bluuebunny/crossref_metadata_2025_split huggingface dataset:
Autoradiographic analysis of 3H‐glutamate, 3H‐dopamine, and 3H‐GABA accumulation in rabbit retina after kainic acid treatment
Authors: Hampton C. K. , Redburn D. A. 
Published: January 2005

AbstractWe have previously reported that exposure of isolated rabbit retina to 10−3M kainic acid produces profound morphological changes in specific retinal neurons (Hampton et al, 1981). We noted specific swelling of horizontal cell bodies and neurites, necrosis of cell bodies in the amacrine and ganglion cell layers, and swelling of elements in the inner plexiform layer. We now report a differential sensitivity to kainic acid of specific subclasses of amacrine cells autoradiographically labeled with 3H‐glutamate, 3H‐GABA, or 3H‐dopamine. Three different effects were observed: (1) Labeling of neurons after incubation in 3H‐glutamate was uniformly reduced while labeling of glia was much less affected. ( 2 ) The accumulation of 3H‐dopamine was also decreased by kainic acid in two of the three labeled bands of the inner plexiform layer. The outermost labeled band was insensitive to kainic acid at the highest concentration tested (10.−2M). These findings provide a basis for the subclassification of dopaminergic amacrine cells into at least two subclasses based on their sensitivity to kainic acid. (3) Kainic acid caused a dramatic increase in the labeling of GABAergic amacrine cell bodies and their terminals. This increased intensity may reflect a compensatory increase in uptake activity in response to kainic acid‐induced depletion of endogenous GABA stores. These results confirm the highly toxic nature of kainic acid and demonstrate a high degree of specificity and complexity in its action in the retina.
Growth, differentiation, and viability of fetal rat cortical and spinal cord implants into adult rat spinal cord
Authors: Patel U. , Bernstein J. J. 
Published: January 2005

AbstractSuccessful transplantation of the fetal brain into adult host brain has been accomplished. These studies explore the growth, differentiation, and viability of E11, E12, and El5 rat fetal cortex and fetal spinal cord implantation into the spinal cord of adult rats (donor and host, Sprague‐Dawley). Under deep Chloropent anesthesia, 70 rats had 1‐mm cubes of fetal cortex inserted with pressure or by stylus injection subpially between the dorsal horn and dorsal column (left side), or implantation of whole segments of fetal spinal cord. Animals were prepared for light microscopy 14 and 21 days and 1, 2, and 3 months later. Implants by both fetal tissues had a 69% survival rate. The younger the fetal implant the higher the success of the implant (E11 > E15). The diameter of fetal spinal cord implants reached the diameter of control postnatal animals after 30 days. The implants not only increased in mass (up to 7‐fold in some cases) but differentiated and matured (apolar, unipolar, bipolar, and multipolar) neurons were observed one to three months postimplantation. By 30 days postimplantation, fetal neurons had large, often crenated nuclei, with a large single prominent nucleolus. The most successful implants were the young E11 fetal spinal cord into the adult host spinal cord. These implants represent an initial successful transplantation of fetal spinal cord into adult spinal cord.
Synaptogenesis and myelination in dissociated cerebral microcarrier cell cultures
Authors: Shahar A. , Reuveny S. , Amir A. , Kotler M. , Mizrahi A. 
Published: January 2005

AbstractA new approach for cultivating dissociated cerebral neurons is described. It is based on a rapid attachment of neurons to the DEAE‐cellulose cylindrical MC and their subsequent interconnection to form cell‐MC conglomerates. Intensive fiber growth followed by synaptogenesis and progressive myelin formation are indicative of optimal conditions of nutrition and oxygenation.
Ganglioside–basic protein interaction: Protection of gangliosides against neuraminidase action
Authors: Yohe H. C. , Jacobson Ronald I. , Yu Robert K. 
Published: January 2005

