bluuebunny/crossref_metadata_2025_split huggingface dataset:
Lack of thyroid hormones but not their excess affects the maturation of olfactory receptor neurons: A quantitative morphologic study in the postnatal rat
Authors: Paternostro Mark A. , Meisami Esmail 
Published: April 2003

AbstractTo study quantitatively actions of thyroid hormones on maturation of olfactory receptor neurons (ORN), surface density and total number of receptor knobs (1 knob/ORN) were measured in 1 μ sections from septal olfactory epithelium of newborn, 12‐ and 25 day normal, hypo‐ and hyperthyroid rats. Hypothyroidism was induced by adding to drinking water n‐propylthiouracil (0.1% w/v) from birth. Hyperthyroidism was induced by daily injection of pups with T4 (1‐thyroxine, 0.3 μg/g b.w. s.c.). Experimental pups showed all the signs of hypo‐ and hyperthyroidism. Between days 1–25, normal pups showed marked increase in surface area of septal olfactory epithelium (6 ×), total number (12 ×) and surface density (#/mm2, 2 ×) of mature ORNs. Thyroid deficient rats showed, by day 12, marked reductions in epithelial surface area and total number of mature ORNs; these and the surface density deficits became very pronounced by 25 day (30% area, 27% density, 47% # mature ORNs). Hyperthyroid rats, however, did not show an increase in any of these parameters over controls. Although total number of ORNs (mature and immature), as measured by number of nuclei, was also reduced in hypothyroid pups, surface density was not altered, indicating that maturation of ORNs, but not their local accretion is altered in thyroid deficiency. The results indicate that thyroid hormones are essential for normal proliferative expansion of olfactory epithelium and for maturation of ORNs postnatally. These actions of thyroid hormones are not increased or accelerated by excess T4 suggesting saturation of the hormone receptor system at the normal plasma level.
A sensitive period in gestation for nicotine acceleration of neuromuscular maturation
Authors: Rose Kenneth J. , Strand Fleur L. 
Published: April 2003

AbstractNicotine, administered to pregnant Sprague‐Dawley rat dams during gestation, altered the maturation of the developing extensor digitorum longus (EDL) muscle‐peroneal nerve complex of the 2‐week‐old offspring. Initial isometric twitch time to peak and rate of rise of tension and tetanus time to peak tension of the group treated with nicotine during gestational (G) days G3–G8 were faster than controls indicating accelerated maturation of EDL muscle. Contractile parameters of the group treated with nicotine during G9–G13, a period immediately prior to muscle innervation, differed little from control. Nicotine administered during G14–G21 significantly increased twitch and tetanus tension and twitch rate of rise. There was little to no effect on motor unit size or number of motor units with nicotine during any of the three prenatal periods. Thus, while late prenatal nicotine administration primarily altered the strength of muscle, early gestational administration of nicotine increased the rate of muscle development suggesting a possible sensitive period for the accelerative action of nicotine on muscle maturation at this time.
Muscle‐derived factors enhance cholinergic neuronal expression in the chick embryo—I. In ovo studies
Authors: Brodie Chaya , Vernadakis Antonia 
Published: April 2003

AbstractThe effects of muscle‐derived factors were studied in the chick embryo in ovo, during early neuroembryogenesis. Limb muscle extract (LME) administration during embryonic period E1–E7 produced a significant increase in choline acetyltransferase activity of both spinal cord and brain in 8‐day‐old chick embryos. Similar treatment failed to induce significant change in the GABAergic phenotypes as assessed by the activity of the enzyme glutamic acid decarboxylase. Administration of limb muscle extract at either embryonic days 1–3 or 4–7 produced a significant increase in choline acetyltransferase activity in the brain, indicating that the critical period of limb muscle extract in the brain to be between embryonic days E1 and E7, a period of neuronal proliferation and differentiation in the brain. On the other hand, LME administration produced no effect on spinal cord choline acetyltransferase activity when given at embryonic days 1–3, whereas it produced a marked increase when given at embryonic days 4–7. Thus, the critical period of limb muscle extract effect in the spinal cord appears to be confined to embryonic days E4–E7, a period of neuronal differentiation and cell death in the spinal cord.These findings indicate that the cholinotrophic activity of muscle‐derived factors is not limited to the muscle target tissues but have a general effect on cholinergic neurons in the CNS. Whether these cholinotrophic effects are mediated by a common factor or by different factors is still under investigation.
The nerve growth factor receptor gene is expressed in both neuronal and non‐neuronal tissues in the human fetus
Authors: Ernfors Patrik , Wetmore Cynthia , Eriksdotter‐Nilsson Maria , Bygdeman Marc , Strömberg Ingrid , Olson Lars , Persson Håkan 
Published: April 2003

