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PubMed1995

Brain chimeras for the study of an avian model of genetic epilepsy: structures involved in sound and light-induced seizures.

The epileptic homozygotes of the Fayoumi strain of chickens (Fepi) are affected by photogenic reflex epilepsy with complete penetrance. Here we demonstrate that they are equally affected by audiogenic reflex epilepsy induced by intense sound stimulation. All the Fepi display sound-induced seizures from hatching to adulthood consisting of initial 'ictal arousal' and running fits usually followed by generalized clonico-tonic convulsions. A running fit is the preconvulsive motor symptom specifically induced by auditory stimulation while neck myoclonus is the preconvulsive motor symptom specifically induced by photic stimulation. The EEG interictal spikes and spike and waves are suppressed and replaced by a desynchronized trace during the seizures of both kinds. Viable neural chimeras were obtained by graft of embryonic brain vesicles from Fepi donors into normal chick embryos. Transfer of the complete audiogenic and photogenic phenotypes was obtained in chimeras resulting from embryonic substitution of both the prosencephalon and mesencephalon. The substitution of the prosencephalon alone resulted in transfer of interictal paroxysmal EEG activity accompanied by the sound and light-induced desynchronization and 'ictal arousal' with no motor seizures. Chimeras with embryonic substitution of the mesencephalon alone displayed running fits and convulsions induced by sound stimulation but only neck myoclonus following light stimulation. The conclusions are reached that: (i) the Fepi is a model of audiogenic and photogenic reflex epilepsy; (ii) in both types, the seizure initiator and the convulsion generator are localized in the brainstem, although reinforcement from telencephalic visual structures is needed to trigger photogenic generalized convulsions.

Acoustic Stimulation↗
PubMed1988

Brain monoamine levels in suckling mice following postnatal exposure to secalonic acid D via the dam's milk.

Mice were gavage-fed on day 13 of pregnancy with 0 (groups N, 15, 25) or 25 (group P) mg/kg of secalonic acid D (SAD) and again while nursing their offspring on postgestational days 1-10 with 0 (N,P), 15(15) or 25(25) mg/kg/day. SAD residues were present in the stomach of pups nursed by SAD-treated dams. Postnatal exposure to SAD decreased (P less than 0.05) body weight gains of offspring. Treatment decreased the developmental levels of norepinephrine and dopamine in the prosencephalon (forebrain) and cerebellum-pons of the offspring on postnatal days (PND) 7 and 7-16, respectively. On PND 7-16 serotonin and 5-hydroxyindoleacetic acid levels decreased in the prosencephalon and cerebellum-pons of offspring exposed prenatally (P) or postnatally (15,25) to SAD.

Animals↗
PubMed1988

Amino acid neurotransmitters and their receptors in the brain synaptosomes of acute hepatic failure rats.

Ammonia contents in the brain stem and prosencephalon markedly increased in a rat model of acute hepatic failure induced by partial hepatectomy following CCl4 intoxication. In hepatic failure rats, synaptosomal glutamic acid (excitatory amino acid neurotransmitter) contents decreased significantly in the prosencephalon, and GABA (inhibitory amino acid neurotransmitter) contents decreased significantly in the brain stem. The molar ratio of glutamic acid to glutamine significantly diminished in the brain stem. Glutamic acid decarboxylase activity in the synaptosomes and the binding of [3H]glutamic acid and [3H]GABA to synaptosomal membrane preparations were unchanged in acute hepatic failure rats. These results indicate than an insufficiency of both excitatory and inhibitory neurotransmitter amino acids is induced by high ammonia contents in the synaptosomes of the brain stem during acute hepatic failure.

Acute Disease↗
PubMedDate not supplied

Secalonic acid D mycotoxin affects ontogeny of brain catecholamines and swimming in mice.

