bluuebunny/crossref_metadata_2025_split huggingface dataset:
effects of NGF and dibutyryl cAMP on neuronal differentiation of embryonal carcinoma cells
Authors: Sharma Shanti , Hansen John T. , Notter Mary F. D. 
Published: April 2003

AbstractThe P19S18O1A1 embryonal carcinoma cell line is capable of neuronal differentiation and is therefore useful in studying neuronal development and the influence of growth modulators on neuronal differentiation. We report here on the effects of nerve growth factor (NGF) and dibutyryl cyclic adenosine monophosphate (db cAMP), individually and combined, on differentiation of P19S18O1A1 cells. NGF alone did not induce any significant neuron‐like changes in cultures exposed to NGF for as long as 12 days. Treatment with db cAMP resulted in changes in a significant population of the cells, including development of a neuron‐like morphology, seen at both the light and electron microscopic level, loss of stage‐specific embryonic antigen expression and the appearance of two neuronal markers, neurofilament protein and neuron‐specific enolase. These changes were similar to changes seen when embryonal carcinoma (EC) cells are treated with retinoic acid. NGF in combination with dibutyryl cyclic adenosine monophosphate brought about similar changes as dibutyryl cyclic adenosine monophosphate alone, and was therefore not synergistic for induction of neuronal properties. In retinoic acid‐treated cultures, the neuron‐like cells had ultrastructural features very similar to neurons in non‐tumorous, normal tissue, with typical organelles, such as one nucleolus, neurotubules and neurofilaments, while db cAMP‐treated EC cells showed similar findings at the electronmicroscopic level. The results suggest that db cAMP can induce the neuronal phenotype in EC cells alone without pre‐treatment with retinoic acid.
Development of neurotransmitter systems in the mouse embryo following acute ethanol exposure: A histological and immunocytochemical study
Authors: Schambra Uta B. , Lauder Jean M. , Petrusz Peter , Sulik Kathleen K. 
Published: April 2003

AbstractAcute maternal ethanol administration to C57B1/6J mice on gestational day 7 (GD7) results in facial and brain abnormalities similar to those reported in human fetal alcohol syndrome (FAS). Using this model, we assessed the damage to brain structures using histological methods and changes in developing neurotransmitter systems with immunocytochemistry. Cholinergic neurons in the forebrain were stained with a monoclonal antibody to choline acetyltransferase (ChAT). Catecholaminergic neurons in the midbrain and serotoninergic neurons in the hindbrain were stained with polyclonal antisera to tyrosine hydroxylase (TH) and serotonin (5‐HT), respectively. Forebrain deficiencies, including loss of midline structures (olfactory bulbs, midline septation, medial septal area) and deficits in lateral and dorsal regions (neostriatum and cerebral cortex) were found in both GD14 embryos and GD18 fetuses. In severely affected offspring, complete loss of the septal region resulted in conjoined lateral ventricles and a reduction in the thickness of the ventricular zone surrounding the single ventricle, as well as a severe loss of ChAT neurons which would normally be located in this territory. However, no consistent changes were seen in the distribution or size of TH or 5‐HT neuronal cell groups in the midbrain and hindbrain. These differences in effects on specific neurotransmitter systems reflect the fact that the forebrain is most severely affected by early ethanol administration, whereas the hindbrain is relatively spared. Such differential effects could produce an imbalance in developing neurotransmitter systems in the embryonic and fetal brain, which could explain some of the functional deficits observed in children with FAS.
The effects of potassium‐induced depolarization, glutamate receptor antagonists and N‐methyl‐d‐aspartate on neuronal survival in cultured neocortex explants
Authors: Ruijter J. M. , Baker R. E. 
Published: April 2003