AbstractIn situ hybridization was used to study expression of β‐nerve growth factor receptor (NGF‐R) mRNA in the early human fetus. In 8‐ to 12‐week old fetuses, high labelling was found over motoneurons along the entire length of the lateral motor column. High levels of NGF‐R mRNA were also seen over most developing nerve cell bodies in both the dorsomedial and ventrolateral part of the dorsal root ganglia. Lower, but clearly specific labelling was detected over a subpopulation of cells in Auerbach's plexus in the intestines. Evidence for a non‐neuronal expression of NGF‐R mRNA came from labelling over a subpopulation of cells in glomeruli of the kidney in a 12‐week old human embryo. Myoblasts in skeletal muscle anlagen were labelled as well as cells along peripheral nerve. The wide‐spread expression of NGF‐R mRNA in the human fetus suggests that the NGF‐R is important for development of a variety of different tissues of both neuronal and non‐neuronal origin.
Tubulin gene expression during synaptogenesis in rat, mouse and chick brain
Authors: Bhattacharya B. , Sarkar P.K. 
Published: April 2003

AbstractStudies on tubulin gene expression in brains from three different species, viz rat, mouse and chick, varying with respect to their periods of synaptogenesis, show that the rise and fall in the level of tubulin during synaptogenesis is closely parallel to that of tubulin mRNA. In all three species, the onset of synaptogenesis is accompanied by a dramatic rise in the level of tubulin which continues till the midphase and then declines to adult level by the end of synaptogenesis. The chick α‐ and β‐tubulin coding region probes, pT1 and pT2, which have a 80–90% homology with rat/mouse sequences, were employed to determine the overall levels of α‐ and β‐tubulin mRNA in all samples. Quantitation of tubulin mRNA by dot hybridization revealed a closely parallel change in the levels of both α‐ and β‐tubulin mRNA. In analogy with that of tubulin, the mRNA levels in rat and mouse brain increased progressively from birth till postnatal day 5 and that in the chick brain increased from day 7 till day 11 of embryonic development. In all three cases, the peak levels of tubulin mRNA corresponded closely with the midphase of synaptogenesis and declined almost to adult levels by the end of synaptogenesis. The sudden decline in the level of tubulin as well as its mRNA during the middle of synaptogenesis suggests that the repression of tubulin gene expression is neither due to cessation of cell division nor cell differentiation. Instead, it is likely to be due to the autoregulatory property of tubulin which leads to rapid turnover of its own mRNA when a sufficient level of intracellular tubulin accumulates during the midphase of synaptogenesis.
The extracellular matrix of cerebral gray matter: Golgi's pericellular net and nissl's nervösen Grau revisited
Authors: Bignami A. , Asher R. , Perides G. , Rahemtulla F. 
Published: April 2003

AbstractGlial hyaluronate‐binding protein (GHAP) and a large aggregating chondroitin sulfate proteoglycan (Ag‐Pg) similar to a fibroblast proteoglycan (versican) were localized in bovine, dog and cat central nervous system (CNS) gray matter by indirect immunofluorescence. The distribution of the two hyaluronate‐binding proteins was identical with that of hyaluronate, an extracellular glycosaminoglycan. All substances formed a finely reticulated mesh in the neuropil with a condensation of the stain around large neurons. It is concluded that in gray matter, as in white matter, the extracellular matrix (ECM) contains hyaluronate‐protein aggregates. We suggest that the hyaluronate‐protein aggregates correspond to the pericellular network first described by Golgi.
Regulation of the low affinity receptor for nerve growth factor, p75NGFR, in the olfactory system of neonatal and adult rat
Authors: Turner Christopher P. , Perez‐Polo J. Regino 
Published: April 2003