Suckling mice exposed to secalonic acid D (SAD) mycotoxin postnatally (by gavaging dams with 0, 15 or 25 mg/kg on postgestational days 1 to 10) or prenatally (by gavaging with 25 mg/kg on gestational day 13 to produce a positive behavioral teratogenic control group) manifested subtle preweaning neurobehavioral, neurochemical and growth deficits. Gestational length, maternal weight gain, neonatal sex ratio and physical appearance of pups at birth were unaffected by treatment. Prenatal SAD (25 mg/kg) delayed (p less than 0.05) ontogeny of swimming on postnatal days (PND) 11 and 13 and reduced norepinephrine (NE) and dopamine (DA) levels in prosencephalon on PND 7 and in cerebellum-pons on PND 7-16. In the postnatal treatment groups, pup body weight gains were decreased from PND 9-22. Swimming was delayed in the 15 mg/kg postnatal exposure group on PND 11 and 13, while 25 mg/kg delayed swimming on PND 11-15. Postnatal exposure to 25 mg/kg also reduced NE and DA levels in prosencephalon and cerebellum-pons on PND 7-16. SAD thus caused concomitant ontogenetic delays in growth, swimming behavior and brain catecholamine levels following either prenatal (transplacental) or early postnatal (transmammary) exposure. These data indicate that both in utero and lactational exposures must be considered when assessing potential risks posed to developing mammals by environmental neurotoxicants.

Animals↗
PubMed2005

Development of the cholinergic system in the brain and retina of the zebrafish.

We have analyzed the distribution pattern of choline acetyltransferase (ChAT) in the zebrafish brain and retina during ontogeny. ChAT-immunoreactive (ChAT-ir) neurons are observed in the prosencephalon from 60 h postfertilization (hpf) onwards, exclusively in the preoptic area (basal plate of p6) derived from the secondary prosencephalon. In the mesencephalon, ChAT-ir cells are observed in both the optic tectum and the tegmentum. Stained cells in the tegmentum are observed from 60 hpf onwards, while in the optic tectum they appear after hatching. In the rhombencephalon, ChAT-ir cells are first observed in the isthmic region (rh1) and in the medulla oblongata (rh5-rh7) at the end of embryonic life. The rhombencephalic cholinergic cell groups develop in a gradual caudorostral sequence. Motoneurons of the spinal cord are ChAT-ir from 48 hpf onwards. The retina displays ChAT-ir neuropil in both the inner and outer plexiform layers from embryonic life, whereas stained amacrine cells are only observed after hatching. The staining in the outer plexiform layer gradually decreases during juvenile development. The optic nerve axons show a transient expression of ChAT at the end of embryonic development. The early presence of ChAT immunolabeling suggests an important neuromodulator role for acetylcholine in the first developmental stages.

Animals↗
PubMed1991

Transfer of genetic epilepsy by embryonic brain grafts in the chicken.

In the Fayoumi chicken, a spontaneous recessive autosomal mutation (F.Epi) is responsible for high susceptibility to seizures that are especially inducible by intermittent light stimulation. Substitution of defined areas of the encephalic neuroepithelium in normal chicken embryos at 2 days of incubation by their counterparts from homozygous F.Epi embryos generates the epileptic phenotype in the chimeras. It was found that grafting primordia of both prosencephalon and mesencephalon of homozygous F.Epi birds is necessary and sufficient for transfer of the full disease. When grafted alone, the homozygous F.Epi prosencephalon, although showing the typical epileptic interictal electroencephalogram, does not allow the complete epileptic seizures to occur in the hosts. Grafts of mesencephalon and/or rhombencephalon modify neither the behavior nor the electroencephalographic pattern of the recipient chickens. Cooperation of forebrain and midbrain activities is therefore required to yield epileptic seizures in this model.

Animals↗
PubMed1982

Anterior pituitary gland secretion after forebrain ablation: periovulatory gonadotropin release.