AbstractThe effects of elevating the potassium concentration of the growth medium of neocortical explants was studied. Under control conditions, 10 mM potassium resulted in ca 20% decrease in the number of surviving neurons. The same potassium concentration, however, was clearly neurotrophic in tetrodotoxin‐grown cultures: tetrodotoxin‐induced neuronal death was significantly reduced. Both effects could be mimicked by the addition of 10 μM N‐methyl‐d‐aspartate (NMDA); lower concentrations were without effect; higher concentrations were neurotoxic under both control and tetrodotoxin conditions. The neurotoxic, as well as the neurotrophic effects of 10 mM potassium appear to be mediated through depolarization‐induced glutamate release since they could be influenced by the application of glutamate receptor antagonists. The addition of the NMDA receptor antagonist d‐2‐amino‐7‐phosphonoheptanoate (APH) blocked the trophic effect of 10 mM potassium in tetrodotoxin‐grown cultures, resulting in low survival. On the other hand, the addition of the non‐NMDA antagonist 6,7‐dinitroquinoxaline‐2,3‐dione (DNQX) resulted in neuronal survival similar to control cultures, indicating that it blocked the toxic effects of glutamate, leaving the trophic effects on the NMDA receptor untouched. Under control (non‐TTX) conditions, neither DNQX nor APH showed significant effects on 10 mM potassium‐induced cell death, indicating that stimulation of the non‐NMDA, as well as the NMDA receptors is neurotoxic. This differential effect of NMDA receptor stimulation on neuronal survival is discussed with respect to the maturational and/or functional state of the neurons in the culture.
Kainic acid lesioning alters development of the outer plexiform layer in neonatal rabbit retina
Authors: Messersmith Elizabeth K. , Redburn Dianna A. 
Published: April 2003

AbstractThe first synaptic relay in the primary visual pathway occurs between terminals of photoreceptors and second‐order neurons within the outer plexiform layer of the retina. During development, one of these types of second‐order neurons, the type A horizontal cell, differentiates and assumes mature characteristics several days before any other cells ramifying in that synaptic layer. In neonates, horizontal cells appear to be GABAergic during the first 5 days of postnatal life and in addition they also are responsive to kainic acid. We have previously suggested that they may play a pioneering role in the postnatal development of the outer plexiform layer, perhaps providing structural guidance or trophic substances such as GABA, for synaptic development. To test this hypothesis, we first demonstrated that a single intraocular injection of kainic acid within 24 hr of birth results in a permanent and selective loss of type A horizontal cells in the outer retina. Retinas from animals maintained for 5 days postinjection were harvested for analysis of postnatal development of the outer plexiform layer in the absence of horizontal cells. One of the major findings was that kainic acid treatment caused a reversal of the normal complement of photoreceptor cell types, resulting in an abnormally high rod/cone ratio. The distribution of cell processes within the outer plexiform layer was also altered and normal synaptic connections were not made. In spite of these changes in the constituents of the outer plexiform layer, the normal position of the synaptic layer was not affected by the loss of horizontal cells. These results rule out the possibility that horizontal cells provide a structural barrier which is an absolute requirement for establishing the location of the outer plexiform layer. Rather, these cells may be more involved in cell differentation and synaptogenesis.
GABA mediated excitation in immature rat CA3 hippocampal neurons
Authors: Cherubini E. , Rovira C. , Gaiarsa J. L. , Corradetti R. , Ari Y. Ben 
Published: April 2003

AbstractIntracellular recordings from rat hippocampal neurons in vitro during the first postnatal week revealed the presence of spontaneous giant depolarizing potentials (GDPs). These were generated by the synchronous discharge of a population of neurons. GDPs reversed polarity at −27 and −51 mV when recorded with KCl or K‐methylsulphate filled electrodes, respectively. GDPs were blocked by the GABAA receptor antagonist bicuculline (10 μM). Iontophoretic or bath applications of GABA (10–300 μM) in the presence of tetrodotoxin (1 μM), induced a membrane depolarization or in voltage clamp experiments an inward current which reversed polarity at the same potential as GDPs. The response to GABA was blocked in a non‐competitive manner by bicuculline (10 μM) and did not desensitize.GABA mediated GDPs were presynaptically modulated by N‐methyl‐d‐aspartate (NMDA) and non‐NMDA receptors. Their frequency was reduced or blocked by NMDA receptor antagonists and by the rather specific non‐NMDA receptor antagonist 6‐cyano‐7‐nitroquinoxaline‐2,3‐dione (CNQX). The frequency of GDPs was enhanced by glycine and d‐serine (10–30 μM) in a strychnine insensitive manner. This effect was blocked by AP‐5, suggesting that it was mediated by the allosteric modulatory site of the NMDA receptor.These observations suggest that most of the ‘excitatory’ drive in immature neurons is mediated by GABA acting on GABAA receptors; furthermore excitatory amino acids modulate the release of GABA by a presynaptic action on GABAergic interneurons.
Comparison of the developmental changes of the brainstem auditory evoked response (BAER) in taurine‐supplemented and taurine‐deficient kittens
Authors: Vallecalle‐Sandoval M.‐H. , Heaney G. , Sersen E. , Sturman J.A. 
Published: April 2003

