QEEG norms for the first year of life.

BACKGROUND: QEEG allows a more objective evaluation of cerebral electrical activity as well as the production of topographical maps for easier comprehension. Here we have developed qEEG norms for the first year of life using methods previously published for other age ranges, including for example, regression for Gausssianity before Z transformation. These norms constitute a non-invasive and low cost tool for the functional evaluation of the infant's brain. RESULTS: Developmental equations were obtained from 101 healthy infants recording at spontaneous quiet sleep stage II. Polynomial regression equations, with age as independent variable, were calculated for full Broad Band Spectral Parameters (BBSP) using the Least Squares technique. Interpolated maps of the BBSP values or their Z transformation were constructed for linked-ear reference, average reference and Laplacian montages. All montages produced similar tendency curves and Z maps of absolute and relative power, and mean frequency at all frequency bands. The norms obtained were validated against an independent group of 50 healthy infants and some pathological cases. 91-98% of cases were well classified as normal across all measures and montages. To exemplify, two pathological cases are presented of which their qEEG maps show resemblance to CT and MRI. CONCLUSIONS: These qEEG norms are highly useful as an aid to visual interpretation and for the study of pathology further evolution as well as for assessment of infants showing brain risk factors. To our knowledge this is the first normative qEEG study for the initial year of life with such large sample and validation-group.

EEG development in children with sociocultural disadvantages: a follow-up study.

OBJECTIVE: The purpose of this work was to find a possible relation between psychosocial risk and any lag or alteration in CNS maturation in a group of children growing up in an economically, socially and culturally disadvantageous environment in a developing country. METHODS: A 6 year prospective study of 42 pre-school children, growing and living under psychosocial and economic impediments, is presented. EEGs were previously recorded at different ages: 18-30 months (Int J Neurosci 79 (1994) 213), 4 years (Electroenceph clin Neurophysiol 102 (1997) 512), and 5 and 6 years (this study). The EEG developmental patterns between high- and low-risk children (HRC/LRC) are compared. RESULTS: The EEG pattern in HRC showed higher delta and theta absolute power (AP) and relative power (RP) values in frontal leads, and less alpha AP and RP in posterior leads. The qEEG differences between HRC and LRC diminished with age, although differences in frontal theta and occipital/left temporal alpha bands persisted at 6 years. CONCLUSIONS: We conclude that an inadequate or insufficient environmental stimulation is a major contributing factor of the developmental lag in HRC brain maturation. SIGNIFICANCE: This is one of the very few longitudinal studies that address the issue of relating sociocultural risk to EEG maturation.

Forskolin-induced expression of tyrosine hydroxylase in human foetal brain cortex.

Brain-derived neurotrophic factor (BDNF) has previously been shown by this and other laboratories to work in concert with dopamine (DA) to induce the dopaminergic phenotype in foetal rat and human cerebral cortex during specified sensitive developmental stages. In the present study this induction by BDNF/DA was found to be greatly amplified by adding forskolin (fsk: 10 microM) to the rat and human cerebral cortex cultures together with DA (10 microM) and BDNF (50 ng/ml). This amplification was 14-fold for human tissue and 2-fold for rat tissue treated over an 80% shorter period. Compared to treatment with BDNF alone, the additional fsk increased tyrosine hydroxylase-positive (TH+) cell numbers by 220-fold in the human and 26-fold in the rat tissue. Parallel reverse transcription-polymerase chain reaction (RT-PCR) measurement of TH mRNA showed substantial increases above control levels when BDNF/DA or BDNF/DA/fsk treatments were applied. Since fsk boosts intracellular levels of cyclic AMP (cAMP), its amplifying action when added together with BDNF/DA is likely to be due to interactions via the cAMP response element/cAMP response element binding protein (CRE/CREB) systems. This is discussed.

Brain-derived neurotrophic factor in human platelets.

A sensitive, capture enzyme-linked immunosorbent assay (CELISA) has been applied to the accurate and reproducible measurement of brain-derived neurotrophic factor (BDNF) protein in normal human blood platelets, a mean concentration of 1.03 +/- 0.04 ng (SEM)/mg of platelet protein being observed. The method, which requires only 10 ml blood, is now suitable for the investigation of a variety of clinical disorders.

The depolarisation-induced release of [125I]BDNF from brain tissue.

The pattern of release of radioactive brain-derived neurotrophic factor ([125I]BDNF) from brain tissue was studied. Rat brain slices from cerebral cortex and synaptosomes from cerebral cortex and hippocampus were preloaded with [125I]BDNF. Depolarising stimulation by veratridine (final conc. 50 microM) and high KCl (final conc. 45 mM) caused a short-term, greatly enhanced depolarisation-induced release of [125I]BDNF during superfusion and batch protocol experiments. The results suggested that the evoked release was independent of the presence of extracellular calcium ions, but dependent on intracellular calcium ion stores, since the intracellular calcium ion chelator BAPTA-AM, but not the extracellular chelator EGTA abolished the high-potassium-induced [125I]BDNF release from synaptosomes. The release was blocked by tetrodotoxin (1 microM) when synaptosomes were stimulated by veratridine or potassium chloride. Short time-fraction (30 s) superfusion experiments showed that the [125I]BDNF release from synaptosomes appeared in two temporal phases.

Selective inhibition of neurite outgrowth on mature astrocytes by Thy-1 glycoprotein.

THY-1, the smallest member of the immunoglobulin superfamily, is a major cell-surface component expressed by several tissues. The protein, carbohydrate and gene structures of this molecule are known, yet its function is not. It is highly expressed in nervous tissue, where it appears on virtually all neurons after the cessation of axonal growth. Here we show that expression of Thy-1 by a neural cell line inhibits neurite outgrowth on mature astrocytes, but not on other cellular substrata which include Schwann cells and embryonic glia. This inhibition of neurite extension on astrocytes can be reversed by low concentrations (nanomolar) of soluble Thy-1. If a similar interaction between neuronal Thy-1 and astrocytes occurs in vivo, it could stabilize neuronal connections and suppress axonal regrowth after injury in the astrocyte-rich areas of adult central nervous system.

Activation of T lymphocytes by cross-linking of glycophospholipid-anchored Thy-1 mobilizes separate pools of intracellular second messengers to those induced by the antigen-receptor/CD3 complex.

T cells can be activated, not only by the conventional (antigen-receptor/CD3 complex) route, but also by cross-linking any one of their lipid-anchored surface glycoproteins. We have compared early transmembrane signalling events mediated through CD3 with those mediated through Thy-1, a lipid-linked surface glycoprotein, on the human lymphoid cell line Jurkat and transfectants expressing higher levels of Thy-1. Cross-linking of Thy-1 causes immediate phosphatidylinositol (PI) turnover and an influx of extracellular Ca2+, while releasing very little Ca2+ from intracellular stores. CD3 activation, on the other hand, causes PI turnover which releases intracellular Ca2+, and only secondarily induces an influx of extracellular ions. The Thy-1 response is detectable at very low levels of surface Thy-1, and is not mimicked by enzymatic removal of lipid-linked proteins from the cell surface. The Thy-1-induced Ca2+ influx is more sensitive to L channel blockers than the CD3-mediated flux. These results indicate that the initial stages of Thy-1-mediated activation involve the rapid and extensive mobilization of the intracellular second messengers, PI and Ca2+, by mechanisms separate to those activated by the antigen-receptor/CD3 complex.