We sought to determine whether the estrous phase of FSH release in cyclic female rats is dependent on the immediate presence of the diencephalon. A piece of forebrain, the diencephalon and part of the telencephalon, was surgically removed from female rats between 1130--1300 or 2000-2200 h on proestrus. Blood was withdrawn through indwelling venous cannulae during the afternoon and evening of proestrus and the early morning of estrus for RIA of plasma LH, FSH, and PRL concentrations. In rats sham operated at either time period, plasma LH, FSH, and PRL levels rose from 1345 to 1800 h on proestrus. Whereas the plasma LH and PRL concentrations fell from 1800 h on proestrus to 0300 h on estrus, the plasma FSH concentrations remained elevated during this period. The removal of the piece of forebrain around noon on proestrus blocked the rises in the plasma LH and FSH levels and caused high plasma PRL concentrations from 1345 h on proestrus to 0300 h on estrus. The removal of the piece of forebrain during the evening of proestrus did not interfere with the fall in plasma LH concentrations or the maintenance of elevated plasma FSH concentrations during either late proestrus or the early morning estrus, but did cause high plasma PRL levels during that time interval. Hypophysectomy combined with removal of the forebrain piece during the evening of proestrus resulted in a drop in plasma FSH and PRL concentrations. The results confirm that in the rat, 1) the prosencephalon plays an acute stimulatory role n causing the preovulatory LH surge and the proestrous phase of FSH release, 2) the prosencephalon exerts effects during the afternoon and/or early evening of proestrus that cause the estrous phase of FSH release, and 3) the estrous phase of FSH release occurs in the absence of acute diencephalic stimulation.

Animals↗
PubMed1990

Patterning of chick brain vesicles as revealed by peanut agglutinin and cholinesterases.

Differentiation of individual rhombomeres of the chicken hindbrain directly follows the emergence of primary brain vesicles. Immediately after the constriction of the prosencephalon at HH9, a series of vesicles of decreasing size is established almost simultaneously between HH9 and HH10, including mesencephalon, four preotic (R2-R5) and one postotic (R6/R7) rhombomeres. Thereby, the cranial neural tube is ventrally embedded in a mesodermal PNA-binding matrix that particularly accumulates underneath vesicular constriction sites, as demonstrated for the segregation of the prosencephalon at HH9 and the cerebellar rhombomere R1 from R2 at HH13. The subsequent period of hindbrain differentiation is analyzed by cholinesterase (AChE, BChE) and peanut lectin histochemistry, by the BrdU and the neurite-specific G4 antibodies. Preotically, differentiation of two pairs of rhombomeres (R4 + R5, R2 + R3) starts in R4, immediately followed by R2. The caudal rhombomeres of both pairs are delayed (R5, R3). Then the postotic rhombomere is subdivided, whereby R7 differentiates before R6. Thus, the development in the direct vicinity of the otic vesicle is delayed (R5, R6). R7 is the last rhombomere that is demarcated caudally. Based on these findings, we postulate two processes that may regulate rhombomere formation in the chicken embryo: (a) an early rostrocaudal wave establishing the major brain vesicles, (b) a superimposed pairwise segmentation emanating rostrally and caudally from the otic vesicle. The segregation of the cerebellar rhombomere is a late step.

Animals↗
PubMed1998

Expression of the Emx-1 and Dlx-1 homeobox genes define three molecularly distinct domains in the telencephalon of mouse, chick, turtle and frog embryos: implications for the evolution of telencephalic subdivisions in amniotes.

Homologies between vertebrate forebrain subdivisions are still uncertain. In particular the identification of homologs of the mammalian neocortex or the dorsal ventricular ridge (DVR) of birds and reptiles is still a matter of dispute. To get insight about the organization of the primordia of the main telencephalic subdivisions along the anteroposterior axis of the neural tube, a fate map of the dorsal prosencephalon was obtained in avian chimeras at the 8- to 9-somite stage. At this stage, the primordia of the pallium, DVR and striatum were located on the dorsal aspect of the prosencephalon and ordered caudorostrally along the longitudinal axis of the brain. Expression of homeobox-containing genes of the Emx, Dlx and Pax families were used as markers of anteroposterior developmental subdivisions of the forebrain in mouse, chick, turtle and frog. Their expression domains delineated three main telencephalic subdivisions in all species at the onset of neurogenesis: the pallial, intermediate and striatal neuroepithelial domains. The fate of the intermediate subdivisions diverged, however, between species at later stages of development. Homologies between forebrain subdivisions are proposed based on the conservation and divergence of these gene expression patterns.

