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PubMed2006

Cortical progenitor cells in the developing human telencephalon.

Radial glial (RG) cells have been demonstrated to be a major neural progenitor cell type, but in the human fetal brain, neither their molecular nor their spatiotemporal characteristics are well known. We used glial and neuronal-specific antibodies to determine the antigen characteristics and distribution of RG cells and other neuronal progenitors in the human brain during the first half of intrauterine development. Proliferating RG (4A4+) cells in the ventricular zone (VZ) showed clear caudorostral and ventrodorsal gradients, spreading from the spinal cord to the ventral rhombencephalon, at embryonic stages (4.5-5.5 gestational weeks [gw]). However, in the same embryo, other dividing cells expressed the neuronal marker SMI-31 and were present throughout the entire CNS, including the rostral prosencephalon. At the beginning of cortical neurogenesis (6 gw), proliferating VZ cells labeled either with neuronal markers (SMI-31, MAP2, beta-III-tubulin), double-labeled 4A4(+)/SMI-31+ cells, or cells not labeled with these antibodies, were in close proximity to each other. At midgestation (17-24 gw), RG divisions were less frequent, but were spread throughout the entire cerebral cortex, including the subventricular and intermediate zones and the subpial granular layer. Several subtypes of RG were co-labeled with vimentin and other glial markers (BLBP, GFAP, or GLAST) and quantified in vitro. In conclusion, the diversity of cortical progenitors in the human brain may, in part, explain the unique complexity of the human cerebral cortex.

Aborted Fetus↗
PubMed2004

Molecular screening of SHH, ZIC2, SIX3, and TGIF genes in patients with features of holoprosencephaly spectrum: Mutation review and genotype-phenotype correlations.

Holoprosencephaly (HPE; 1 out of 16,000 live births; 1 out of 250 conceptuses) is a complex brain malformation resulting from incomplete cleavage of the prosencephalon, affecting both the forebrain and the face. Clinical expressivity is variable, ranging from a single cerebral ventricle and cyclopia to clinically unaffected carriers in familial dominant autosomic HPE. The disease is genetically heterogeneous, but additional environmental agents also contribute to the etiology of HPE. In our cohort of 200 patients, 34 heterozygous mutations were identified, 24 of them being novel ones: 13 out of 17 in the Sonic hedgehog gene (SHH); 4 out of 7 in ZIC2; and 7 out of 8 in SIX3. The two mutations identified in TGIF have already been reported. Novel phenotypes associated with a mutation have been described, such as abnormalities of the pituitary gland and corpus callosum, colobomatous microphthalmia, choanal aperture stenosis, and isolated cleft lip. This study confirms the great genetic heterogeneity of the disease, the important phenotypic variability in HPE families, and the difficulty to establish genotype-phenotype correlations.

Adult↗
PubMed1978

The pineal-paraphyseal complex of sea turtles. I. Light microscopic description.

The pineal-paraphyseal complex of sea turtles is an impressively large structure which projects dorsally and anteriorly above the prosencephalon. The complex was examined by light microscopy in several age classes of green sea turtles (Chelonia mydas) and from juvenile loggerhead turtles (Caretta caretta). The paraphysis is extensively fused to the distal portion of the pineal body, suggesting an interrelated function for these two tissues. No duct or canal was observed connecting the pineal lumen to the third ventricle. Two pineal cell types are described which appear to correspond to the neuroglial supportive cells and the secretory rudimentary photoreceptor cells of other amniotic vertebrates. A possible luminal secretion in the form of apical protrusions is produced by the latter cell type. No typical photoreceptive outer segments were observed.

Animals↗
PubMed1981

Arterial circulation of the spinal cord and brain in the Monodontidae (order Cetacea).

