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At least 127 records · Page 7Linked to original sources
PubMed2000

Neural tube defects among Mexican Americans living on the US-Mexico border: effects of folic acid and dietary folate.

Populations of Mexican descent have high occurrences of neural tube defects (NTDs). A recent study suggested that folic acid supplements may not protect these populations from NTDs. In a case-control study, the authors investigated the role of folic acid and dietary folate intake in NTD risk among Mexican Americans living along the Texas-Mexico border. From January 1995 to February 1999, 148 Mexican-American women with NTD-affected pregnancies and 158 women with normal live births were interviewed in person about use of vitamin supplements and dietary intakes during a 6-month periconceptional period (from 3 months before conception to 3 months after conception). Daily preconceptional consumption of vitamin supplements containing folic acid was 2.5% in control women and 2.0% in case women (odds ratio = 0.77; 95% confidence interval (CI): 0.19, 3.22). With adjustment for maternal age, education, obesity, and previous stillbirth or miscarriage, the risk estimate was essentially null (odds ratio = 1.12; 95% CI: 0.22, 5.78). Combined folic acid intake from diet and supplements showed only a modest risk reduction for intakes of > or = 1.0 mg per day (adjusted odds ratio = 0.73; 95% CI: 0.31, 1.72). The fact that the primary folic acid exposure was in the form of dietary polyglutamates rather than the more easily absorbed supplemental monoglutamates may explain an apparent decreased effect in this population.

Adult↗
PubMedDate not supplied

A role for cortical crosstalk in the binding problem: stimulus-driven correlations that link color, form, and motion.

The putative independence of cortical mechanisms for color, form, and motion raises the binding problem-how is neural activity coordinated to create unified and correctly segmented percepts? Binding could be guided by stimulus-driven correlations between mechanisms, but the nature of these correlations is largely unexplored and no one has (intentionally) studied effects on binding if this joint information is compromised. Here, we develop a theoretical framework which: (1) describes crosstalk-generated correlations between cortical mechanisms for color, achromatic form, and motion, which arise from retinogeniculate encoding; (2) shows how these correlations can facilitate synchronization, segmentation, and binding; (3) provides a basis for understanding perceptual oddities and binding failures that occur for equiluminant and stabilized images. These ideas can be tested by measuring both perceptual events and neural activity while achromatic border contrast or stabilized image velocity is manipulated.

Animals↗
PubMed2000

The olfactory placodes of the zebrafish form by convergence of cellular fields at the edge of the neural plate.

The primary olfactory sensory system is part of the PNS that develops from ectodermal placodes. Several cell types, including sensory neurons and support cells, differentiate within the olfactory placode to form the mature olfactory organ. The olfactory placodes are thought to arise from lateral regions of the anterior neural plate, which separate from the plate through differential cell movements. We determined the origins of the olfactory placodes in zebrafish by labeling cells along the anterior-lateral edge of the neural plate at times preceding the formation of the olfactory placodes and examining the later fates of the labeled cells. Surprisingly, we found that the olfactory placode arises from a field of cells, not from a discrete region of the anterior neural plate. This field extends posteriorly to the anterior limits of cranial neural crest and is bordered medially by telencephalic precursors. Cells giving rise to progeny in both the olfactory organ and telencephalon express the distal-less 3 gene. Furthermore, we found no localized pockets of cell division in the anterior-lateral neural plate cells preceding the appearance of the olfactory placode. We suggest that the olfactory placodes arise by anterior convergence of a field of lateral neural plate cells, rather than by localized separation and proliferation of a discrete group of cells.

Animals↗
PubMed2004

Prevalence of craniorachischisis in a Texas-Mexico border population.