AbstractUsing MAb192, a monoclonal antibody to the rat low affinity receptor for nerve growth factor (p75NGFR), we determined the expression of p75NGFR in rat neonatal and adult olfactory system. In neonates and adults, we observed discrete p75NGFR‐immunoreactivity (p75NGFR‐ir) in the glomerular layer of the main olfactory bulb. The intensity and organization of glomerular p75NGFR‐ir increased with age. This was in keeping with the general ontogeny of the main olfactory bulb. Generally, granule cells, mitral cells and periglomerular cells of the main olfactory bulb were not specifically stained. However, in early neonates, granule cells close to the lateral olfactory tract exhibited p75NGFR‐ir. Additional specific staining was found in the olfactory receptor neurons of neonatal and adult olfactory neuroepithelium, the olfactory fascicles and in the glomeruli of the accessory olfactory bulb. The intensity, but not the organization, of specific staining in the accessory olfactory bulb increased as the animal matured. We believe that p75NGFR‐ir in the olfactory system is associated with its unique capacity to regenerate its peripheral input to the main olfactory bulb. The presence of p75NGFR‐ir in the accessory olfactory bulb would suggest a broader role for this protein. Here we discuss the implications of these findings with regards to nerve growth factor, other trophic molecules, and their receptors. The data presented provide a foundation for studies involving manipulation of regenerative phenomena while monitoring the expression of neurotrophic factors and their receptors.
Neonatal prazosin exposure reduces ovarian weight and estrogen receptor binding in adult female rats
Authors: Fitch Roslyn Holly , Feder Harvey 
Published: April 2003

AbstractExposure of estrogen treated adult female guinea pigs to the alpha‐1 antagonist prazosin has been shown to reduce levels of estrogen binding in the hypothalamus and preoptic area. To further investigate this interaction between the noradrenergic and neuroendocrine axes, newborn female rat pups received an s.c. implant of prazosin (0.0125 mg/day for 5 days) or placebo. In adulthood, subjects were sacrificed by perfusion with DMSO on the morning of proestrous. Tissue analysis of the medial preoptic area, corticomedial amygdala, and mediobassal hypothalamus revealed that cytosolic estrogen binding was significantly reduced in all three areas for the prazosin treated group as compared to controls. Ovarian weight was also significantly reduced in the prazosin treated group, although uterine weight was unaffected. Interestingly, prazosin treated females showed a post‐pubertal increase in body weight characteristic of ovariectomized females, while controls showed no such increase.These results support the existence of a significant developmental interaction between the noradrenergic system and the neuroendocrine axis as measured by ovarian weight and estrogen binding in the brain.
Postnatal laminar development of cholinergic receptors, protein kinase C and dihydropyridine‐sensitive calcium antagonist binding in rat visual cortex. Effect of visual deprivation
Authors: Kumar Ashok , Schliebs Reinhard 
Published: April 2003

AbstractThe postnatal ontogeny of 3H‐pirenzepine and 3H‐oxotremorine‐M binding to M1‐ and M2‐muscarinic acetylcholine receptors, respectively, as well as 3H‐nicotine binding to neuronal nicotinic acetylcholine receptors, 3H‐phorbol‐12,13‐dibutyrate binding to protein kinase C and 3H‐PN200‐110 binding to dihydropyridine‐sensitive calcium channels was studied in individual layers of the visual cortex in both normally raised and monocularly deprived rats (one eyelid sutured at the age of 11 days) using quantitative receptor autoradiography. Postnatal ontogeny of M1‐muscarinic receptors is similar in each visual cortical layer reaching the highest receptor density at the age of 15 days, whereas M2‐muscarinic binding sites increase gradually from day 7 up to day 34. Highest 3H‐nicotine binding is reached in all visual cortical layers at postnatal day 15 followed by a considerable decrease in binding sites until day 25. Phorbol ester binding rises considerably from birth until the age of 15 days reaching nearly the adult value in the upper layers, whereas in layers V and VI a marked decrease in binding levels until adulthood can be observed. The developmental course of 3H‐PN200‐110 binding sites is similar in all visual cortical layers and exhibits a moderate rise in binding sites between postnatal days 7 and 15. Monocular deprivation results in permanent changes in the developmental profiles of phorbol ester as well as calcium antagonist binding sites, whereas the alterations in muscarinic and nicotinic cholinergic receptors folloing monocular deprivation are only of transient nature. The data presented suggest that acetylcholine plays a modulatory role during a certain period of early postnatal maturation of the visual cortex by affecting both cholinergic receptors and associated second messenger cascades.
Differences in vimentin distribution in glial cells in culture revealed with an antibody against a phosphorylated epitope
Authors: Ciesielski‐Treska Jaroslava , Ulrich Gabrielle , Aunis Dominique 
Published: April 2003

