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1. |
Cultured peripheral nervous system cells support peripheral nerve regeneration through tubes in the absence of distal nerve stump |
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Journal of Neuroscience Research,
Volume 14,
Issue 4,
1985,
Page 393-401
H. D. Shine,
P. G. Harcourt,
R. L. Sidman,
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摘要:
AbstractAxons of a cut peripheral nerve will grow across a gap ( ≤ 10 mm in adult rodents) formed when the proximal and distal stumps are placed at opposite ends of an impermeable, inert tube, but will not grow to the end of a blind‐ended tube in the absence of the distal stump [Williams et al, 1984]. Work reported here demonstrates that cultured peripheral nervous system (PNS) cells suspended in a collagen matrix will provide an effective milieu that directs and supports axonal regeneration from a severed nerve into a blind‐ended tube in the absence of a distal stump. Adult mouse sciatic nerves were cut and the proximal stumps were inserted into close‐ended tubes that contained either a collagen matrix containing dissociated cells from embryonic mouse dorsal root ganglia (DRG), a collagen matrix saturated with medium conditioned by cultured DRG cells, or a collagen matrix saturated with fresh medium. In all three cases cellular cables formed that ran the full length of the tubes, but myelinated and unmyelinated axons regenerated the length of the tubes only when cultured cells had been added. The critical factor in influencing axonal regerneration through the length of the tubes was the presence of cultured cells, since collagen alone or collagen saturated with conditioned medium did not support axonal regrowth even though cells had migrated into the chambers from the proximal stumps in all cases. Ordered structure was not a requisite for axonal growth, since the cultures consisted of random arrays of dissociate
ISSN:0360-4012
DOI:10.1002/jnr.490140402
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1985
数据来源: WILEY
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2. |
Transplantaion of embryonic chick spinal cord into transection adult chicken into transection adult chicken spinal cords: A useful model for transplantation research |
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Journal of Neuroscience Research,
Volume 14,
Issue 4,
1985,
Page 403-414
M. S. Grady,
O. Steward,
J. A. Jane,
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摘要:
AbstractAdult chicken spinal cords were completely transected under direct visualization. One week later, embryonic chick spinal cords 6 days, 9 days, or 11 days old were implanted into the site of transection. The animals were allowed to survive for 2 months and then killed and the spinal cords were prepared for histologic analysis. The survival and outgrowth of the embryonic transplants were compared with regard to the age of the implant, and its effects on the host tissue. Six‐day embryonic tissue survival and integrated far better than 9‐day or 11‐day, and adult spinal cord subjacent to the early age embryo showed fewer degenerative changes. The chick embryo may provide a model for use in CNS transplant
ISSN:0360-4012
DOI:10.1002/jnr.490140403
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1985
数据来源: WILEY
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3. |
Effects of nitrendipine on the voltage‐sensitive calcium channel in mammalian sensory neurons |
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Journal of Neuroscience Research,
Volume 14,
Issue 4,
1985,
Page 415-422
M. J. Litzinger,
P. G. Nelson,
R. Y. K. Pun,
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摘要:
AbstractWe examined the ability of nitrendipine, a calcium antagonist believed to block the voltage‐sensitiv calcium channels in a number of excitable membranes, to affect the calcium spike duration and rate of rise (Dv/Dt) in 4‐week‐old cultured mouse dorsal root ganglion neurous. Concentrations of 10 nM‐1:0 μM intrendipine reduced but did not eliminate calcium spike as measured by the rate of rise. These results were obtained at either 22° rate of rise (Dv/Dt) in 4‐week‐old cultured mouse dorsal root ganglion neurous. Concentrations of 10 nM‐1:0 μM intrendipine reduced but did not eliminate calcium spike as measured by the rate of rise. These results were obtained at either 22° or 37°C in solutions containing 5 mM calcium. A similar lack of total block was seen with prolonged incubation in sodium‐free recording media containing 1 μM tetrodotoxin (TTX), 1.8 mM calcium, and 1 μM nitrendipine. Calcium spike duration was affected in an inconsistent manner by nitrendipine and other 1,4 dihydropyridines. Cobalt (10 mM) totally blocked the voltage‐dependent calcium mechanism as measured by either the spike duration or the rate of rise. We conclude that calcium influx through the voltage‐sensitive calcium channel in mouse dorsal root ganglion neurons is not blocked by even high conc