AbstractThe ability of acidic phospho‐ and sphingolipids to interact with basic proteins was studied by double diffusion analysis. The phospholipids, tri‐ and diphosphoinositide, and the sphingolipid, sulfatide, interacted with myelin basic protein as evidenced by precipitin line formation. Of the sialoglycosphingolipids (gangliosides) tested, only the myelin‐specific monosialoganglioside, GM4The ganglioside nomenclature used here is according to the system of Svennerholm [1963]. The gangliosides are designated as follows: GM4 = I3NeuAcGalCer; GM3 = II3NeuAcLacCer; GM1 = II3NeuAcGgOse4Cer; GD1a = IV3 NeuAc, II3NeuAcGgOse4Cer; GD1b = II3(NeuAc)2GgOse4Cer; and GT1b = IV3NeuAc, II3(NeuAc)2GgOse4Cer.
, formed a precipitin line with myelin basic protein. In addition, myelin basic protein retarded the activity of Clostridium perfringens neuraminidase against GM4 and the disialoganglioside, GD1b. Examination of purified rat brain myelin suggested the presence of a neuraminidase activity intrinsic to myelin. This finding, in concert with ganglioside‐myelin basic protein complexes which selectively protect against neuraminidase, may provide a physiological explanation for the simplified ganglioside pattern found in myelin.
Presynaptic modulation of activity and molecular forms of acetylcholinesterase in the rat superior cervical ganglion during early postnatal development
Authors: Klinar B. , Sketelj J. , Sket D. , Brzin M. 
Published: January 2005

AbstractPreganglionic nerve trunk of the rat superior cervical ganglion was transected shortly after birth in order to evaluate the influence of preganglionic nerves on the development of acetylcholinesterase and choline acetyltransferase in ganglionic neurons. In spite of an early decentralization, specific activity of acetylcholinesterase in the ganglion is increasing during the first 3 wk of life until it is about equal to the activity which remains in the superior cervical ganglion decentralized in an adult animal. Thus, the preganglionic nerves, which per se contribute the presynaptic fraction of total ganglionic AChE activity in normal innervated ganglia, apparently exert no significant regulatory effect on the specific activity of the fraction of acetylcholinesterase affiliated with the developing ganglionic cells. However, the absence of innervation during development is strongly reflected in the pattern of acetylcholinesterase molecular forms. The activity of the 16 S molecular form of AChE remains high in the developing superior cervical ganglion, decentralized at birth, in contrast to the substantial absolute and relative decrease of specific activity of this form during development of a normally innervated ganglion. A high proportion of 16 S AChE probably reflects a shift of decentralized immature ganglion nerve cells toward a cholinergic character. In accordance with this assumption, choline acetyltransferase activity in early decentralized ganglia is significantly higher than that in the ganglia decentralized in adult animals.
Effects of blinding and pinealectomy on regional brain monoamine concentrations
Authors: Niles Lennard P. , Brown G. M. , Mishra R. K. 
Published: January 2005

AbstractThe effects of blinding with or without pineal ablation on brain monoamine levels were studied in male rats. Brain dopamine (DA), norepinephrine (NE), epinephrine (E), and serotonin (5‐HT) were measured by radioenzymatic assays. Four weeks following pinealectomy, E levels were significantly enhanced in the frontal cortex. Chronic blinding decreased striatal DA levels and increased striatal 5‐HT levels in both sham‐operated and pinealectomized (Px) animals.In a second experiment Px animals were sacrificed 1 or 7 d after pinealectomy in order to examine the short‐term effects of pinealectomy. There were no differences between controls and Px animals in their cortical levels of DA, NE, and E and their hippocampal and hypothalamic 5‐HT levels. However, the E concentrations measured 1 d after surgery were significantly greater than after 7 d. The implications of these findings with regard to the reported role of the pineal and melatonin in brain homeostasis and endocrine regulation are discussed.
Some factors affecting the concentrations of para‐hydroxyphenylacetic acid and meta‐hydroxyphenylacetic acid in the mouse caudate nucleus
Authors: McQuade P. S. , Juorio A. V. 
Published: January 2005

AbstractAcid hydrolysis of mouse caudate homogenates results in a significantly increased concentration of para‐hydroxyphenylacetic acid (p‐HPAA). Thus p‐HPAA appears to be significantly present as an acid‐labile conjugate in the mouse caudate nucleus. Saline injection also increased the concentration of the acid metabolite of the tyramines.The subcutaneous injection of either meta‐hydroxyphenylacetic acid (m‐HPAA) or p‐HPAA or both produced at 0.5 hr and 2.0 hr large increases in the mouse caudate nucleus concentrations of m‐ and/or p‐HPAA. Similarly at 2.0 hr the injection of a combination of para‐ and meta‐tyramine caused large increases in the acid metabolite concentrations.Probenecid, at a dose of 500 mg/kg, increased striatal p‐HPAA and m‐HPAA concentrations. Probenecid, injected prior to the administration of p‐HPAA and m‐HPAA, did not reduce the increased concentrations of these two acid metabolites previously observed after the administration of the acid metabolites alone. It thus appears that p‐HPAA and m‐HPAA are transported from the brain by a probenecid‐sensitive mechanism, but in the presence of high blood concentrations, p‐HPAA and m‐HPAA may enter the brain by a mechanism that is not affected by probenecid.
Cell proliferation in growing cultures of dissociated embryonic mouse brain: macromolecule and ornithine decarboxylase synthesis and regulation by hormones and drugs
Authors: Bhat N. R. , Shanker G. , Pieringer R. A. 
Published: January 2005