AbstractWe have previously described that spatial and temporal changes in the organization of vimentin that are correlated with protein kinase C (PKC)‐induced phosphorylation of vimentin can be detected with the mouse monoclonal antibody B3 in cultures of amoeboid microglia [Ciesielski‐Treska et al. (1991) J. Neurosci. Res.29, 362–378]. The antibodies were generated to native form of vimentin‐containing filaments and antibody B3 reveals a restricted immunostaining of vimentin in glial cells from human, rat and mouse origin. In the present study we show the distribution of epitope B3 analyzed by immunofluorescence within defined populations of rat glial cells. Relatively high immunoreactivity was found in Type 1 astrocytes, Type 2 astrocytes and oligodendrocytes had low immunoreactivity. Although the results suggested that in Type 1 astrocytes the phosphorylated epitope is prominent, its phosphorylation was not found to be cell cycle‐dependent, and appeared unrelated to the organizational changes of intermediate filaments associated with the morphological conversion of polygonal to stellate astrocytes. As expected, the immunofluorescence was increased by exposition of astrocyte cultures to an activator of PKC, confirming our previous conclusion that the immunoreactivity of the epitope B3 depends on PKC‐mediated phosphorylation. In addition, the finding that the immunofluorescence of vimentin was more homogeneous in quiescent, serum‐deprived astrocytes and also in astrocytes exposed to an inhibitor of protein synthesis, cycloheximide, may suggest that phosphorylation of the epitope B3 depends on a protein factor present in fetal calf serum. The immunofluorescence studies on cultures enriched in Type 2 astrocytes and in oligodendrocytes indicate that the epitope B3 is hypophosphorylated in glial cells of this lineage and becomes dephosphorylated after terminal differentiation of oligodendrocytes. These observations suggest that in Type 2 astrocytes and in oligodendrocytes the low level of phosphorylation of vimentin could be related to the down regulation in vimentin expression.
Activity‐dependent plasticity of inhibitory and excitatory amino acid transmitter systems in cultured rat cerebral cortex
Authors: Ramakers G.J.A. , van Galen H. , Feenstra M.G.P. , Corner M.A. , Boer G.J. 
Published: April 2003

AbstractChronic suppression of spontaneous bioelectric activity in cultures of dissociated fetal rat cerebral cortex increases neuronal cell death and results in electrophysiological changes which indicate an altered balance between excitatory and inhibitory neurotransmission in culture. To delineate whether alterations in neurotransmitter release could underlie this imbalance, we investigated the effects of chronic tetrodotoxin (TTX) treatment on the content and release of glutamate, aspartate and γ‐aminobutyric acid (GABA) in culture. Chronic TTX treatment decreased the content of all amino acids investigated. However, only GABA was decreased relative to the neuronal marker NSE (neuron‐specific enolase), indicating a disproportionate loss of GABA production following chronic silencing. Depolarization‐induced release of GABA, glutamate and aspartate increased about 10‐fold between 7 and 21 days in control cultures. Chronic TTX treatment significantly increased the depolarization‐induced release of glutamate and aspartate at 7 days in vitro relative to control levels. At all ages it caused a two‐fold increase in the ratio of evoked excitatory amino acid release to that of GABA. These observations suggest that chronic silencing of developing neocortex cell cultures increases the ratio of excitatory to inhibitory synaptic activity either by differential cell death or by reduced synaptic efficiency, on which a decrease in GABA neurotransmission appears to play a major role. Since similar mechanisms may be involved in activity‐dependent plasticity in vivo, these cultures provide a useful model to analyse this phenomenon at the cell biological and molecular level.
Early nutritional changes modify the kinetics and phosphorylation capacity of tryptophan‐5‐hydroxylase
Authors: Manjarrez G.G. , Chagoya G.G. , Hernández R. J. 
Published: April 2003