ISSN:0360-4012
DOI:10.1002/jnr.490140404
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1985
数据来源: WILEY
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4. |
Rat brain α2‐pre‐ and postsynaptic receptors are different or differently modulated? |
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Journal of Neuroscience Research,
Volume 14,
Issue 4,
1985,
Page 423-431
F. Cerrito,
P. Preziosi,
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摘要:
AbstractIn order to get better characterization of α2‐pre‐ and postsynaptic noradrenergic receptors in the rat brain, we investigated the α2‐receptor changes which take place during a 12‐day treatment with the α2‐antagonists yohimbine (4 mg/kg) and mianserin (10 mg/kg). These treatments caused a significant increase in the sensitivity of hypothalamic synaptosomes to the inhibitory action of the noradrenergic agonist clonidine on the3H‐noradrenaline release elicited by K depolarization. Frontal cortex α2‐autoreceptors were not affected by drug treatments. However, the3H‐p‐aminoclonidine (3H‐PAC) bindig to membranes from hypothalamus or frontal cortex from treated animals was the same as in controls.Changes in neural firing, elicited by the α2‐antagonists on noradrenergic neurons, could explain our results.The presynaptic autoreceptors may thus become hypersensitive to counteract the enhanced neurotransmitter release in the hypothalamus, where the noradrenaline is accumulated at the synaptic cleft. In the frontal cortex, where it seems that only 5% of the noradrenergic terminals make synaptic contacts with postsynaptic elements, the α2‐autoreceptors are less sensitive to an enhanced neurotransmitter release. Alternatively, they have scarce functional importance because the noradrenaline release is effectively modulated by the inhibitory recurrent locus coeruleus collaterals.At the postsynaptic level, the receptor down‐regulation might be prevented by chronic presence of the antagonist drug.Thus the different behavior between pre‐ and postsynaptic α2‐receptors and between α2‐receptors of different brain areas may be ascribed to a different modulation rather t
ISSN:0360-4012
DOI:10.1002/jnr.490140405
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1985
数据来源: WILEY
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5. |
Purification and characterization of cultures of oligodendroglia from rat brain |
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Journal of Neuroscience Research,
Volume 14,
Issue 4,
1985,
Page 433-447
S. E. Poduslo,
R. Curbeam,
K. Miller,
P. Reier,
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摘要:
AbstractIt is possible to purify dary cells from rat brain which by ultrastructural criteria are oligodendroglia. The modified technique involves the use of an isolation medium less damaging to the initial cell suspension and then differential plating of a stratified primary cell culture obtained from 1–3‐day‐old rat brain which has been described. Five percent serum encourages the growth of oligodendroglia. In this system, the oligodendroglia can be harested several times from the primary cultures. To retain the homogeneous populations of oligodendroglia, it is necessary to constantly manipulate the cultures by hitting the flasks and replating the suspended cells. Electron microscopy reveals that the small dark cells are differentiated oligodendroglia with prominent microtubules. Immunofluorescence staining of the cells shows that the majority of the cells are negative for known surface markers which include cerebrosides and 04 antigen (markers for oligodendroglia), glial fibrillary acidic protein, and fibronectin. Interestingly, it is possible to increase the number of 04‐positive cells by the addition of dibutyryl cyclic AMP to the medium. Rat oligodendroglia are able to incorporate about 20% of the radioactivity into cerebrosides, using the substrate, [3H]galactose; this is a biochemical feature unique to oligodendroglia. The expression of all the oligodendroglial antigens should be remarkably enhanced when the cells are induced to produce
