OBJECTIVE: To examine the cultural ideals for body size held by urban Senegalese women; to determine the body size that women associate with health; and to estimate the change in prevalence of female obesity in an urban neighbourhood of Dakar. DESIGN: Cross-sectional, population-based study in the subject's home, using a structured interviewer-administered questionnaire, conducted in the same Dakar neighbourhood as that of a previous survey conducted in 1996. SUBJECTS: A total of 301 randomly selected women, aged 20-50 y, living in a specific Dakar neighbourhood, Senegal. MEASUREMENTS: A total of 32 items concerning body satisfaction, social status, health and individual attributes to associate with one of six photographic silhouettes; body mass index (BMI), waist circumference, waist-to-hip ratio by anthropometry; and measures of economic status. RESULTS: In all, 26.6% of women were overweight (BMI 25-29.9 kg/m 2 ) and 18.6% were obese (BMI Z30 kg/m 2 ) compared with 22.4 and 8.0% respectively in 1996. Overweight was the most socially desirable body size, although obesity itself was seen as undesirable, associated with greediness and the development of diabetes and heart disease. Lay definitions of overweight and normal weight differed substantially from health definitions, as one-third of the sample saw the 'overweight' category as normal. Over a third of women with BMI Z25 kg/m 2 wanted to gain more weight. CONCLUSION: There has been a sharp rise in the prevalence of obesity in Senegalese women living in a Dakar neighbourhood over the last 7 y. In general, overweight body sizes (but not obese) were seen in a positive light. The finding that the term 'overweight' made little sense to these Senegalese women could have important implications for developing public health policies.

The neurotrophin (NT) brain-derived neurotrophic factor (BDNF) plays an essential role in the formation of long-term potentiation (LTP). Here, we address whether this modulation by BDNF requires its continuous presence, or whether a local increase in BDNF is necessary during a specific time period of LTP initiation. Using electrical field stimulation of primary cultures of hippocampal neurons, we demonstrate that short high-frequency bursts of stimuli that induce LTP evoke also an instantaneous secretion of BDNF. In contrast, stimuli at low frequencies, inducing long-term depression, do not enhance BDNF secretion, suggesting that BDNF is specifically present, and thus required, at the time of LTP induction. The field-stimulation-mediated BDNF secretion depends on the formation of action potentials and is induced by IP 3-mediated Ca 2؉ release from intracellular stores. Experiments, aimed at determining the sites of NT secretion that use NT6, showed similar patterns of surface labeling by field stimulation to those shown previously by high potassium.

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The precise polarization and orientation of developing neurons is essential for the correct wiring of the brain. In pyramidal excitatory neurons, polarization begins with the sprouting of opposite neurites, which later define directed migration and axo-dendritic domains. We here show that endogenous N-cadherin concentrates at one pole of the newborn neuron, from where the first neurite subsequently emerges. Ectopic N-cadherin is sufficient to favour the place of appearance of the first neurite. The Golgi and centrosome move towards this newly formed morphological pole in a second step, which is regulated by PI3K and the actin/microtubule cytoskeleton. Moreover, loss of function experiments in vivo showed that developing neurons with a non-functional N-cadherin misorient their cell axis. These results show that polarization of N-cadherin in the immediate post-mitotic stage is an early and crucial mechanism in neuronal polarity.

The establishment of neuronal connectivity depends on the correct initial polarization of the young neurons. In vivo, developing neurons sense a multitude of inputs and a great number of molecules are described that affect their outgrowth. In vitro, many studies have shown the possibility to influence neuronal morphology and growth by biophysical, i.e. topographic, signaling. In this work we have taken this approach one step further and investigated the impact of substrate topography in the very early differentiation stages of developing neurons, i.e. when the cell is still at the round stage and when the first neurite is forming. For this purpose we fabricated micron sized pillar structures with highly reproducible feature sizes, and analyzed neurons on the interface of flat and topographic surfaces. We found that topographic signaling was able to attract the polarization markers of mouse embryonic neurons -N-cadherin, Golgi-centrosome complex and the first bud were oriented towards topographic stimuli. Consecutively, the axon was also preferentially extending along the pillars. These events seemed to occur regardless of pillar dimensions in the range we examined. However, we found differences in neurite length that depended on pillar dimensions. This study is one of the first to describe in detail the very early response of hippocampal neurons to topographic stimuli.

Deficiencies in fragile X mental retardation protein (FMRP) are the most common cause of inherited intellectual disability, fragile X syndrome (FXS), with symptoms manifesting during infancy and early childhood. Using a mouse model for FXS, we found that Fmrp regulates the positioning of neurons in the cortical plate during embryonic development, affecting their multipolar-to-bipolar transition (MBT). We identified N-cadherin, which is crucial for MBT, as an Fmrp-regulated target in embryonic brain. Furthermore, spontaneous network activity and high-resolution brain imaging revealed defects in the establishment of neuronal networks at very early developmental stages, further confirmed by an unbalanced excitatory and inhibitory network. Finally, reintroduction of Fmrp or N-cadherin in the embryo normalized early postnatal neuron activity. Our findings highlight the critical role of Fmrp in the developing cerebral cortex and might explain some of the clinical features observed in patients with FXS, such as alterations in synaptic communication and neuronal network connectivity.

Neurotrophins (NTs) play an essential role in modulating activity-dependent neuronal plasticity. In this context, the site and extent of NT secretion are of crucial importance. Here, we demonstrate that the activation of phospolipase C (PLC) and the subsequent mobilization of Ca 2+ from intracellular stores are essential for NT secretion initiated by both Trk and glutamate receptor activation. Mutational analysis of tyrosine residues, highly conserved in the cytoplasmic domain of all Trk receptors, revealed that the activation of PLC-g in cultured hippocampal neurons and nnr5 cells is necessary to mobilize Ca 2+ from intracellular stores, the key mechanism for regulated NT secretion. A similar signalling mechanism has been identi®ed for glutamate-mediated NT secretionÐwhich in part depends on the activation of PLC via metabotropic receptorsÐleading to the mobilization of Ca 2+ from internal stores by inositol trisphosphate. Thus, PLC-mediated signal transduction pathways are the common mechanisms for both Trkand mGluRI-mediated NT secretion.

In previous experiments the activity-dependent secretion of nerve growth factor (NGF) from native hippocampal slices and from NGF-cDNA transfected hippocampal neurons showed unusual characteristics [