Animals↗
PubMed1989

Initial development of capillaries in the neuroepithelium of the mouse.

The developmental stage of the mouse embryo at which capillaries first occurred and their localisation in the neuroepithelium were investigated on serial sections of 9 and 10 days old embryos embedded in paraffin and Epon. In addition, areas of the neuroepithelium in which capillaries had been observed at the light microscopical level were investigated by electron microscopy carried out on embryos fixed with glutaraldehyde supplemented with tannic acid. In 5-7 microns serial sections of paraffin-embedded embryos, capillaries were initially seen in the CNS anlage at Theiler's Stage 14 (1972). At this stage, capillaries also occurred in the prosencephalon, the rhombencephalon and in the developing spinal cord. In 1 micron serial sections of resin-embedded embryos, capillaries could be identified in the neuroepithelium one stage earlier, i.e. at Stage 13. These very early capillaries were seen in the dorsal part of the lateral wall of the prosencephalon which later forms the diencephalon. At the ultrastructural level, those areas of the neuroepithelium in which leptomeningeal capillaries first started to spread into the neuroepithelium were characterised by the disintegration of the basement membrane of the neuroepithelium and the appearance of tannic acid-positive extracellular structures between the neuroepithelium and the adjacent leptomeningeal capillaries.

Animals↗
PubMed1987

[A case of holoprosencephaly with parietal encephalocele].

Holoprosencephaly, as described by DeMyer, is a cerebral malformation in which the embryonic prosencephalon fails to divide into cerebral hemispheres. According to the degree of division in the prosencephalon, he classified holoprosencephaly into three types; alobar, semilobar and lobar type. We have experienced a case of holoprosencephaly with parietal encephalocele. The patient was admitted to our hospital 4 hours after birth because of parietal encephalocele. A radical operation was carried out and encephalocele was diagnosed histologically. After discharge from our hospital, his psychosomatic development was remarkably delayed. On Oct. 20, 1985, he was re-admitted for further examination. CT-scan and cerebral angiography showed characteristic findings. The classification of holoprosencephaly and dorsal cyst malformation is discussed. On encephalocele with holoprosencephaly, it is said that there may be an extra-calvarial extension of the dorsal sac or ventricular system. But, Hutchinson stated in his experience that first, a closure disorder of the neural tube caused encephalocele. And later a disorder of diverticularization produced the holoprosencephalic abnormality. He suggested that there were two independent disorders of organogenesis which might rarely occur in the same patient. We also reported a similar case of holoprosencephaly with parietal encephalocele which has some controversial problems.

Abnormalities, Multiple↗
PubMed1987

The morphology of Australian aboriginal brains--documentation of eight cases.

Cortical morphology of the brains of eight Western Australian Aboriginals was documented. Sulcal patterns permitted classification of the brains into separate groups. Characteristic patterns were found for the shape of the prosencephalon and for the insular, parietooccipital, and frontal cortex in the aboriginal group. The length of the frontal, parietal, and occipital lobes and the width of the temporal lobes was measured. Length, width, and height of the Aboriginal prosencephalons were compared to measurements of eleven Caucasian brains. Postmortem changes, genetic differences, and factors influencing brain development were discussed.

Adult↗
PubMed1982

[Fusion of the ventricular walls at the level of the dorsal and ventral telodiencephalic sulci].