AbstractA similar development of the brainstem auditory evoked response is present in taurine‐supplemented and taurine‐deficient kittens between the second postnatal week and the third month of life. Between birth and the second postnatal week kittens from mothers fed the 1% taurine diet showed earlier maturation of the brainstem auditory evoked response as indicated by lower threshold, shorter P1 latency and shorter central conduction time when compared to the kittens from mothers fed the 0.05% taurine diet. These results suggest an important role of taurine in the anatomical and functional development of the auditory system.
Ontogeny of β‐adrenergic receptor‐mediated cyclic AMP generating system in primary cultured neurons
Authors: Ma Fu‐Hai , Ohkuma Seitaro , Kishi Masataka , Kuriyama Kinya 
Published: April 2003

AbstractThe developmental changes in the β‐adrenergic receptor/cyclic AMP generating system were examined using mouse cerebral cortical neurons in primary culture. During neuronal growth in vitro, the number of binding sites for [3H]dihydroalprenolol (DHA) showed a tendency to increase (Bmax), while the affinity (Kd) for [3H]DHA did not show any noticeable changes. Basal and isoproterenol‐stimulated adenylate cyclase activities as well as the activation of adenylate cyclase by 5′‐guanylylimidodiphosphate (GppNHp), NaF and forskolin showed progressive and parallel increases during neuronal growth on a polylysine‐coated surface. The treatment of primary cultured neurons with islet‐activating protein (IAP), one of the pertussis toxins, attenuated the inhibitory effect of carbachol, a muscarinic agonist, on isoproteronol‐induced activation of adenylate cyclase activity. These results indicate that primary cultured neurons possess a cyclic AMP generating system coupled with β‐adrenergic and muscarinic receptors, which is regulated via stimulatory and inhibitory GTP‐binding proteins, respectively. The results described above also suggest that the β‐adrenergic receptor, stimulatory and inhibitory types of GTP‐binding proteins and adenylate cyclase may develop in a parallel fashion during neuronal growth on a polylysine‐coated surface.
A comparison of substance P peptide and preprotachykinin mRNA levels during development of rat medullary raphe and neostriatum
Authors: Walker Paul D. , Green Todd L. , Jonakait G. Miller , Hart Ronald P. 
Published: April 2003

AbstractSubstance P (SP) and the mRNA coding for its precursor peptide, preprotachykinin (PPT), were measured in medullary raphe nuclei (MRN) and neostriatum (NS) over development in order to determine (1) whether PPT mRNA levels correlate with peptide development, and (2) whether changes in PPT mRNA might help to account for the apparent decline in SP seen immunohistochemically in certain brain areas postnatally. Total RNA was quantified in dissected tissue pieces using the sensitive orcinol reaction. When MRN PPT mRNA levels measured by Northern blot analysis were adjusted to total RNA levels, PPT mRNA per MRN increased over development with a profile similar to that seen for SP peptide. Moreover, both peptide and mRNA levels exhibited a similar decline after postnatal day 15. Therefore, developmental regulation of SP biosynthesis in the MRN may, in part, explain previous evidence documenting a postnatal decline in SP there.In the NS, SP peptide and PPT mRNA increased with a similar profile from E18 through the first post‐natal week. Thereafter, SP increased less rapidly than its mRNA, indicating incongruities in prohormone message and processed peptide in the NS.
The role of taurine in the survival and function of cerebellar cells in cultures of early postnatal cat
Authors: Trenkner E. , Sturman J.A. 
Published: April 2003

AbstractThe role of taurine and β‐alanine was analyzed in kitten cerebellar cultures. Since in contrast to mouse, cats (and primates including man) cannot synthesize sufficient taurine to maintain their body pools, we considered the cat an ideal species for the analysis of the role of taurine during early postnatal cerebellar development under controlled conditions. Unexpectedly, we found that the presence of taurine was toxic to neurons but that compounds, considered to be competitors for the β‐amino acid uptake system, support cell survival and cell function in vitro, the opposite of the results found in mice. This could be explained by the finding that only minute amounts of [3H]taurine were taken up by both cat neurons and glial cells under optimal culture conditions but that in the presence of the taurine analogues β‐alanine and guanidinoethane sulfonic acid (GES) significant amounts of taurine were found in all cell types. These differences between mouse cerebellar cells and cat cerebellar cells in vitro suggest that a reevaluation of the mechanisms that control taurine function in cats and primates is warranted.
Lipid peroxidation in rat cerebral cortex during post‐ischemic reperfusion: Effect of exogenous antioxidants and Ca++‐antagonist drugs
Authors: Vanella A. , Sorrenti V. , Castorina C. , Campisi A. , Di Giacomo C. , Russo A. , Perez‐Polo J.R. 
Published: April 2003