BACKGROUND: The most severe neural tube defect (NTD), craniorachischisis, is characterized by anencephaly confluent with spina bifida open from the cervical to the lumbar region. We describe the prevalence of craniorachischisis among the Texas-Mexico border population during the period 1993-1999. METHODS: An active surveillance system identified all clinically apparent NTD-affected fetuses and infants born to mothers residing and delivering in any of the 14 Texas-Mexico border counties. Craniorachischisis cases included live-born, stillborn, and therapeutic abortions. RESULTS: A total of 16 craniorachischisis cases were identified for a total prevalence of 0.51 per 10,000 live births (Mexican American prevalence, 0.52 per 10,000) and a prevalence of 0.28 per 10,000 live births for cases of 20 weeks gestation or greater. CONCLUSIONS: The prevalence of craniorachischisis was higher than that reported in Atlanta (0.1 per 10,000 live births), but much lower than that reported in Northern China (10.7 per 10,000 births). In this high NTD prevalence region, it is possible that a multiplicity of risk factors, mostly related to poverty, contribute to a high prevalence of craniorachischisis.

Black or African American↗
PubMed2004

Morphological features of tail bud development in truncate mouse mutants.

A key malformation in the homozygous truncate mouse mutants is a partial lack of the notochord in the embryo tail. In order to analyze if tail bud development was affected by the truncate (tc) mutation, serial semithin sections of tails of the homozygous mutant embryos were compared to the wild-type controls. In the wild-type embryos morphologically uniform mesenchyme of the tail bud was continuous via the medullary cord to the secondary neural tube, and via the tail cord to the notochord and the gut. In truncate embryos the tail cord was not continuous to the notochord, but to the additional lumen of the tail gut resulting in tail gut duplication. Toward the base of the tail two tail guts subsequently fused together or the additional one disappeared. If present in the tip of the tail, the notochord in truncate embryos ended near the ventral border of the secondary neural tube. The rest of the tail notochord was fragmented and the posterior ends of the fragments were frequently adjacent or even continuous to the neural tube. We suggest that the improper regionalization of the tail bud, where notochord is associated with the neural tube rather than with the tail gut, is related to the subsequent segmental lack of the notochord in truncate mutants.

Animals↗
PubMed2004

A new model for olfactory placode development.

The peripheral nervous system of vertebrate animals arises primarily from the interaction of cranial neural crest and sensory placodes. Placodes are described as thickenings of ectoderm that arise through cell division during neural tube formation. The olfactory sensory system is one component of the peripheral nervous system that arises from paired sensory placodes during development. The olfactory placodes give rise to the primary sensory neurons, support cells and basal cells of the olfactory epithelium. Recent evidence from work in zebrafish and chick suggests that the olfactory and auditory placodes arise from large fields of cells that converge to form the sensory placode. The olfactory placodes arise from within the neural plate, and cell division is apparent only after the sensory placodes are morphologically distinct. As the olfactory placode is forming, its precursors must segregate from their neighboring fields which will give rise to the adenohypophyseal placode, cranial neural crest, and telencephalon. Analysis has shown that the endocrine cells thought to arise from the olfactory placode originate in the neighboring adenohypophyseal and cranial neural crest domains. The borders separating the domains are plastic, where cells sort as they move, and cell fate is dependent on the identity of neighbors once the cells have converged to form the sensory placode. Thus there is degeneracy built into the system such that cells accommodate changes in the environment until cell migrations controlling the formation of the sensory placodes are complete.

Animals↗
PubMed2006

Differential expression of muscarinic acetylcholine receptors across excitatory and inhibitory cells in visual cortical areas V1 and V2 of the macaque monkey.

Cholinergic neuromodulation, a candidate mechanism for aspects of attention, is complex and is not well understood. Because structure constrains function, quantitative anatomy is an invaluable tool for reducing such a challenging problem. Our goal was to determine the extent to which m1 and m2 muscarinic acetylcholine receptors (mAChRs) are expressed by inhibitory vs. excitatory neurons in the early visual cortex. To this end, V1 and V2 of macaque monkeys were immunofluorescently labelled for gamma-aminobutyric acid (GABA) and either m1 or m2 mAChRs. Among the GABA-immunoreactive (ir) neurons, 61% in V1 and 63% in V2 were m1 AChR-ir, whereas 28% in V1 and 43% in V2 were m2 AChR-ir. In V1, both mAChRs were expressed by fewer than 10% of excitatory neurons. However, in V2, the population of mAChR-ir excitatory neurons was at least double that observed in V1. We also examined m1 and m2 AChR immunoreactivity in layers 2 and 3 of area V1 under the electron microscope and found evidence that GABAergic neurons localize mAChRs to the soma, whereas glutamatergic neurons expressed mAChRs more strongly in dendrites. Axon and terminal labelling was generally weak. These data represent the first quantitative anatomical study of m1 and m2 AChR expression in the cortex of any species. In addition, the increased expression in excitatory neurons across the V1/V2 border may provide a neural basis for the observation that attentional effects gain strength up through the visual pathway from area V1 through V2 to V4 and beyond.

