Neonatal brain

The distribution of NMDAR subtypes offers one explanation for regional brain vulnerability to HIV-associated injury. Neonatal brain predominantly expresses... 

Neonatal brain damage results in compensatory plasticity 524... 

Neonatal brain damage results in compensatory plasticity. Although, without intervention, axonal growth in the injured adult CNS is limited, the immature CNS responds to injury with a remarkable rerouting of neuronal pathways from undamaged areas to re-innervate... 

Eriksson P, Viberg H, Jakobsson E, et al. 1999. PBDE 2,2, 4,4, 5-pentabromodiphenyl ether, causes permanent neurotoxic effects during a defined period of neonatal brain development. Organohalogen Compounds 40 333-336. 

T. Nakamoto, A.D. Hartman, H.I. Miller, T.E. Temples and G.E. Quinby, Chronic caffeine intake by rat dams during gestation and lactation affects various parts of the neonatal brain. Biol. Neonate, 49 (1986) 277-283. 

Xu G, Ong J, Liu YZ, Silverstein FS, Barks JD (2005) Subventricu-lar zone proliferation after alpha-amino-3-hydroxy-5-mediyl-4-isoxazolepropionic acid receptor-mediated neonatal brain injury. Dev Neurosci 27 228—234. 

The effects of low concentrations of epidural bupivacaine on the developing neonatal brain has been studied in infant rhesus monkeys, to decide if there was a detrimental relation between perinatal analgesia with epidural bupivacaine and later infant development (160). The monkeys, whose mothers had been given epidurals at term (but not during labor) were subjected to a battery of neurobehavioral tests for 1 year. The authors concluded that epidural bupivacaine did not cause neonatal abnormalities or specific cognitive defects, but that it may delay the normal course of behavioral development. It is difficult to extrapolate the results of this small study to human obstetrics. 

P2X, receptors show an order of potency for the natural ligands ATP > ADP and the unnatural ligands a.P-methylene-ATP and ATP-y-S are useful investigational agonists, but desensitization is very evident. These receptors are found in a number of smooth muscle preparations including arterioles, vas deferens and the urinary bladder, where they cause depolarization and contraction. They are found only in neonate brains. The form of the receptor here seems to be a homopolymer formed of identical units. At these sites, the ejps (excitatory junction potentials) seen on sympathetic nerve stimulation are caused in response to ATP action at P2X purinoceptors when it is liberated - as a cotransmilter - from sympathetic varicosities. 

S. van Huffel et al., Changes in Oxygenation and Hemodynamics in Neonatal Brain by Means of Near-Infrared Spectroscopy a Signal Analysis Study, Dept, of Pediatrics and Neonatal Medicine, University Hospital Gasthuisberg, Leu-... 

Brain. - An historical review of developments in the field of cerebral blood flow and metabolism has been produced with 34 references. The use of NMR and magnetic resonance imaging in the study of function and dysfunction in the neonatal brain has been reviewed with 40 references. The potential of and NMR in the assessment of cerebral metabolism in experimental models and human hydrocephalus has been reviewed with 110 references.A review of the applications of C-labelling to studies of the human brain has been produced with 90 references. The detection of choline-containing phospholipids in acute and chronic neurodegeneration has been reviewed with 231 references.The role of and NMR in the study of schizophrenia has been reviewed in two parts. A review of the use of NMR in the study of phenylketonuria has been produced with 26 references and comments on the text have also been published. 

The levels of these receptors are substantially higher than those seen in the adult rat brain (Berrendero et al. 1999). Moreover, in the fetal and early neonatal brain, there is an atypical distribution of CBi receptors compared to the adult brain, particularly with regard to the location of receptor binding in white matter areas (Romero et al. 1997) and mRNA expression in subventricular zones of the forebrain (Berrendero et al. 1998,1999), areas in which these receptors are scarce or undetectable in the adult brain (Herkenham et al. 1991 Mailleux and Vanderhaeghen 1992b). This atypical location of CBi receptors is a transient phenomenon, since during the course of late postnatal development these receptors progressively acquire the classic pattern of distribution observed in the adult brain (Romero et al. 1997 Berrendero et al. 1998). 

It has been known for several years through in vivo tracer studies that human term and preterm infants are capable of synthesizing C20 and C22 LCP from the Cjg precursors (Carnielli et al., 1996 Salem et al., 1996 Sauerwald et al., 1997). These and more recent studies suggest that this capability is highly variable from individual to individual (Uauy et al., 2000). However, all studies to date have sampled blood compartments, and estimates of relative conversion based on such measurements are tenuous at best. We recently reported the bioequivalence of dietary LN A and DHA as precursors for primate neonate brain DHA accretion based on direct measurements of brain DHA accretion (Su et al., 1999a). Neonate baboons were fed a commercial infant formula with 18% of total fatty acids by weight as LA and 1.8% as LNA, which gives an LA/LNA ratio of 10 for 6 wk. Doses of LNA or DHA were administered orally at 4 wk and animals were sacrificed at 6 wk. 