AbstractAlthough the role of oxidant‐antioxidant metabolism in total ischemia and reperfusion in the central nervous system and cardiac myocardium have been well studied, less is known about the consequences of partial ischemic episodes. Here we show that reperfusion contributes to free radical formation as judged by conjugated diene formation. Also, antioxidants and Ca++ antagonists were able to reduce free radical formation. These results would suggest that free radical generation following ischemia and reperfusion may result from more than one injury process in cerebral cortex.
Effect of seizure activity and calpain inhibitor I on LTP in juvenile hippocampal slices
Authors: Fitzpatrick John S. , Shahi Kavian , Baudry Michel 
Published: April 2003

AbstractKainic acid‐induced seizure activity in adult rats produces an impairment of long‐term potentiation induction in hippocampal slices. As the consequences of seizure activity are different in adult and juvenile rats, we tested the ability of hippocampal slices prepared from kainate‐treated juvenile rats to exhibit long‐term potentiation. Long‐term potentiation was induced by theta‐burst stimulation and was not significantly different in slices prepared from control or kainate‐injected juvenile rats (16–18 postnatal days). Short‐term potentiation, however, was reduced in the kainate‐treated juveniles. Calpain inhibitor I has been shown to prevent long‐term potentiation formation in adult hippocampal slices, and we evaluated its effect on long‐term potentiation in hippocampal slices from juvenile rats. Calpain inhibitor I produced a significant reduction in the degree of long‐term potentiation induced by theta‐burst stimulation in hippocampal slices prepared from 14–20 postnatal day‐old animals. The results are consistent with the notion that, although similar mechanisms participate in the formation of long‐term potentiation in juvenile and adult animals, juvenile animals are much more resistant than adult animals to the consequences of seizure activity.
Serotoninergic reinnervation of regenerating tentacular sensory organs in a pulmonate snail, Cryptomphalus aspersa
Authors: Flores Vladimir , Brusco Alicia , Scicolone Gabriel , Saavedra Jorge Pecci 
Published: April 2003

AbstractSeveral ontogenetic studies performed in different species suggest a developmental role for 5‐HT neurons. The 5‐HT system interconnecting the CNS and the tentacular sensory organs in pulmonates is a suitable model for studying the postulated developmental role of 5‐HT neurons. In this paper we describe the behavior of the 5‐HT fibers during the early stages of blastema reinnervation, primordium formation and differentiation of regenerating tentacular sensory organs in the pulmonate snail Cryptomphalus aspersa. Our results show that the regeneration process allows the development of a normal pattern of 5‐HT innervation of the regenerated sensory organs and suggest that 5‐HT could be involved in reciprocal developmental interactions with regenerating tentacular tissues.
Neurochemical changes of long‐term adrenalectomy in rat brain: Effects on neurotransmitter amino acids
Authors: Zonta N. , Ferrario P. , Di Giulio A.M. , Zecca L. , Gorio A. , Mantegazza P. 
Published: April 2003

AbstractThe levels of five amino acids together with glutamine synthetase activity, were measured in brain regions of rats with bilateral adrenalectomy, performed in newly weaning rats on postnatal day 22 and sacrificed 3 months later. Adrenalectomy caused a general decrease of glutamine concentration in three hippocampal regions (CA1‐CA2, CA3, CA4‐dentate gyrus), in hypothalamus, striatum and cerebellum. This reduction, which was particularly significant in hippocampus and cerebellum, was paralleled by a decrease of glutamine synthetase activity. Treatment with corticosterone reversed the effect of adrenalectomy. Little or no change was observed in the tissue levels of taurine, aspartic, glutamic or gamma‐amino butyric acids.
The developing chick brain shows a dramatic increase in the ω‐conotoxin binding sites around the hatching period
Authors: Azimi‐Zonooz A. , Litzinger M.J. 
Published: April 2003