Animals↗
PubMed1990

Effects of retinoic acid on the distribution of glycoconjugates during mouse tail bud development.

Retinoic acid (RA), a potent teratogen of caudal axial development in rodents, has been shown to alter glycoconjugates in a variety of embryonic tissues and teratocarcinomas. In this study, we examined its effects on the expression of cell surface and extracellular matrix glycoconjugates during tail bud development in mouse embryos by using lectin histochemistry. The lectins WGA, sWGA, and PNA showed striking differences in binding between RA-exposed and control embryos. Computer-assisted densitometry revealed a significant increase in binding of all three lectins to the extracellular material of the luminal and abluminal borders of the secondary neural tube and surrounding the notochord in RA-exposed embryos. RA-treated embryos also showed an increased binding affinity for the lectins sWGA and PNA to the cells of the notochord, while WGA showed increased binding to the neuroepithelial cells of the secondary neural tube. The results suggest that RA affects the expression of lectin binding sites during the early development of RA-induced caudal axial defects.

Animals↗
PubMed1997

Border controls at the mammalian spinal cord: late-surviving neural crest boundary cap cells at dorsal root entry sites may regulate sensory afferent ingrowth and entry zone morphogenesis.

Boundary caps (BCs) form when neural crest cells, migrating ventrally alongside the neural tube, arrest at sites where axons will enter and exit. However, nothing is known of their subsequent fate and functions. We have found late-surviving neural crest BC cell clusters at proximal dorsal root entry sites throughout rat spinal cord development. Sensory afferents cross BCs to enter the spinal cord, while exiting astrocyte processes, destined to form the dorsal root entry zone (DREZ) after birth, are temporarily stalled in their vicinity. To test whether contact with BC cells influences neurite outgrowth from dorsal root ganglia, neurons were cultured on embryonic dorsal root/spinal cord cryosections. Neurites that entered CNS territory preferentially extended over BC cells. Thus, BC cells could be instrumental in regulating afferent ingrowth and DREZ morphogenesis in mammalian spinal cord development.

Animals↗
PubMed1997

Detached retina affects morphologic and biochemical changes in the retina adjacent to bullous retinal detachment in rabbits.

PURPOSE: Long-term results, more than 10 years after successful retinal detachment surgery, have shown gradually decreasing visual acuity in some cases. It is unclear if reduced functional recovery postoperatively is caused by anatomic changes or biochemical disorders. To determine the etiology of the reduced visual acuity, we cytochemically examined the changes in the cellular responses of the edges of retinal detachments. METHODS: We histochemically studied the glucose-6-phosphatase (G6P) and 5'-nucleotidase (5'-Nase) activity in the rabbit retina. Experimental rhegmatogenous retinal detachment was produced in a rabbit model after partial vitrectomy, followed by retinal tear formation. RESULTS: Although 5'-Nase activity gradually decreased during the period of detachment, activity was still detectable after 24 weeks. G6P activity increased in the region of the detached neural retina. Around the border of the detached retina, the decrease in 5'-Nase activity extended approximately 140 micrometers into the adjacent attached retina at 2 weeks after detachment and 270 micrometers at 24 weeks. CONCLUSIONS: These observations suggest that some anatomical and biochemical damages may occur in the retina adjacent to bullous retinal detachment and may explain the reduction in postoperative vision in some clinical cases.