ISSN:0360-4012
DOI:10.1002/jnr.490140406
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1985
数据来源: WILEY
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6. |
Cerebral citric acid cycle enzymes in methionine sulfoximine toxicity |
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Journal of Neuroscience Research,
Volume 14,
Issue 4,
1985,
Page 449-459
L. Ratnakumari,
G. Y. C. V. Subbalakshmi,
Ch. R. K. Murthy,
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摘要:
AbstractThe activity levels of pyruvate dehydrogenase, enzymes of the citric acid cycle, aspartate and alanine aminotransferases, and NADP+‐isocitrate dehydrogenase were determined in the cerebral cortex, cerebellum, brain stem, corpus striatum, hippocampus, and midbrain regions of normal rats and rats injected with acute and subacute doses of methionine sulfoximine (MSI). In both conditions there was an elevation in the activities of pyruvate dehydrogenase and all the enzymes of the citric acid cycle except malate dehydrogenase, whereas the activities of aminotransferases and NADP+‐isocitrate dehydrogenase were suppressed in all the cerebral regions. It is suggested that the operational rates of the citric acid cycle would be enhanced in MSI‐induced hyperammonemia and that there might be a derangement in the transport of reducing equivalents across mitochondrial membranes. It has been suggested that the convulsant action of the drug is due to its effects on ionic gradients and may not be due to depletion of α‐ketoglutarate from the citric ac
ISSN:0360-4012
DOI:10.1002/jnr.490140407
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1985
数据来源: WILEY
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7. |
Amino acid incorporation during morphine intoxication. I : Dose and time effects of morphine on protein synthesis in specific regions of the rat brain and in astroglia‐enriched primary cultures |
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Journal of Neuroscience Research,
Volume 14,
Issue 4,
1985,
Page 461-477
L. Röunnbäck,
E. Hansson,
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摘要:
AbstractUptake and incorporation of3H‐valine into soluble protein were studies in normal and in physically dependent rat brain, or in astroglial primary cultures at various times after the administration of morphine at different doses. There was an increased protein synthesis in striatum and brain stem of previously untreated rats 2–3 hr after low‐dose morphine administration (10mg/kg bw IP). The changes were completely reversed by naloxone (5 mg/kg bw, IP) administered 10 min prior to the morphine. During the first hour after IP administration of 25 mg morphine/kg bw there was a decrease in striatum and brain stem protein synthesis, followed by an increase in brain stem protein synthesis between 2 and 3 hr later. These changes were blocked by naloxone. In all brain regions studied 40 mg morphine/ 1kg bw, IP inhibited protein synthesis, an effect partially reversed by naloxone (5 mg/kg bw, IP).Similar dose‐ and time‐dependent effects were pbtained from primary astrogliaenriched cultures from cerebral hemispheres, suggesting that low or moderate doses of morphine affect brain cell protein synthesis. At least one phase of increased synthesis was seen, but within a few hours of a high morphine dose the protein synthesis was decreased.After long‐term morphine intoxication (13 days; final dose 340 mg/kg bw/day po) incorporation of3H‐valine in vivo into TCA‐precipitable soluble proteins during 60 min decreased in the hypothalamus and in occipital and entorhinal cortex, and was unchanged in other brain regions examined. An IP injection of morphine (10 or 25 mg/kg bw/day) to such animals resulted in a pronounced and rapidly occurring increase in protein synthesis in many brain regions. This was further demonstrated with gel electrophoresis in brain stem and hypothalamus, where higher3‐labeling was seen in many protein bands. The labeling of one band from brain stem having approx 80,000 MW was especially pronounced. Incorporation of3−H‐valine into mambrance‐bound proteins of brain stem changed in a similar way to the soluble proteins, but was not as pronounced.Similar, although less pronounced, effects were seen after IP administration of 25 mg morphine/kg bw to rats intoxicated for 4 days (final dose 130 mg/kg bw/day