Critical periods, brain development

Schmitt, C.A. and A.A. McDonough. Thyroid hormone induces Na,K-ATPase during a critical period of development in neonatal rat brain. Fed. Proc. 46 361, 1987. 

The determination of fhe embryonic "critical period of development" for the brain structures involved in learning and memory processes in mice is based on the original work by Rodier (1976). This study identified fhe embryonic time frames for peak neurogenesis and neuroepithelial proliferation for cerebral corfex, hippocampus, septum, amygdala, corpus striatum, thalamus, hypothalamus, cerebellum, and olfactory bulb as the period from embryonic day E14 fhrough E17. Rodier documented almost 40 years ago that the specific time of the central nervous system (CNS) insult is an important factor in subsequent effects on both anatomy and behavior. Therefore, this early work established what we refer to as the embryonic "critical period of development." The report suggested that the behavioral effects of toxicants such as benzo(a)pyrene (B(a)P) are similar in both rats and mice. This study was one of the first to demonstrate that mice could be used successfully as subjects in a variety of behavioral evaluation experiments. 

Schiefermeier M. and Yavin E. (2002). n-3 Deficient and docosahexaenoic acid-enriched diets during critical periods of the developing prenatal rat brain. J. Lipid Res. 43 124-131. 

These studies offer a new model of concomitant behavioral, chemical, and morphological abnormalities associated with a defined Insult at a critical period 1n dendritic development. This model may have some special Importance 1n relation to minimal brain dysfunctions, particularly since no blood-brain barrier protects the fetal brain from antibodies 1n the maternal circulation. 

Iodine deficiency has its most devastating effects on babies while they are in the womb and during their first three months oflife. These are the critical periods of brain development and lack of iodine leads to irreversible effects and permanent mental retardation and on average such children have an IQ of around 85 compared to the IQ of 100 of children who develop normally. Many exhibit the symptoms of brain damage due to lack of iodine, and this condition affects as many... 

It has long been known that thyroid hormone deficiency, when established prior to the critical period of brain development, produces severe and permanent mental retardation both in humans ( cretinism ) and in experimental animals (see Refs. 6 and 101). Most of the early studies aimed at describing the behavioural, physiolog-... 

In conclusion, these genetic and functional results support the concept that a dysregulation of GSH metabolism, and in particular GSH synthesis, is one of the vulnerability factors that could contribute to the development of schizophrenia. These markers may contribute to obtain a complete picture of genetic risk factors of schizophrenia and may help to identify critical period and specific brain locations during development, where GSH deficits are important to the emergence of the disease. 

Most of these neurobehavioral effects presumably stemmed from changes in the development of several neurotransmitter systems caused by exposure to cannabinoids during critical prenatal and early postnatal periods of brain development. A large number of studies have demonstrated effects of cannabinoids on the maturation of dopamine (DA) (Fernandez-Ruiz et al. 1992, 1994, 1996 Walters and Carr 1988 Garcfa-Gil et al. 1998), serotonin (5-HT) (Molina-Holgado et al. 1997),... 

A new era of pharmacological interventions in autism is possible due to increasing understanding of molecular events regulating critical periods of brain development. 

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