In this paper we document retial supply of the spinal cord and describe the arterial vascular pattern of the brain in the whale family Monodontidae. Observations are based on gross dissections of four brains, two each of Monodon monoceros and Delphinapterus leucas, and one spinal cord from M. monoceros. Vessels of the spinal cord arise from extradural retia in the neural canal. Arteries originating from the retia penetrate the dura between successive spinal roots (mainly ventral) and not in association with them, unlike radicular arteries of other mammals. Also, these vessels are uniformly distributed and contribute equally to a plexus surrounding the cord. An A. radicularis magna is not present, and neither are distinct anterior or posterior spinal arteries. Circulation to the brain is effected by two pairs of arteries originating from intracranial retia. The rostral pair supplies most of the forebrain (prosencephalon), whereas the more caudal pair supplies mainly the midbrain (mesencephalon) and hindbrain (rhombencephalon). The circulatory pattern is characterized by 1) complete independence of anterior cerebral arteries (no anastomoses); 2) extensive cortical supply by the anterior choroidal arteries; 3) absence of subdural communicating vessels between rostral and caudal trunks; 4) union of caudal trunks to form a small basilar artery; and 5) absence of vertebral arteries and hence of a vertebral basilar system. There are some obvious differences between subdural arteries in the Monodontidae and those in other mammals; however, their general patterns of distribution are similar, and we suggest that most of the vessels, at least in the cranium, are homologous.

Animals↗
PubMed1991

Development of paleocortical projections through the anterior commissure of hamsters adopts progressive, not regressive, strategies.

The perinatal development of anterior commissure projections was studied in hamsters by use of carbocyanine crystals implanted either into the commissure or into the ventrolateral prosencephalon. The earliest fascicles of growing commissural fibers had reached the midline on day 14 of gestation (E14). On E15, these fibers had entered the opposite hemisphere and reached the borders of their target regions. No waiting period was observed, since on E16 axons were already collateralizing into most targets. On P1, labelled cells were seen in all regions projecting through the anterior commissure in adults, namely, the anterior olfactory nucleus, olfactory tubercle, piriform cortex, nucleus of the lateral olfactory tract, bed nucleus of the stria terminalis, insular, perirhinal, entorhinal, and temporal cortices, as well as the amygdaloid complex. No evidence of topographical exuberance was detected. Counts of labelled neurons showed that the number of commissural cells increased gradually after birth. It is concluded that the development of paleocortical connections through the anterior commissure employs progressive strategies, lacking the regressive phenomena that are characteristic of the neocortical projections through the corpus callosum.

Aging↗
PubMed2005

Lobar holoprosencephaly: prenatal MR diagnosis with postnatal MR correlation.

Holoprosencephaly is a congenital anomaly characterized by lack of cleavage of the prosencephalon. Although, relatively rare, it is the most common anomaly that involves both the brain and the face. Prenatal diagnosis of this anomaly using ultrasonography, particularly of the less severe forms, is difficult. Magnetic resonance imaging has recently become an important complement to US in prenatal diagnosis of CNS anomalies. We herein report a patient in whom, at 23 weeks of gestation, US suggested agenesis of the corpus callosum and in whom, at 24 weeks of gestation, MRI correctly diagnosed lobar holoprosencephaly, which was confirmed by a postnatal MRI at 3 weeks of age.

Adult↗
PubMed1991

Early transvaginal sonographic diagnosis of alobar holoprosencephaly.

Holoprosencephaly is a cerebral anomaly resulting from incomplete cleavage of the primitive prosencephalon or forebrain. Early detection of this anomaly is very important since the most severe form is incompatible with life. The diagnosis also signals the need for a chromosomal determination since chromosomal abnormalities have been associated with this anomaly. An early diagnosis of alobar holoprosencephaly at 14 weeks' gestation, employing transvaginal sonography, is reported. Our findings are compared with prenatal transabdominal sonographic findings of holoprosencephaly which have been reported during the last decade in the literature.

Adult↗
PubMed2003

Ethmocephaly caused by de novo translocation 18;21--prenatal diagnosis.

Ethmocephaly is a rare anomaly associated with partial failure of cleavage of the prosencephalon. Morphologically, it is closely related to cyclopia. We present an extremely rare case of ethmocephaly diagnosed in utero and caused by an unbalanced de novo translocation 18;21.

Chromosomes, Human, Pair 18↗
PubMed1975

Teratogenesis in cats associated with griseofulvin therapy.