5'-Nucleotidase↗
PubMed1998

Hoxd-4 expression during pharyngeal arch development in flounder (Paralichthys olivaceus) embryos and effects of retinoic acid on expression.

Teleost fish develop seven pharyngeal arches (mandible, hyoid and five gill arches) which give rise to the jaw and gills, and skeletal cell populations which originate from the cranial neural crest. The anterior border of expression of the Deformed (Dfd) group is located in the hindbrain and pharyngeal region. To investigate pharyngeal skeletal formation in the teleost fish, we cloned the cDNA coding Hoxd-4 from a cDNA library for flounder (Paralichthys olivaceus) embryos, and analyzed gene expression pattern during embryogenesis and the effects of retinoic acid (RA) on this gene expression. Between the 21-somite and prim-5 stages, Hoxd-4 was expressed in the central nervous system from rhombomere 7 to the spinal cord, and in the pharyngeal region posterior from gill arch 2. Its expression then became restricted to cartilage precursor cells of gill arches 2-5. When embryos in the early shield stage were exposed to RA at concentrations above 10(-7) M, the anterior border of Hoxd-4 expression shifted anteriorly in a dose-dependent manner, both in the central nervous system and pharyngeal region. We propose that, during gill skeleton formation, Hoxd-4 functions in the specification of regional identity between gill arches 1 and 2, and that their identity is affected by treatment with RA.

Animals↗
PubMed1999

Neural modulation of cephalexin intestinal absorption through the di- and tripeptide brush border transporter of rat jejunum in vivo.

Intestinal absorption of beta-lactamine antibiotics (e.g., cefixime and cephalexin) has been shown to proceed through the dipeptide carrier system. In a previous study, nifedipine (NFP), an L-type calcium channel blocker, enhanced the absorption of cefixime in vivo but not in vitro, and it was suggested that neural mechanisms might be involved in the effect of NFP. The aim of the present study was to assess the involvement of the nervous system on the intestinal absorption of cephalexin (CFX). To investigate this, we used a single-pass jejunal perfusion technique in rats. NFP and diltiazem enhanced approximately 2-fold the plasma levels of CFX in treated rats versus untreated controls. NFP also increased approximately 2-fold the CFX level in portal plasma and increased urinary excretion of CFX, thus indicating that CFX did effectively increase CFX intestinal absorption. Perfusing high concentrations of dipeptides in the jejunal lumen competitively reduced CFX absorption and inhibited the enhancement of CFX absorption produced by NFP. Hexamethonium and lidocaine inhibited the effect of NFP, whereas atropine, capsaicin, clonidine, and isoproterenol enhanced CFX absorption by the same order of magnitude as NFP. Thus, complex neural networks can modulate the function of the intestinal di- and tripeptide transporter. Sympathetic noradrenergic fibers, intestinal sensory neurons, and nicotinic synapses are involved in the increase of CFX absorption produced by NFP.

ATP-Binding Cassette Transporters↗
PubMed1990

Origin of infrasound sensitive neurones in the papilla basilaris of the pigeon: an HRP study.

Infrasound sensitive afferent fibres recorded in the pigeon cochlear ganglion were marked by intracellular injections of horseradish peroxidase (HRP). All stained fibres were found to innervate hair cells in the basilar membrane between 90 and 950 microns from its apical end. No fibres to the macula lagenae were found. Nine of the 10 completely stained fibres contacted hair cells located abneurally on the free basilar membrane, the tenth ended over the neural limbus near its abneural border. All fibres innervated between two and nine hair cells. This is in contrast to common auditory fibres in the bird that were reported to innervate only one hair cell located neurally over the neural limbus. This paper, therefore, demonstrates, for the first time, physiologically defined fibres that do not end on 'inner' hair cells.

Animals↗
PubMed1995

Identification of the border between fibronectin type III homologous repeats 2 and 3 of the neural cell adhesion molecule L1 as a neurite outgrowth promoting and signal transducing domain.