Abstractω‐Conotoxin CVIA, a 27 amino acid neuropeptide toxin believed to target voltage sensitive calcium channels (Cruz et al., 1987, Biochemistry26(3), 820–824) was bound to developing chick brain at embryonic day 9‐post hatch day 10. A two‐fold increase was observed in ω‐Conotoxin binding sites around chick hatching, embryonic days 18–20. Depolarization induced 45Ca fluxes also increased around hatching. ω‐Conotoxins block ⩾‐80% of these 45Ca fluxes throughout development. Competition binding did not detect large differences in the binding affinity of sites during development. We conclude from these data that the increases in ω‐Conotoxin binding sites and 45Ca fluxes around chick hatching are related to one of the presynaptic mechanisms of neuronal maturation necessary for normal neuronal function and chick behavior after hatching.
Microcephalic cerebrum with hypomyelination in the pygmy mouse (pg)
Authors: Sugisaki Tetsuro , Beamer Wesley G. , Noguchi Tetsuya 
Published: April 2003

AbstractTo determine whether somatomedin has a direct action on cerebral development instead of an indirect action of a growth hormone, we examined the central nervous system of the pygmy mouse (pg), a mutant with normal somatomedin activity. Our findings are: (A) the weights of the pg/pg cerebrum and cerebellum weighed were significantly less than those of the normal controls (pg/+), 14 and 15% less, respectively; (B) the total DNA content was reduced by 17% in the cerebrum and cerebellum of the pg/pg mouse; (C) the total RNA content was also reduced in the cerebrum and cerebellum, proportional to the reduction in DNA; (D) CNPase activity was reduced selectively in the cerebrum of the pg/pg mouse by 25%; and (E) the pg/pg mice exhibited a strikingly reduced level of activity with an indistinct diurnal periodicity. Therefore, the present findings suggest that the action of somatomedin on the pro‐liferation and maturation of glial cells might be a necessary precondition to myelin formation.
Developmental and strain‐specific heterogeneity of rat adrenal chromaffin cells recognized by a monoclonal antibody against intact chromogranin B
Authors: Hansen Barbara , Lietzke Rolf , Unsicker Klaus , Westermann Reiner 
Published: April 2003

AbstractWe have raised a monoclonal antibody (MAB‐1E10) reactive with the intact forms but not the processing products of the chromaffin cell vesicle protein chromogranin B (CgB). The antibody recognizes rat and human, but not bovine and chick adrenal chromaffin cells. In addition, MAB‐1E10 immunoreactivity was detected in rat PC 12 pheochromocytoma cells and in pituitaries. Several other tissues, including pancreas, small intestine and superior cervical ganglia, which are known to contain CgB in endocrine cells or neurons, respectively, were found not to be reactive with MAB‐1E10. Using short‐term cultures of dissociated adrenal chromaffin cells from Hannover‐Wistar rats, we found that the expression of intact CgB is developmentally regulated. Between embryonic day 19 and postnatal day 40, about 80% of adrenal chromaffin cells — identified by their reactivity with an antibody against the enzyme dopamine‐β‐hydroxylase — were found to be reactive with MAB‐1E10. The proportion of positive cells subsequently decreased to about 5% at postnatal day 90. In the presence of glucocorticoids, this decrease was reduced to about 45% CgB‐positive cells at postnatal day 90. In another rat strain, Sprague‐Dawley rats, the proportion of MAB‐1E10‐immunoreactive chromaffin cells (about 50%) remained constant from birth to adulthood. Our results indicate that CgB is differentially expressed and/or processed in different rat tissues, strains and during development, and furthermore, that expression or processing in rat chromaffin cells might be regulated by glucocorticoids. Intact CgB appears to be a marker for a subpopulation of chromaffin cells, but its function(s) remains to be clarified.
Endothelin modulates dihydropyridine receptor decreased binding in hippocampal slices from normotensive and spontaneously hypertensive rats
Authors: Huguet Francois , Brisac Anne‐Marie , Dubar Michel , Ingrand Pierre , Piriou Alain 
Published: April 2003

AbstractPrevious studies in rats have demonstrated both the link between voltage‐operated calcium channels and endothelin and their cerebral involvement in the pathophysiology of spontaneous hypertension. In the present study, the interaction of endothelin with specific dihydropyridine (DHP) binding sites was investigated using the brain slices model. In rat hippocampal slices, pre‐incubation with Bay K 8644 decreased [3H] (+) PN 200‐110 binding. There was no difference in agonist‐induced decrease of DHP binding in normotensive and spontaneously hypertensive (SH) rats. The effect of Bay K 8644 was partially inhibited by endothelin but not by angiotensin in both normotensive and hypertensive rats. These data compared to those of other studies suggest that DHP binding sites which are regulated by endothelin are post‐synaptic. We conclude that brain slices provide a good in vitro model to study DHP receptor regulation and to explore endothelin interactions with DHP‐sensitive Ca2+ channels.