AbstractPrimary cultures of cells dissociated from embryonic mouse brain were demonstrated to be a useful system for studying cell proliferation and its regulation. Ornithine decarboxylase activity was closely correlated with the rate of DNA and RNA synthesis during cell growth, suggesting that the enzyme is as good an indicator of cell proliferation in these cultures as it is in vivo. Both DNA synthesis and ornithine decarboxylase activity were stimulated by insulin. The enzyme was stimulated five‐ to sixfold by insulin and approximately twofold by butyrate, cis‐retinoic acid, and 12‐O‐tetradecanoylphorbol‐13‐acetate. No effect on the enzyme activity was observed with triiodothyroinine, hydrocortisone, growth hormone, cyclic AMP, or cyclic GMP.
Development of synaptic transmission by cholinergic neurons in culture
Authors: Puro D. G. , Yeh H. H. 
Published: January 2005

AbstractWe examined the development of cholinergic transmission at synapses formed in culture by retinal neurons derived from the embryonic chick. In our experimental system, striated muscle cells served as postsynaptic targets for cholinergic retinal neurons. Functional retina‐muscle synapses could be formed in cultures containing either retinal explants or dissociated retinal cells. Plating a low density of dissociated cells permitted the study of relatively isolated, visually identifiable, cholinergic neurons. We found that, early in the functional maturation of retina‐muscle synapses, the release of acetylcholine occurs spontaneously, but cannot be evoked by the putative excitatory transmitter, glutamate. This stage is followed by the emergence of transmitter release that is evocable by glutamate in a receptormediated and calcium‐dependent manner. This ability to transmit excitatory information across a synapse is expressed in culture by neurons derived from retinas that are at an early stage of morphogenesis.
Evidence from phospholipid metabolism changes for muscarinic cholinergic receptors on rat anterior pituitary cells
Authors: Hauser G. , Parks J. M. 
Published: January 2005

AbstractIn incubations of dissociated adult rat anterior pituitary cells with [32P]orthophosphate, carbamylcholine causes an increase in phosphatidic acid labeling accompanied by a small reduction in phosphatidylinositol labeling. Carbamylcholine and oxotremorine produce about the same maximum change while that caused by pilocarpine is smaller. Low concentrations of atropine, quinuclidinyl benzilate, and scopolamine completely inhibit the effect caused by carbamylcholine, whereas d‐tubocurarine does not decrease the stimulation, even at higher concentrations. The muscarinic antagonists alone produce a rise in phosphatidylinositol labeling and a drop in phosphatidic acid labeling, an effect opposite from that produced by the agonists, but d‐tubocurarine alone has no effect. Thus changes in phospholipid metabolism are mediated through muscarinic cholinergic receptors in dissociated rat anterior pituitary cells, confirming the presence of functional binding sites. The present studies also demonstrate the utility of experiments on precursor incorporation into phospholipids in identifying the existence on cells or tissues of certain receptor classes.
Serum vulnerability and time‐dependent stabilization of neurites induced by nerve growth factor in PC12 pheochromocytoma cells
Authors: Skaper S. D. , Selak I. , Varon S. 
Published: January 2005

AbstractCultures of PC12 pheochromocytoma cells were established on a polyornithine substratum in medium supplemented with the chemically defined N1 mixture in the presence or absence of Nerve Growth Factor (NGF). Normal cell proliferation in the absence of NGF was equally competent when fetal calf serum (FCS) was replaced with N1‐supplemented medium. The differentiation of PC12 cells, which occurs upon NGF treatment, ultimately results in cell death without the addition of 0.1% FCS to the N1‐supplemented medium. The combination of N1, 0.1% FCS, and NGF permits the PC12 cells to develop a neuritic outgrowth much earlier than when higher (1—10%) FCS levels are used. Neurite retraction is caused in a dose‐dependent manner by a delayed presentation of FCS. Within 2 days of serum presentation, however, neurites regrow to achieve that percentage of neurite‐bearing cells which is seen without a serum challenge. Moreover, the retraction response becomes less pronounced with time over the 8‐day culture period for any given serum concentration. Among the N1 ingredients, only insulin and transferrin are needed by PC12 cells for survival whether in the dividing state or not. Neurite growth was not dependent on any of the N1 components.
Taurine uptake by chick embryo retinal neurons and glial cells in purified culture
Authors: Adler R. 
Published: January 2005

