristics, prenatal & current substance use, and mother & child’s IQ Prenatal marijuana exposure was significantly score. associated with increased CD1 scores for each trimester. Further ANCOVA analyses indicated a significant linear relationship. This study revealed an unreported long-term consequence of prenatal marijuana use on child depressive symptomatology. These findings add to the reports of effects of prenatal marijuana exposure on behavior (Fried, 1995) and cognitive development (Day, 1994) and may be a further marker of the teratogenic effects of exposure.
NBTS 22 Adams, J. and D. Annis. Dept of Psychology, Univ. of Massachusetts, Boston, MA. Hindbrain abnormalities: a shared neuropathology across cognitive developmental disorders.
245 A review of genetic mental retardation syndromes, certain brain malformation syndromes, and teratogen-induced syndromes involving cognitive dysfunction reveals a shared neuropathology in This paper hindbrain structures. will examine the neuropathological and neuropsychological characteristics of children with autism, Down, Fragile X, Turner, and Williams Syndrome, the Arnold Chiari malformation, isotretinoin, All and ethanol teratogenesis. share hindbrain abnormality and reduced intelligence: most share a profile of relative weaknesses in organizational, and attentional, visuospatial processing. The mediating role of hindbrain structures and projection pathways in these processes will be It will be argued that discussed. hindbrain abnormality can account for these cognitive deficits: deficits which are commonly attributed to frontal and/or cortical pathology when adult models are applied. Supported by NIH: ROl-HD29510.
NBTS 23 FUKUMURA*, M., G.D. CAPPON*, H.W. BROENING and C.V. VORHEES. Div. of Dev. Biol., Children’s Hosp. Res. Found. and Univ. of Cincinnati, Cincinnati, Ohio. Lack of aender difference in methamphetamine (MA)-induced caudate-putamen (CPU) dopamine and serotonin reductions in rats. In mice, it has been reported that MA-induced CPU DA reduction is greater in males than in females. We examined MA-induced neurotransmitter alterations in Sprague-Dawley CD rats (saline, MA 5, and MA 10 mg/kg, N=8/group; expressed as free base). The treatments were administered S.C. four times at 2 hr intervals. Body temperatures were measured every 30 min from the first MA administration until 3 hr after the final dose. If rectal temperatures 241.5X, subjects were placed on ice. Animals were sacrificed 3 days post-treatment. MA induced significant DA and 5-HT reductions in CPU but the magnitude of these reductions were not significantly different between the sexes. In the MA 5 mg/kg groups, CPU DA content was reduced by 44.8% and 51.2%, and CPU 5-HT content was reduced by 23.9% and 30.5% of controls for females and males, respectively. In the MA 10 mg/kg