摘要:

AbstractNerve‐intact muscle regenerates were prepared by ischemic‐toxic injury of slow soleus (SOL) and fast extensor digitorum longus (EDL) muscles of the rat. Rapid innervation of regenerating myotubes modified intrinsic patterns of AChE molecular forms, revealed by velocity sedimentation in linear sucrose gradients. Regarding their onset, the effects of innervation can be classified as early and late. The earliest changes in the SOL regenerates appeared a few clays after inner vation by their motoneurons: The activity of the 13 S AChE form (A 8) increased significantly in compari son to non‐innervated regenerates. The pattern of AChE molecular forms became similar to that in the normal SOL muscle during the 2nd week after in jury. In contrast, no major differences were observed between 8 day‐old innervated and non‐innervated EDL regenerates. Their patterns of AChE molecular forms resembled that in the normal EDL. However, the predominance of the 10 S AChE form (G 4) char acteristic for the 2‐week old non‐innervated regener ates was prevented by innervation. Early effect of innervation observed in the SOL regenerates but not in the EDL may be due to intrinsically different re sponse of the regenerating SOL myotubes to innerva tion. Rather high extrajunctional activity of the asymmetric 16 S (A 12) molecular form of AChE in early regenerates was reduced to adult level in about 3 weeks in the SOL, and nearly completely sup pressed in 5 weeks after innervation in the EDL re generates. This reduction is assumed to be a late ef fect of innervation, as well as a decrease of the activity of the 4 S AChE form (G 1) in the SOL regenerates. A suppressive mechanism is activated in the extra junctional regions of the innervated muscle regener ates during their maturation. This mechanism coun teracts the enhancing influence of contractile activity on the expression of the asymmetric AChE forms in immature muscle cells, and is more efficient in the EDL than in the SOL. Its onset may be apparently delayed by protracted fusion of the satellite cells with

ISSN:0360-4012    

DOI:10.1002/jnr.490280302

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1991

数据来源: WILEY

摘要:

AbstractThere is growing evidence on the existence of endog enous ouabain‐like factors that modulate Na+, K+‐ATPase activity. In this laboratory, two soluble sub‐fractions (peaks I and II) were previously separated from rat cerebral cortex, which, had opposite effects on Na,+K+‐ATPase activity. Peak I stimulated and peak II inhibited the enzyme (Rodríguez de Lores Arnaiz and Antonelli de Gomez de Lima, Neurochem Res 11:933‐947, 1986). The same effects are now re ported for K+‐p‐nitrophenyphosphatase activity. Lo calization of high‐affinityouabain binding in rat brain was done by quantitative atitoradiography us ing amicrocomputer digital imaging system. Peak I did not modify, whereas peak II blocked ouabain binding in areas 3–4 of cerebral cortex, dentate gyrus, stria terminalis, thalamic nuclei, and basal gan glia. Similar results were obtained when ouabain binding was determined in rabbit cerebral cortex and by a conventional filtration assay in nerve ending membranes obtained from rat cerebral cortex. These results favour the idea that the factor present in peak II fraction might behave as an ouab

ISSN:0360-4012    

DOI:10.1002/jnr.490280303

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1991

数据来源: WILEY

摘要:

AbstractBiochemical analysis indicates that lithium ion (Li+) has deleterious effects on the metabolism of at least two elements of the cytoskeleton in cultured chick dorsal root ganglia (DRG) neurons. Phosphorylation ofnewly synthesized middle molecular mass neurofilament polypeptide (NF‐M) is inhibited by 10‐25 mM LiCl, and tubulin (Tb) synthesized in the presence of Li+is subject to rapid degradation. These Li+‐in duced metabolic abnormalities are accompanied by alterations in cellular and cytoskeletal morphology. Treatment of cultures having vigorously growing neurites with 25 mM LiCl results in the cessation of net neurite growth, without causing neurite retrac tion. Indirect immunofluorescence reveals that in these cultures Li+provokes an aggregation of NF protein into a dense knot in the cell body/proximal neurite region. The knots contain accumulations of all three NF polypeptides and electron microscopic observation demonstrates that the knots contain in tact, but disorganized, filaments. Both the inhibition of neurite outgrowth and NF collapse are reversible. Tubulin and intact microtubules are redistributed in immature cultures treated with Li+insofar as they are excluded from the NF knots. Neurons in estab lished cultures (e.g., 7 days and beyond) fail to show any difference between Li+treatment and control conditions in the morphology of the cytoskeletal ele ments exa