po). After an IP injection of 40 mg morphine/kg bw to the long‐term intoxicated rats, the depression in protein synthesis was less pronounced than that seen in previously untreated rats. Naaloxone (5 mg/kg bw IP) gave the rats symptoms of withdrawal. In sensory‐motor cortex and in cerebellum the effects on protein synthesis caused by 10 or 25 mg/kg bw morphine were practically reversed by naloxone, whereas in striatum and brain stem, naloxone in the dose used was not able to compleely restore the changes in protein synthesis. Protein synthesis was not restored to control values in any brain region after naloxone treatment prior to 40 mg morphine/kg bw.After 2 days of withdrawal of morphine‐intoxicated rats, amino acid incorporation into soluble protein increased in the occipital cortex, decreased in the frontal cortex, and was unchanged in the other brain regions examined compared to long‐term‐intoxicated rats.It is concluded that the machinery for protein synthesis is sensitized after long‐term morphine treatment. The sensitization was especially pronounced in brain regions rich in opiate receptors, although it could no
ISSN:0360-4012
DOI:10.1002/jnr.490140408
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1985
数据来源: WILEY
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8. |
Amino acid incorporation during morphine intoxication. II: Electrophoretic separation of extracellular proteins from cerebral hemisphere slices and astroglia‐enriched primary cultures |
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Journal of Neuroscience Research,
Volume 14,
Issue 4,
1985,
Page 479-490
E. Hansson,
L. Rönnbäck,
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摘要:
AbstractRadioactively labeled proteins were identified in a broad molecular weight range in the incubation medium of rat cerebral hemisphere slice preparations or primary cultures after incubation with radioactive valine. Morphine chloride caused an increase in labeled media proteins with MW ˜40,000 and 65,000 in both preparations, whereas a fraction with MW, ˜80,000 decreased in amount. In the culture preparation a MW ˜15,000 fraction also decreased after morphine treatment. The effects on the MW 40,000 and 65,000 fractions by morphine could not be blocked by naloxone hydrochloride, an opiate antagonist. Labeled media proteins from primary cultures obtained from various brain regions showed many similarties. After 10−5or 10−6M morphine, protein fractions with MW ˜15,000, 25,000, 40,000, 65,000–70,000, 80,000, and 100,000 changed with increases or decreases in the various morphine concentrations. The3H‐labeling of the MW ˜40,000 fraction increased in all cultures, where it decreased.In conclusion, proteins synthesized within cells in brain slices or in astrogliaenriched cultures are released or secreted into the incubation media. Some protein fractions are affected in different directions by morphine. The effects were not correlated with the presence of classical opiate receptors on the cells. This was so even though more changes in media proteins occurred in astroglial cultures from opiate receptor‐rich brain regions than in similar cultures from opiate receptor‐poor regions. The possible significance of proteins synthesized in astroglial cells and released extracellulary in opiate act
ISSN:0360-4012
DOI:10.1002/jnr.490140409
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1985
数据来源: WILEY
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9. |
Bacteria, plasmids and phages. Edmund C.C. Lin, Richard Goldstein, and Michael Syvanen. Cambridge, MA: Harvard University Press, 1984, ix + 316 pp, $35.00 cloth, $18.50 paper |
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Journal of Neuroscience Research,
Volume 14,
Issue 4,
1985,
Page 491-491
V. Holoubek,
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ISSN:0360-4012
DOI:10.1002/jnr.490140410
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1985
数据来源: WILEY
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10. |
Genetics and neurology. Sarah Bundey (Chapter 3 by E.M. Brett). New York: Churchill Livingstone, 1985, 340 pages, $50.00 |
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Journal of Neuroscience Research,
Volume 14,
Issue 4,
1985,
Page 492-493
R. Fabian,
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ISSN:0360-4012
DOI:10.1002/jnr.490140412
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1985
数据来源: WILEY
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