Prenatal brain

The neurodevelopmental hypothesis of schizophrenia posits that the disorder is due to a subtle defect in prenatal brain development but is not clinically manifest until many years later (Murray and Lewis, 1987 Weinberger, 1987). This theory has two essential components a presumption of developmental neuropathology and an expectation that this developmental neuropathology results in a pattern of brain malfunction which ultimately produces the symptoms of schizophrenia. 

We know that in the mature brain, neurotransmitters are released by nerve cell endings and act at synapses to mediate the interaction between nerve cells. There s now evidence that during the development of the prenatal brain, neurons can release transmitters before any connections are made, and that such released transmitters, acting as trophic factors, guide the formation of connections.17 Any environmental impact or mutation that affects the synthesis or release of neurotransmitters can be expected to have an effect on the development of the fetal brain. For example, during fetal development in Down syndrome, reductions apparently occur in the levels of various neurotransmitters. This may be one mechanism for the impaired brain development characteristic of this syndrome.18... 

If an inflammatory response to infection affects brain neuromotor white matter to produce lesions responsible for cerebral palsy, what do inflammatory responses to noninfectious toxins produce elsewhere in the prenatal brain The effects of... 

Neurodevelopmental models of schizophrenia have for the most part emphasized prenatal brain development, focusing on effects that may alter gene expression.15 For example, according to one idea, individuals with schizophrenia inherit genes that cause structural brain deviations that may be compounded by early environmental impact.16 Much of the focus of this hypothesis has been on postnatal impact, such as stress, that changes brain chemistry, but the idea can also accommodate a focus on prenatal impact. 

Yavin, E., Glozman, S., and Green, P. (2001) Docosa-hexaenoic Acid Accumulation in the Prenatal Brain, J. Mol. Neurosci. 16,229-235. 

It is well known that the timing of brain development differs between species. In the human, maximum growth occurs at the time of parturition which is also the time of maximum growth of the pig brain (hence termed "perinatal brain developer"). In the rat and rabbit the maximum growth period is postnatal (termed "postnatal brain developer"). In the sheep and the monkey the maximum growth period is prenatal (termed "prenatal brain developer"). 

TAYLOR H, QUINTERO E M, lAcopiNO A M, LEPHART E D (1999) Phytoestrogeus alter hypothalamic calhindin-D28k levels during prenatal development . Brain Res Develop Brain Res. 114 277-81. 

Deficiency of manganese may lead to vitamin K deficiency (Chiswell and Johnson 1994) and to problems in prenatal and neonatal development of the brain. 

Lee, B., el al. (2002). Prostaglandin D synthase in the prenatal ovine brain and effects of its inhibition with selenium chloride on fetal sleep/wake activity in utero. 

Stressful early life events, involving abuse or neglect, can have a life-long influence on the stress response, and lead to elevated levels of allostatic load for the lifespan. Overactivity of the stress hormone axis has been linked to prenatal stress or poor maternal care in rodent models, and this overactivity contributes to increased rates of brain and body aging [39]. 

Beagles, prenatal and early neonatal stages, given single acute dose of 0.2-1.0 Gy, then observed over 11-year life span Irradiation at all ages was associated with increased risk of decreased fertility inhibited growth and development lower brain weight and increase in fatal neoplasms 5... 

Mole, R.H. 1990. The effect of prenatal radiation exposure on the developing human brain. Inter. Jour. Radiation Biol. 57 647-663. 

McCormick, C.M. et al., Sex-specific effects of prenatal stress on hypothalamic-pituitary-adrenal responses to stress and brain glucocorticoid receptor density in adult rats, Dev. BrainRes., 84, 55, 1995. 

Yorty, J.L. and Bonneau, R. H., Prenatal transfer of low amounts of herpes simplex vims (HSV)-specific antibody protects newborn mice against HSV infection during acute maternal stress, Brain Behav. Immun., 18, 15, 2004. 

Okonmah AD, Brown JW, Blyden GT, Soliman KF. (1988). Prenatal effects of acute harmaline exposure on fetal brain biogenic amine metabolism. Pharmacology. 37(3) 203-8. 

Neonatal (Desaulniers et al., 2005) or prenatal (Johrl et al., 2006) exposure to AFIR agonist imprints adult brain mRNA expression in rat. 

Brzezinski MR, Boutelet-Bochan H, Person RE, Fantel AG, Juchau MR. 1999. Catalytic activity and quantitation of cytochrome P-450 2E1 in prenatal human brain. J Pharmacol Exp Ther 289 1648-1653. 

Johri A, Dhawan A, Lakhan Singh R, Parmar D. 2006. Effect of prenatal exposure of deltamethrin on the ontogeny of xenobiotic metabolizing cytochrome P450s in the brain and liver of offsprings. Toxicol Appl Pharmacol 214 ... 

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