To determine the domains of the neural cell adhesion molecule L1 involved in neurite outgrowth, we have generated monoclonal antibodies against L1 and investigated their effects on neurite outgrowth of small cerebellar neurons in culture. When the 10 antibodies were coated as substrate, only antibody 557.B6, which recognizes an epitope represented by a synthetic peptide comprising amino acids 818 to 832 at the border between the fibronectin type III homologous repeats 2 and 3, was as efficacious as L1 in promoting neurite outgrowth, increasing intracellular levels of Ca2+, and stimulating the turnover of inositol phosphates. These findings suggest that neurite outgrowth and changes in these second messengers are correlated. Such a correlation was confirmed by the ability of Ca2+ channel antagonists and pertussis toxin to inhibit neurite outgrowth on L1 and antibody 557.B6. These observations indicate for the first time a distinct site on cell surface-bound L1 as a prominent signal-transducing domain through which the recognition events appear to be funneled to trigger neurite outgrowth, increase turnover of inositol phosphates, and elevate intracellular levels of Ca2+.

Amino Acid Sequence↗
PubMed1989

The morphogenesis of hindbrain crowding associated with lumbosacral myeloschisis.

The teratogenicity of ethylenethiourea (ETU) was investigated in Sprague-Dawley rats and Landrace pigs. Pregnant rats each received a single intragastric dose of ETU on a given day from day 8 to day 19 of gestation, and pregnant pigs were given a single dose of ETU from day 15 to day 19. Control animals received an ETU-free vehicle. The newborn pigs were all normal, whereas there were high incidences of specific types of congenital malformation of the central nervous and other systems in the rats. A high incidence of lumbosacral myeloschisis associated with hindbrain crowding was observed in rat fetuses exposed to ETU on day 11 of gestation. This abnormality is considered comparable to Chiari type II malformation associated with spinal dysraphism (Arnold-Chiari malformation) in humans. Morphogenetic fetuses were examined by light and scanning electron microscopy and interactive image analysis. At gestational days 12 and 13, the volume of the caudal end of the neural tube from the anterior border of the hindlimb bud to the most caudal portion of the fetus was significantly greater in ETU-exposed than in control rat embryos. Experimental rat embryos also exhibited disturbance in closure of the posterior neuropore, with extrusion of neural tissue through the opening. An apparently unrelated abnormality in ETU-exposed rat fetuses was underdevelopment of the cranium, leading to hindbrain crowding.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2005

Resolving border disputes in midlevel vision.

Two papers in this issue of Neuron specify the coding of border ownership, the basis of figure-ground segmentation, in early extrastriate visual cortex (area V2). Recording from a population of neurons, Qiu and von der Heydt show that border ownership assignments based on 2D images show the same bias when tested with stereopsis. Zhaoping shows that a neural model of V2 can make appropriate border assignments based on 2D images.

Form Perception↗
PubMed1978

Central neural pathways for angiotensin-induced thirst.

Evidence is reviewed implicating the preoptic region in angiotensin-induced thirst. The most responsive area according to results obtained with behavioral, electrophysiological, and autoradiographic mapping techniques is at the caudal border of the medial preoptic region and rostral border of the anterior hypothalamus. The neural pathway from this preoptic site for angiotensin-induced thirst extends along the medial forebrain bundle through the midlateral hypothalamus to the paramedial midbrain tegmentum and to an area ventrolateral to the central gray. Lesions of this pathway in the midlateral hypothalamus and rostral midbrain significantly attenuated drinking induced by microinjections of angiotensin II into the preoptic area but did not disrupt water intake induced by microinjections of angiotensin II into the subfornical organ or cerebral ventricles. Although the efferent pathways from angiotensin-receptive sites in the subfornical organ and cerebral ventricles are unknown, it appears from these observations that the medial forebrain bundle is not involved. Lesions of the medial forebrain bundle-lateral hypothalamus also do not disrupt drinking induced by microinjections of hypertonic saline into the preoptic region although lesions placed 1 mm further lateral do. Since fat lateral hypothalamic lesions are without effect on drinking induced by centrally administered angiotensin II, this suggests that intracellular and extracellular thirst signals are subserved by separate neural pathways in the hypothalamus.

Action Potentials↗