In the course of development of the mouse embryo prosencephalon, the walls of the dorsal and ventral telodiencephalic sulci fuse along their ependymal surfaces. This study is based on 1 mu semithin sections of the prosencephalon and on ultrathin sections of the fusion zone of mice of 13 days postconception. Ultrathin sections of the rostral part of the fusion zone present two rows of junctions (maculae adhaerentes) in opposition belonging to each of the two walls. On either side of these rows of junctions is found a row of cells, many in various stages of mitosis. In the caudal part of the fusion zone, intercellular spaces are wide and are occupied by numerous cytoplasmic prolongations that present mitochondria, granular endoplasmic reticula, and Golgi apparatus. Many of these prolongations establish contacts between themselves and with the cell bodies.

Animals↗
PubMedDate not supplied

Metabolism of 3H-catecholamines in the brain of spontaneously hypersensitive rats (SHR) after running stress.

The influence of stress on the metabolism of adrenaline (A) and noradrenaline (NA) in the prosencephalon (PC) and rhombencephalon (RC) of SHR and normotensive Wistar rats (WR) was studied. After intraperitoneal injection of 3H-tyrosine, radioactivity of 3H-adrenaline (3H-A), 3H-noradrenaline (3H-NA), total 3H-3-methoxy-4-hydroxyphenylglycol (3H-MHPG), total 3H-3,4-dihydroxyphenylglycol (3H-DHPG) and 3H-vanillylmandelic acid (3H-VMA) was measured in PC and RC of SHR and WR, non-stressed or subjected to running stress. Stress induced a significant decrease of 3H-A level in PC and RC of 8-week-old SHR while no stress-related changes in 3H-NA level were found in either part of the brain of SHR. In RC, 3H-A level was lower in older than in younger non-stressed SHR and decreased further after stress. In all SHR, stress enhanced formation of total 3H-MHPG and/or 3H-DHPG in PC, while increased 3H-VMA level was found only in PC of 24-week-old and in RC of 8-week-old stressed SHR. The results suggest that the decrease of the level of 3H-A in the brain of SHR is involved in their reaction to stress and may depend on increased metabolism mainly to glycols but also to VMA. The lower 3H-NA and 3H-A levels in the prosencephalon of non-stressed young and older SHR, concomitant with unaltered or elevated formation of their metabolites, may suggest higher release of the transmitters involved in the pathogenesis of spontaneous hypertension.

Animals↗
PubMed1981

Cranial differentiation in chick embryos with experimentally induced median facio-cerebral anomalies. A preliminary note.

In an effort to answer the question whether prosencephalic neural crest cells play an essential part in the differentiation of the facial skeleton, in twenty 2- to 6-somite stage chick embryos the anteriormost part of the neural crest was eliminated. Observations on 10 of these embryos, sacrificed 2 hours after the microlaser irradiation, showed that often also some damage is done to the prosencephalic neural tissue. Among the remaining 10 embryos, 6 survived until the age of 12 days. One of these embryos showed unilateral microphthalmia, two bilateral microphthalmia, two synophthalmia and one cyclopia. In the microphthalmic embryos, the facial skeleton proved to have differentiated normally; in the other embryos, several facial bones were entirely lacking, while others only had developed rudimentarily. All affected eyes lacked a cartilaginous sclera. On the basis of these results, the question posed could not be answered. On the other hand, however, the experiments revealed that (1) prosencephalic neural crest cells are indispensable for a normal differentiation of the scleral cartilage, (2) elimination of the prosencephalic neural crest and a part of the prosencephalon does not affect the development of the mandible and the hyoid, and (3) the mesodermal mesenchyme bordering the prosencephalon, has no developmental capacities of its own. Finally, the craniofacial anomalies observed in the synophthalmic and cyclopic chick embryos, proved to be highly similar to the corresponding anomalies in man.

Abnormalities, Multiple↗
PubMed1994

The arterial pattern at the base of arhinencephalic and holoprosencephalic brains.