AbstractThe properties and cellular distribution of a high‐affinity uptake mechanism for taurine have been investigated using separate populations of purified chick embryo neural retina neurons and glia. Purified neuronal monolayers, cultured in serumfree medium, were incubated in radioactive taurine under different conditions and studied autoradiographically and biochemically. Labeling with radioactive taurine was detected in the perikaryon of most of the neurons present in the cultures. Neuronal uptake occurred by means of a high‐affinity mechanism which was completely inhibited at low temperatures or in the absence of sodium ions. The uptake was linear for at least 1 hr and, as is the case in vivo, could be inhibited by γ‐aminobutyric acid (GABA) or β‐alanine. Incubation in ouabain, glutamate, or high K+ concentrations failed to cause any increase in the amount of taurine released by neurons preloaded with the radioactive amino acid. The rather widespread distribution of high‐affinity taurine uptake was confirmed using separate retinal cultures rich in glial cells. Practically 100% of the glial cells appeared labeled after incubation in 10−7 M [3H] taurine, and this uptake was also inhibited by low‐temperature, Na+‐free medium, GABA, or β‐alanine. Several pieces of evidence indicate that high‐affinity taurine uptake coexists with uptake mechanisms for other amino acids, such as GABA, glutamate, and aspartate, in retinal neurons as well as glial cells. These in vitro populations offer a promising experimental system for the investigation of the effects of taurine on retinal cells.
Increased adhesion response of anaplastic glioma cells to nerve growth factor and the presence of specific receptors
Authors: Vinores S. A. 
Published: January 2005

AbstractA trypsin‐degradable nerve growth factor (NGF) receptor associated with the phospholipid component of the surface membrane has been detected on F98 anaplastic glioma cells. NGF also bound to the nucleus of F98 cells. Bound NGF was not displaceable by insulin, cytochrome C, growth hormone, or bovine serum albumin. Specific binding of NGF occurred with a Kd of 8.79 x 10−12 M as determined by Scatchard analysis with approximately 34,000 receptors per cell. Specific NGF binding was also evident to C6 rat glioma cells and IMR‐32 human neuroblastoma cells, but not to 3T3 mouse fibroblasts. These observations coupled with previous findings suggest that the NGF receptor may be a marker found on cells of neural derivation.As little as 1 ng/ml NGF caused an increase in the adhesiveness of F98 cells to culture flasks. Increased adhesiveness could be observed in as little as 5 min and was apparent for at least 45 min. At 25 min in NGF‐containing medium, 24 ± 3% of the cells adhered to the flasks compared to 13 ± 1% of control cells. The NGF‐induced increase in adhesiveness was not duplicated by epidermal growth factor, insulin, cytochrome c, bovine serum albumin, dibutyryl cyclic AMP, or sodium butyrate. Oxidized NGF blocked the effect of native NGF, but had little or no adhesion‐promoting activity itself. Pretreatment of the cells with NGF was also effective in promoting adhesion, even though nerve growth factor was not added to the binding medium. The effect of this pretreatment was reversible; when NGF‐pretreated cells were grown in medium without supplemental NGF, the adhesiveness of the cells returned to control levels or lower.
Modulation of protein synthesis in a cell‐free system derived from rat brain by corticotropin (ACTH), magnesium, and spermine
Authors: Schrama L. H. , Edwards P. M. , Schotman P. 
Published: January 2005