Multiple congenital malformations occurred in kittens of three cats treated orally at weekly intervals with 500-1000 mg of the antifungal drug griseofulin. Malformations of the brain included exencephaly, malformed prosencephalon, caudal displacement, and hydrocephalus. Skeletal malformations included cranium bifidium, spina bifida (C1 through C4, and sacral), abnormal atlantooccipital articulation, cleft palate, absence of maxillae, and lack of tail vertebrae. Cyclopia and anophthalmia with absence of optic nerves and rudimentary optic tracts were also observed. Atresia ani, atresia coli, lack of atrioventricular valves in the heart, and absence of external nares and soft palate were other abnormalities present.

Abnormalities, Drug-Induced↗
PubMed1982

Facial duplication: case, review, and embryogenesis.

The craniofacial anatomy of an infant with facial duplication is described. There were four eyes, two noses, two maxillae, and one mandible. Anterior to the single pituitary the brain was duplicated and there was bilateral arhinencephaly. Portions of the brain were extruded into a large frontal encephalocele. Cases of symmetrical facial duplication reported in the literature range from two complete faces on a single head (diprosopus) to simple nasal duplication. The variety of patterns of duplication suggests that the doubling of facial components arises in several different ways: Forking of the notochord, duplication of the prosencephalon, duplication of the olfactory placodes, and duplication of maxillary and/or mandibular growth centers around the margins of the stomatodeal plate. Among reported cases, the female:male ratio is 2:1.

Eye Abnormalities↗
PubMed1985

Morphological and biochemical aspects of monofunctional phosphoramide mustard teratogenicity in rat embryos cultured in vitro.

Day 10 rat embryos were exposed in vitro to a monofunctional analog of phosphoramide mustard (MPM) at concentrations of 25 to 200 micrograms/ml (144 to 1,156 X 10(-6) M). After a 24-hour exposure, embryos exhibited a dose-dependent decrease in growth parameters (crown-rump length, number of somites, and protein content) as well as incidence of malformations. Abnormal embryos were characterized by hypoplasia of the prosencephalon as well as hypoplasia of the mandibular arches, tail, and limb buds. Histological analysis revealed abnormal levels of necrotic cells, particularly in the neuroepithelium and surrounding mesenchyme. In all respects embryos exposed to MPM could not be distinguished from embryos exposed to phosphoramide mustard. We also determined using mouse L1210 cells that at the maximum nonlethal concentration used in our embryo exposure experiments, MPM did not cause DNA cross-linking but did cause single-strand DNA breaks. Phosphoramide mustard, at concentrations teratogenic to embryos in vitro, did produce DNA cross-linking. Taken together, our results indicate that although cyclophosphamide (CP)-induced DNA cross-linking may play a role in CP teratogenesis, DNA cross-linking is not an absolute requirement.

Animals↗
PubMed1986

Methacrylic acid as a teratogen in rat embryo culture.

Using day 10 rat embryos cultured in vitro, we have shown that methacrylic acid is teratogenic at concentrations ranging from 1.2 to 2.1 mM. At these concentrations, methacrylic acid produced concentration-dependent decreases in growth parameters, i.e., crown-rump length, number of somites, and embryo protein content. In addition, methacrylic acid exposure produced malformed embryos characterized primarily by abnormal neurulation. Less frequent abnormalities included hypoplasia of the prosencephalon, edema, malpositioned heart, abnormal flexion, and dilated otic vesicles. Accompanying these abnormalities was an underlying increase in methacrylic acid-induced cell death.

Acrylates↗
PubMed1989

Embryotoxicity of phenyl ketone analogs of cyclophosphamide.

Phenylketophosphamide and phenylketoisophosphamide are preactivated acyclic ketone analogs of cyclophosphamide and isophosphamide with antitumor activity. These compounds undergo an elimination reaction to yield phosphoramide or isophosphoramide mustard and phenyl vinyl ketone. In this study, the embryotoxicity of phenylketophosphamide, phenylketoisophosphamide, and phenyl vinyl ketone were determined. Embryotoxicity was assessed in vitro in whole rat embryos cultured on day 10.5 of gestation in the absence and presence of an activating system derived from maternal liver. Both phenylketophosphamide and phenylketoisophosphamide were embryotoxic in the absence of metabolic activation. Moreover, there was no enhancement of this embryotoxicity in the presence of an activating system. A 10-microM concentration of phenylketophosphamide produced 100% malformed embryos, while this concentration of phenylketoisophosphamide was not teratogenic. At 25 microM phenylketoisophosphamide, all the surviving exposed embryos were malformed. Phenylketophosphamide was embryolethal to more than 50% of the exposed embryos at a concentration of 50 microM. In contrast, a concentration of phenylketoisophosphamide of 100 microM was required to produce significant embryolethality. Phenyl vinyl ketone was not embryotoxic at any of the concentrations tested. The major malformation observed, a hypoplastic prosencephalon, and the growth retardation effects were not only similar for phenylketophosphamide and phenylketoisophosphamide, but also similar to those previously reported for "activated" cyclophosphamide. Unlike the results with cyclophosphamide, where both phosphoramide mustard and the aldehydic metabolite of cyclophosphamide, acrolein, are toxic, the embryotoxic effects of phenylketophosphamide and phenylketoisophosphamide are mediated only by the mustard metabolite.