The term bioequivalence, as used here, is chosen to imply a relative efficacy in accretion between two sources of brain DHA, in analogy to the use of the term in reference, for instance, to retinol and fl-carotene. The crucial clinical issue for infant formulations is to establish the amount of DHA to be added to LCP-free formulas as a precursor for neonate brain development. In our neonate study, the commercial formula contained 1.8% of calories as LNA, and the only dietary DHA that these animals consumed was from the dose. Thus, the bioequivalence of 7 1 applies directly to the addition of small amounts of DHA to formula, meaning that the addition of DHA at 0.26% of calories may provide an equal amount of brain DHA as the entire 1.8% calories as LNA. Factors driving the addition of less DHA include possible interference with A A metabolism, the possibility of contaminants added incidentally in DHA oils, and expense. The potency of DHA relative to LNA suggests that the addition of amounts as small as 0.1% of calories would support brain growth, a figure similar to the lowest levels of DHA found inhuman breast milk. Finally, we note that the purely biochemical nature of our studies to date cannot establish whether LNA can completely substitute for DHA. Studies in human preterms suggest that it cannot, whereas those in term infants remain controversial (Cunnane, Francescutti, Brenna, Crawford, 2000). 

Gilmore JH, Lin W, Prastawa MW, Looney CB, Vetsa YS, Knickmeyer RC, Evans DD, Smith JK, Hamer RM, Lieberman JA, Gerig G (2007) Regional gray matter growth, sexual dimorphism, and cerebral asymmetry in the neonatal brain. J Neurosci 27 1255-1260. 

Han BH, Holtzman DM. BDNF protects the neonatal brain from hypoxic-ischemic injury in vivo, via the ERK pathway. J Neurosci 2000 20 5775-5781. 

The ability to maintain glucose homeostasis during the first few days of life also depends on the activation of gluconeogenesis and the mobilization of fatty acids. Fatty acid oxidation in the liver not only promotes gluconeogenesis (see Chapter 31) but generates ketone bodies. The neonatal brain has an enhanced capacity to use ketone bodies relative to that of infants (fourfold) and adults (40-fold). This ability is consistent with the relatively high fat content of breast milk. 

Abdel-Rahman. A., Dcchkovskaia. A, M Mehia-Simmons. H., Guan. S., Khan, W. A., and Abou-Donia, M. B. (2003). Increased expression of glial fibrillary acidic protein in cerebellum and hippocampus DilTerential effects on neonatal brain regional acetylcholinesterase following maternal exposure to ciimbincd chlorpyrifos and nicotine. J. Toxicol. Environ. Health A 66, 2047-2066. 

The Effects of Hypothyroidism Due to Iodine Deficiency in Neonatal Brain The Changes in Brain Metabolites Detected by Magnetic Resonance Spectroscopy... 

Mayer, A.M., The marine toxin domoic acid may affect the developing brain by activation of neonatal brain microglia and subsequent neurotoxic mediator generation, Med. Hypothe., 54, 837, 2000. 

Fetal or neonatal brain prior to myelination contains relatively little cholesterol and in this respect the composition is similar to that of other body tissues. However, during this period before myelin is laid down, microscopic examination shows that small lipid droplets appear in variable number within the nervous tissue. In the human spinal cord droplets appear up to the twenty-second week of fetal life and in the chick embryo up to the sixteenth day of incubation. It would appear from histochemical reactions (Adams and Davison, 1959) that these droplets contain hydro-phobic lipids such as cholesterol esters or triglyceride. Chemical analyses... 

The number of binding sites per mg of DNA varies widely from one tissue to another. Of the tissues studied, the anterior pituitary contains the highest density of receptor sites (6,000 per cell) and the testis the lowest (16 per cell). The number of nuclear binding sites in spleen is small, and close to that in circulatory lymphocytes (about 400 per cell). The adult brain contains about 2,000 binding sites per cell. In neonatal brain their number (4,000 per cell) is higher than in adults and close to that in adult liver [24]. The receptor density -expressed in binding capacity (ng T3/mg DNA)- is not uniform in different brain areas. The anterior pituitary and the cerebral cortex contain more receptors than the cerebellum and the brain stem. The difference spans from 0.5 ng T3 to 0.05 ng T3/mg DNA. The Ka of the receptors in different parts of the brain appears quite similar [25-29]. 

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