AbstractGestational malnutrition induces an acceleration of the serotonin biosynthetic pathway in the developing brain with an increase in brain L‐tryptophan (L‐Trp), tryptophan‐5‐hydroxylase (TrpOH) activity and serotonin content. In the present work we report results on the possible mechanism of TrpOH activation. Kinetic experiments were done with different L‐Trp concentrations in the rat brain at different ages. Also various phosphorylating conditions of the enzyme were tested in order to compare its activation in developmentally malnourished and normal brains. The results showed lower Km values and no changes in the Vmax in the malnourished as compared to controls. Interestingly, in the malnourished group, TrpOH showed an increased activity under the phosphorylating conditions employed. We propose that in the activation of brain TrpOH by developmental malnutrition, not only is an elevation of L‐Trp involved, but also a change in the enzyme itself reflected in a higher affinity for L‐Trp and in a greater response to phosphorylation. This allows us to propose the possibility that early chronic malnutrition induces structural changes in the enzymatic molecule.
Development of the gabaergic phenotype in murine spinal cord‐dorsal root ganglion cultures
Authors: Caserta Maria T. , Barker Jeffery L. 
Published: April 2003

AbstractMurine spinal cord and dorsal root ganglion GABAergic neurons, derived from 12‐day‐old fetuses, were examined autoradiographically, biochemically and immunocytochemically in vitro to determine the timecourse of appearance and maturation of this phenotype and the extent and mode of its innervation of target neurons. Specific 3H‐GABA uptake into spinal cord neurons was the first property to develop and was present at the earliest time studied, one day in vitro. Immunocytochemical localization of glutamic acid decarboxylase (GAD) revealed positively stained neurons beginning at four days. At five days in vitro, electron microscopic immunocytochemistry revealed GAD‐immunoreactive (GAD‐IMR) boutons investing neuronal perikarya as well as neuronal processes. By one week in vitro, GAD‐IMR neurons constituted 27% of the total population and GAD‐IMR boutons could be seen contacting every cell with a neuronal morphology. The mode of investment of target neurons by GAD‐IMR boutons was not circumscribed to either soma or dendrites but usually involved the entire neuronal perimeter and did not change with time in culture. Three morphologically distinct types of GAD‐IMR neurons were evident: a small, bipolar type; a medium‐sized multipolar neuron which was the most common and a large, multipolar type, resembling a motoneuron. A small population (8%) of dorsal root ganglion neurons was found to contain GAD both biochemicaly and immunocytochemically but was never invested by GAD‐IMR boutons. GAD activity in vitro paralleled in vivo levels with maximal activity being reached at four weeks in vitro and 10 days postnatally in the intact mouse spinal cord. Murine spinal cord GABAergic neurons are a morphologically diverse and abundant neuronal population with extensive, precocious innervation of all other neuronal phenotypes in vitro suggesting that GABA has a widespread influence over other developing neuronal systems in the murine spinal cord.
Postnatal development of NMDA, AMPA and kainate receptors in individual layers of rat visual cortex and the effect of monocular deprivation
Authors: Kumar Ashok , Schliebs Reinhard , Bigl Volker 
Published: April 2003

AbstractThe postnatal development of the ligand binding to n‐methyl‐d‐aspartate (NMDA), alpha‐amino‐3‐hydroxy‐5‐methylisoxazole‐4‐propionic acid (AMPA), and kainate receptor sites was studied in individual layers of rat visual cortex with [3H]MK‐801, [3H]CNQX and [3H]kainate, respectively. The studies were performed by quantitative receptor autoradiography in the different visual cortical layers from normally raised rats and from monocularly deprived animals.In normally raised rats, in all visual cortical layers, [3H]MK‐801 and [3H]CNQX binding increased significantly from birth to around postnatal day 20, at which age already the adult values are reached. In contrast, the increase in [3H]kainate binding from day 1 to day 15 is followed by a significant decrease in binding sites up to day 25; at this age the adult binding level is nearly attained.Monocular deprivation, by unilateral eyelid suture at the age of 11 days onwards, leads to a transient decrease in [3H]CNQX binding in all visual cortical layers, whereas [3H]kainate binding results to a permanent decrease in AMPA receptor sites in cortical layers II to VI in both sides of the cortex. In contrast, only long‐term monocular deprivation until the age of 90 days resulted in decreased [3H]MK‐801 binding levels as compared to age‐matched controls. The data suggest that the laminar development of glutamate receptor subtypes is differentially affected by visual experience during early brain maturation.