The mechanisms by which the anatomical variations of the circle of Willis develop is considered to be related to haemodynamic factors, i.e. the differential growth of the various parts of the brain will continuously change the haemodynamic demands and consequently the flow patterns in the cerebral arteries. It is therefore to be expected that, if a selected part of the brain does not develop, the change in the haemodynamic demand will affect the development of some cerebral arteries. Consequently the arteries at the base of 2 arhinencephalic and 8 holoprosencephalic brains were studied in conjunction with the brain malformations. The defects of holoprosencephaly are believed to arise from a failure of the prosencephalon to separate fully into the telencephalon and diencephalon and become manifest at the time that the prosencephalon normally starts to separate into the hemispheres, i.e. 28-34 d p.c. Arhinencephalic brains are fully diverticulated. There is only a partial or complete agenesis of the olfactory tracts and bulbs. The defect causing arhinencephaly starts at 43 d p.c. In the arhinencephalic brains no particular vascular abnormalities were found. However, at the base of the holoprosencephalic brains no complete circle of Willis was present; the anterior part was lacking and was replaced by anterior branches which emerged unilaterally or bilaterally from the internal carotid artery. The choroidal arteries were of very large calibre and ran to the highly vascularised wall of the dorsal cyst which is usually present in holoprosencephalic brains. In contrast to the anterior part, the posterior arterial pattern was almost identical to the posterior part of the circle of Willis of normal brains. The basic vascular patterns found in the holoprosencephalic brains displayed the features of Padget's developmental stages 2 and 3 of the cerebral vasculature, i.e. the pattern that has normally developed within 28-40 d p.c. The further modification of this pattern could largely be understood from the functional demand imposed on the circulation by the enlarged anterior choroidal arteries. Because the development of the anterior part of the circle of Willis precedes the developmental derangement causing arhinencephaly, a complete circle was found in these brains.

Brain↗
PubMed1994

Holoprosencephaly and septo-optic dysplasia.

Holoprosencephaly is a rare brain anomaly, which may be seen in liveborn neonates, although it is more common in stillbirths and abortions. It may occur alone or as part of a large number of genetic syndromes and associations. It is thought to arise early in embryogenesis (6 weeks), as the prosencephalon is separating into the two hemispheres. It is a complex anomaly with markedly varying degrees of severity. The most severe alobar form affects the entire prosencephalon. The brain shows no evidence of division into two hemispheres. The central thalami and basal ganglia remain undivided and confluent, and there is a large, dorsally located cyst connected to the large single ventricle. These infants usually die shortly after birth. The semilobar form has variable amounts of hemispheric formation with normalization occurring from dorsal to ventral. Some posterior falx, occipital, and temporal horn formation and evidence of a third ventricle are present. It is compatible with life. The lobar form has the most nearly normal appearance. It often exhibits a well-formed ventricular system, absence of the septum pellucidum, a shallow falx, abnormal connection of gray and white matter across the midline, and partially formed frontal lobes. Facial anomalies, especially hypotelorism and midline clefts, generally parallel the brain malformation in severity. Visual and olfactory symptoms plus pituitary abnormalities are often present. Septo-optic dysplasia is a related entity. It has a constellation of symptoms of hypotelorism, severe visual problems, and short stature or other pituitary symptoms. Primary imaging findings include optic nerve hypoplasia and absent septum pellucidum. Septo-optic dysplasia somewhat resembles lobar holoprosencephaly. Septo-optic dysplasia is more common than holoprosencephaly. Isolated absence of the septum pellucidum is also thought to be a mild brain anomaly.

Abnormalities, Multiple↗
PubMed1996

[Nitric-oxide synthase in the developing human cerebral cortex].

Distribution of nitric oxide synthase in the forming cortex of human embryo brain was studied after the paraformaldehyde fixation by histochemical method of NADPH-diaphorase revealing. Since week 7 of the development in the prosencephalon up to week 12 the enzyme was located in the vessel endotheliocyte cytoplasm and presumably in the radial glia cell processes. During this period of embryogenesis no nerve cells containing nitric oxide synthase are present in the prosencephalon.

Cerebral Cortex↗