Animals↗
PubMed1989

Developmental study of neural tube closure in a mouse stock with a high incidence of exencephaly.

About 17% of embryos and fetuses in the SELH/Bc mouse stock have the anterior neural tube defect, exencephaly. No other malformations are seen. The genetic liability to exencephaly was shown to be probably genetically fixed in the SELH/Bc stock. This means that SELH/Bc embryos with successful neural tube closure are genetically the same as exencephalics. Females were significantly more likely to be affected than males (66% females). The pattern of morphological developmental events during anterior neural tube closure on days 8 and 9 of gestation was compared among 322 ICR/Bc (normal), 304 SWV/Bc (normal), and 265 SELH/Bc embryos. Anterior neural tube closure was found to follow a strikingly different pattern in almost all SELH/Bc embryos than in either of the normal strains or in previous published studies. SELH/Bc embryos lack the initial contact between the anterior folds in the posterior prosencephalon/anterior mesencephalon region (Closure 2). In spite of this, all but 17% manage to close the anterior neural tube by extending caudally the later occurring normal anterior zone of contact and fusion at the most rostral aspect of the prosencephalon (Closure 3) through the region of Closure 2 to meet the zone of closure of the rhombencephalon, Closure 4. Anterior neural tube closure was completed late, and in some SELH/Bc embryos, elevation and fusion in the mesencephalon did not occur at all. In histological sections of six- and eight-somite embryos, elevated numbers of pyknotic cells in the neuroepithelium and mesenchyme, and elevated numbers of unstained inclusions in the neuroepithelium were found; but their relationship, if any, to the abnormal pattern of neural tube closure is not clear.

Animals↗
PubMed1990

Embryotoxic effects of sodium arsenite and sodium arsenate on mouse embryos in culture.

Embryotoxic effects of two inorganic arsenic compounds, sodium arsenite (Asi) and sodium arsenate (Asa), on the development of mouse embryos during early organogenesis were studied using the whole embryo culture technique. Embryos with three to five somites exposed to 1-40 microM Asi or to 10-400 microM Asa were cultured for 48 hours and their development was compared with that of control embryos. Asi proved to be teratogenic between 3 and 4 microM and embryolethal at higher concentrations; Asa had similar activity but at concentrations ten times higher than for Asi. Both compounds produced a growth retardation and a similar pattern of defects. Growth retardation was indicated by a statistically significant reduction in crown-rump length, head length, and yolk sac diameter. Abnormal embryos were characterized by hypoplasia of the prosencephalon with open neural tube, hydropericardium, somite abnormalities, and failure of development of limb buds and sensory placodes. These results confirm that both Asa and Asi are embryotoxic compounds and that the Asi activity occurs at concentrations ten times lower than for Asa. Our results suggest that in humans both of these compounds may be involved in part of "unaccountable" early abortions and malformations claimed to be due to the toxicity of heavy metals.

Animals↗
PubMed1990

Embryotoxicity of the intercalating agents m-AMSA and o-AMSA and the epipodophyllotoxin VP-16 in postimplantation rat embryos in vitro.