AbstractModulation of protein synthesis by fragments of the ACTH molecule has been studied in a cell‐free system obtained from subcortical brain tissue of rats. Both the activity of the protein‐synthesizing system and its sensitivity to ACTH‐like peptides appeared to be highly dependent on the Mg2+ and spermine concentrations. At optimal Mg2+ concentrations (4 mM) the peptide sequences ACTH(1–24) and (11–24) were both inhibitory, the latter being the more active. The inhibitory effect was reduced or abolished at higher (suboptimal) Mg2+ concentrations.Spermine, like ACTH, inhibited protein synthesis at the optimal Mg2+ concentration. However, at lower Mg2+ concentrations spermine had a stimulatory effect and maximal activity was obtained at 0.75–1.0 mM Mg2+. In the presence of spermine (60 μM) and Mg2+ (0.75 mM), a half‐maximal inhibition of protein synthesis was obtained with a peptide concentration of 5 μM. A structure‐activity study showed that the peptides ACTH(7–16)‐NH2, (11–24), (5–18, 17Lys18Lys)‐NH2 and (15–24) were active in inhibiting protein synthesis, whereas the fragments ACTH(1‐16)‐NH2 and (17–24) were inactive. The results are discussed in terms of an interaction between ACTH, Mg2+, and spermine, and intracellular processes involved in protein synthesis.
Covalent attachment of 125I‐β nerve growth factor to its receptors on sympathetic neurons
Authors: Stach R. W. , Rusenko K. W. 
Published: January 2005

AbstractWhen 125I‐β nerve growth factor binds to sympathetic and sensory neurons, some labeled ligand is sequestered (becomes inaccessible to the external milieu) in a time‐ and energy‐dependent manner. It would appear that the higher affinity receptor (type I) participates in this process to a greater extent than does the lower affinity receptor (type II) [Olender and Stach, 1980; Olender et al., 1981]. A small portion of the sequestered 125I‐β nerve growth factor is found as part of a high molecular weight complex. When cells, which have been incubated with 125I‐β nerve growth factor, are solubilized with Triton X‐100 and subjected to sodium dodecyl sulfate (SDS) polyacrylamide gel electrophoresis, a complex with an apparent molecular weight of approximately 240,000 is obtained. The formation of the covalent complex can be prevented by the prior addition of excess unlabeled β nerve growth factor or sodium fluoride and dinitrophenol. The covalent 125I‐β nerve growth factor‐receptor complex is dissociated in 50 mM dithiothreitol indicating that disulfide linkages are involved. At concentrations of β nerve growth factor (3.8 × 10−11 −3.8 × 10−10 M) where maximal fiber outgrowth occurs in vitro, approximately 50‐266 attomoles (0.3‐1.6% of the type I receptors) of the covalent complex are formed per 107 nerve cells. These data suggest that a small portion of the 125I‐β nerve growth sequestered by sympathetic neurons becomes covalently attached to its receptor subsequent to its sequestration in a manner which appears to involve type I receptors.
Sodium transport in astrocytes
Authors: Walz Wolfang , Hertz L. 
Published: January 2005

AbstractSodium transport in astrocytes in homogenous primary cultures from mouse brain cortex were investigated with radiotracer (22Na) and electrophysiological methods. The equilibrated Na+ content was 190 nmol × mg−1 protein and the influx and efflux rates were identical at about 560 nmol × mg−1 × min−1. No significant change was observed in Na+ efflux or influx when external K+ was raised from 5.4 to 12 or 54 mM, but the Na+ content decreased. Intracellular Na+ loading, evoked by previous exposure to ice‐cold K+‐free medium, doubled the Na+ efflux. Ouabain, a Na+ ‐K+ exchange inhibitor, exerted a small, nonsignificant inhibition of Na+ efflux at both 5.4 and 12 mM K+ and caused a large increase in Na+ content. At 5.4 mM K+, amiloride, a Na+‐H+ exchange inhibitor, decreased both influx and efflux of Na+ and caused an increase in Na+ content. Furosemide, an inhibitor of a cation‐Cl− carrier, decreased both content and influx of Na+ slightly but had no significant effect on Na+ efflux. The effects of amiloride or furosemide on Na+ influx were abolished at elevated (12 and 54 mM) K+. Attempts to stimulate the Na+−K+ pump with elevated external K+ or internal Na+ produced no electrogenic component of the membrane potential. Probably owing to the high K+ permeability. Based on the present results and earlier experiments on K+ influx, it is concluded that 1) the Na+−K+ pump of astrocytes under normal conditions transports more K+ than Na+; 2) intracellular Na+ loading increases Na+ efflux; 3) some Na+−H+ exchange and cotransport of Na+ and Cl− seem to occur at 5.4 mM K+; and 4) neither of the latter two transport mechanisms is enhanced at elevated K+ concentrations.