The intercalating agent, m-AMSA, and the epipodophyllotoxin, VP-16, both topoisomerase II-reactive anticancer agents, are also embryotoxic agents in rat embryos cultured in vitro. Quantifying the embryotoxic effects of these drugs revealed that the no observed adverse effect level (NOAEL) for m-AMSA is 10 nM, the embryotoxic concentration range is 50-500 nM, and complete lethality is observed at 1 microM. In contrast, the NOAEL for o-AMSA, an inactive isomer of m-AMSA, is 1.0 microM, the embryotoxic concentration range is 10-100 microM, and complete lethality occurs at 200 microM. Based upon the concentrations of drugs required to produce 50% embryotoxicity or 50% malformed embryos, m-AMSA exhibits a 200-500-fold-higher embryotoxicity compared to o-AMSA. VP-16 exhibits a NOAEL of 1.0 microM, an embryotoxic concentration range of 2-5 microM, and complete lethality at 10 microM. Compared to m-AMSA, VP-16 is approximately 10-fold less embryotoxic. At appropriate concentrations, all three drugs were dysmorphogenic resulting in embryos that were characterized by hypoplasia of the prosencephalon with associated microopthalmia and dilation of the rhombencephalon. and dilation of the rhombencephalon. As a prelude to future studies focusing on the mechanism of drug-induced embryotoxicity, we have used established biochemical and immunologic methods to identify and quantify topoisomerase II in rat embryos. In addition, we have demonstrated that the embryo topoisomerase II can be inhibited by both m-AMSA and VP-16. Finally, we have used a human cDNA probe to detect topoisomerase II mRNA in the rat embryo. Thus, the combination of the in vitro whole embryo culture and these biochemical/molecular assays should allow us to explore the role of a specific nuclear target, i.e., topoisomerase II, in the teratogenic effects of some commonly employed chemotherapeutic agents.

Abnormalities, Drug-Induced↗
PubMed1990

Effects of pulsed ultrasound and temperature on the development of rat embryos in culture.

Rat embryos in culture were exposed to pulsed ultrasound at SPTA intensity of 1.2 W/cm2 for 5, 15, and 30 min on day 9.5 of development. The whole embryo culture system allowed precise temperature control for directly examining the effects of ultrasound on the developing neural plate. After exposure, embryos were maintained in culture for a further 48 hr. No major morphological abnormalities were observed but a reduction in somite number occurred in the group insonated for 30 min, which was equivalent to a 2 hr delay in embryonic development. Similar delay in growth and "blistering" in the prosencephalon region of some embryos were observed after insonation for 15 min at 40.0 degrees C, an elevation of 1.5 degrees C over the temperature used for controls. Exposure to ultrasound for 15 min at 40 degrees C caused significant reduction in the growth of the head compared with that of control embryos. Heat shock genes for hsps 71/73 and 88 kD were induced after insonation for 30 min at 38.5 degrees C. Insonation did not cause any temperature changes in the culture medium. However, when the temperature of the culture medium was increased during insonation, defective development occurred. The results of these in vitro experiments suggest that ultrasound if resulting in significant hyperthermia could affect the development during early organogenesis of the neural plate and in particular they suggest that the embryo is at greater risk of damage during hyperthermic conditions. These results should provoke discussion of the concept that ultrasound in the febrile patient may present an increased embryonic risk which should be considered when deliberating on the use of diagnostic ultrasound procedures in the pregnant patient.

Animals↗
PubMed1991

Normal mouse strains differ in the site of initiation of closure of the cranial neural tube.

The scanning electron microscopic study of day 9 embryos reported here documents differences among normal mouse strains in morphology of cranial neural tube closure. The site of initiation of contact and fusion of the cranial neural folds, previously defined as Closure 2 (Macdonald et al., '89), is located in the region of the junction between the forebrain (prosencephalon) and midbrain (mesencephalon) in three normal strains: LM/Bc, AEJ/RkBc, and ICR/Bc. However in a fourth normal strain, SWV/Bc, Closure 2 is initiated much further rostral, in the prosencephalic region. In addition, the anterior neuropore, rostral to Closure 2, closes late in ICR/Bc embryos, relative to the posterior progress of development of the Closure 2 seam. Initiation of closure from the most rostral end of the neural tube (Closure 3) appears to be relatively delayed in ICR/Bc embryos. We hypothesize that the observed genetic polymorphism in location of the first site of fusion between the cranial neural folds in normal mouse embryos may be one basis for differences among normal strains in liability to exencephaly induced by teratogens.

Animals↗