ISSN:0360-4012    

DOI:10.1002/jnr.490280304

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1991

数据来源: WILEY

摘要:

AbstractThe in situ C‐1300 murine neuroblastoma (MNB) tumor model was used to investigate the influence of exogenously administered nerve growth factor (NGF) on tumor growth and tissue catecholamine concentra tion in mice Sympathectomized with 6‐hydroxy‐dopamine (6‐OHDA) on postnatal days 4–10. Mice were implanted with 1 × 106disaggregated MNB cells 3 days after termination of 6‐OHDA administra tion. NGF (12‐15 μg/mouse/day) treatment was ini tiated at the time of MNB cell implantation and con tinued until sacrifice of the animal. The time interval between tumor cell implantation and detection of pal pable tumor (tumor onset time), transverse tumor diameter, tumor weight, tumor weight to body weight ratio, and tumor catecholamine concentration were determined. Neonatal sympathectomy caused a de crease in myocardial norepinephrine concentration of 88% compared with vehicle‐treated animals as well as a significant reduction in total body and organ weight Average body, brain, heart, and spleen weights were decreased 31% 16%, 25%, and 42%, respectively, below control values. The daily injection of NGF, from the time of MNB tumor implantation to sacrifice, did not prevent these effects of chemical sympathectomy from being expressed. Tumor onset time following implantation of MNB cells was signif icantly increased in neonatally Sympathectomized mice and was not altered by treatment with NGF. In contrast, the decrease in MNB tumor growth rate observed in Sympathectomized mice was reversed by administration of NGF. Mean tumor weight and mean tumor to body weight ratio were 89% and 115% of comparable control values, respectively, in Sympathectomized mice receiving exogenous NGF. The norepinephrine (NE) and dopamine (DA) con centrations of tumors removed 8 days after tumor onset were increased 2.8‐ and 3. 6‐fold, respectively, in neonatally Sympathectomized mice. Administration of NGF prevented the increase in tumor NE and DA concentration associated with chemical sympa thectomy. Cell surface receptors for NGF were present on cultured C‐1300 MNB cells. These data suggested the presence of two types of binding sites with KDvalues of 45.9 pM (high affinity) and 2.4 nM (low affinity). The inhibition of MNB tumor growth and elevation in tumor catecholamine content pro duced by neonatal sympathectomy may be Immorally mediated since they were selectively reversed by th

ISSN:0360-4012    

DOI:10.1002/jnr.490280305

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1991

数据来源: WILEY

摘要:

AbstractRat forebrain astrocytes synthesize heat shock proteins with molecular weights 97,89,70,68, and 30‐34 kilodaltons. The stress inducible 68‐kDa heat shock protein (HSP‐68) was vigorously expressed by astro‐cytes in culture after a 45°C, 20 min heat shock. HSP‐68 synthesis was poorly inducible by a second heat shock given 16 hr after the initial heat shock. Decreased [35S]methionine incorporation into HSP‐68 correlated with low levels of HSP‐68 mRNA present after the second heat shock. The data suggest that control of HSP‐68 mRNA levels by transcriptional/ posttranscriptional mechanisms is a major site for regulation of

ISSN:0360-4012    

DOI:10.1002/jnr.490280306

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1991

数据来源: WILEY

摘要:

AbstractEstrogen stimulates expression of proenkephalin mRNA in neurons of the hypothalamic ventromedial nucleus, and evidence is accumulating that synaptic release of one of the peptide end products, met‐en‐kephalin, influences events that regulate reproductive behavior. To address the question of whether estrogen acts directly on neurons that synthesize met‐en‐kephalin or indirectly through a separate neuronal population, we combined estrogen autoradiography with endogenous opioid peptide (EOP) immunohistochemistry. In agreement with previous studies, the ventrolateral subdivision of the hypothalamic ventromedial nucleus was densely packed with EOP‐immunoreactive cells. In males, 48% of the estrogen‐concentrating cells of the ventrolateral subdivision of the hypothalamic ventromedial nucleus contained EOP, and, in females, 27% of the estrogen‐concentrating cells contained EOP. These findings indicate that estrogen acts directly on neurons that express EOP and suggest a mechanism that underlies sexually differentiated reproduc

ISSN:0360-4012    

DOI:10.1002/jnr.490280307

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1991

数据来源: WILEY

摘要:

AbstractIn the present work the distribution of L‐glutamate binding sites in the different layers of human cerebellum of normal individuals and of seven patients who died with olivopontocerebellar atrophy (OPCA) was examined with the technique of quantitative autora‐diography. Specific L‐[3H]glutamate binding was higher in the molecular than in the granule cell layer of normal cerebellar tissue. A significant decrease of L‐[3H]glutamate specific binding was observed in me molecular layer of ail OPCA tissues. In the granule cell layer L‐[3H]glumate binding was decreased only in two patients who suffered from late‐onset sporadic OPCA and in one patient who suffered from a form of OPCA inherited in a dominant manner.Quisqualate‐sensitive binding sites were the most abundant binding sites in the molecular layer of normal cerebella, whereas N‐methyl‐D‐aspartic acid (NMDA)‐sensitive binding sites were the most abundant type in the granule cell layer. A significant decrease of quisqualate‐sensitive and an increase in NMDA‐sensitive binding sites were observed in the molecular layer of OPCA cerebellar tissues. No significant changes were observed in the granule ce

ISSN:0360-4012    

DOI:10.1002/jnr.490280308

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1991

数据来源: WILEY

摘要:

AbstractStriatal slices from the rat were loaded with [3H]glutamate ([3H]Glu) superfused measure release of radioactivity at rest and during potassium‐evoked depolarization. Addition of KC1 (22‐40 mmol/liter) to the perfusion fluid enhanced the release of tritium in a concentration‐dependent manner, and this release was abolished by omission of CaCl2. High‐performance liquid chromatography (HPLC) separation coupled with radiochemical delection revealed that 23% and 41% of the tritium efflux detected in the perfusion fluid under resting conditions and during potassium stimulation, respec‐lively, was due to [3H]Glu. At the end of the super‐fusion about 63% of residual tritium content in the tissue was [3H]Glu. Tritium efflux in response to KCI excess was significantly higher from striatum dissected from 6‐hydroxydopamine‐pretreated rats. Apomorphine decreased, the KCl‐evoked release of [3H]Glu haloperidol exerted the opposite effect, Yohimbine, which antagonized the decrease of dopa accumulation elicited by apomorphine in NSD‐1015 and γ‐butyrolactone‐pretreated rat caudate nucleus, also reversed the appmprphine inhibition of the, re‐lease of [3H]Glu evoked by depolarization. The selective α2‐adrenoceptor antagonist CH‐38083, however, did not modify the apomorphine inhibition of [3H]GIu release or dopa accumulation, andthe α2‐adrenoceptor agonist xylazine did not alter tritium efflux from striatum preloaded with [3H]Glu. These findings suggest that release of glutamate (Glu) from the corticostriatal pathway is under tonic control of dopamine released from nigrostriatal neurons, and α2‐adrenoceptors are not involved in the regulation of glutamatergic transmission in the rat striatum. The effect of yohimbine on Glu release is attributed to its antidopaminergic rathe

ISSN:0360-4012    

DOI:10.1002/jnr.490280309

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1991

数据来源: WILEY

摘要:

AbstractThe present investigation was designed to determine the effect of lesions localized to the nucleus basalis/ substantia innominata (NB) on resting and cholin‐ergically activated regional cerebral cortical blood flow (rCBF). Ibotenic acid (l0μg) was infused locally at 1 mm caudal to bregma, 3 mm lateral to the midline, and 8 mm below the cortical surface. Effectiveness of lesions was demonstrated by histological verification of lesion sitesand determination of choline acetyltransferase activity in cerebral cortex homogenates. rCBF was measured with the autoradiographic iodo‐14C‐antipyrine technique. Resting rCBF was similar in the hemisphere that received the NB lesion and in the contralateral (intact) side in all regions examined. Physostigmine intravenous infusion (33 μg kg−1min−1) enhanced rCBF in frontal, parietal, occipital, and temporal cortex. The increase was symmetrical, however, indicating inability of NB lesion to affect this phenomenon. It is concluded that the cortical cholinergic afferents originating in the NB are not involved in the cont

ISSN:0360-4012    

DOI:10.1002/jnr.490280310

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1991

数据来源: WILEY

摘要:

AbstractWe have previously shown that neuroblasts from cerebral hemispheres of 6‐day‐old chick embryos are able to proliferate when grown in the presence of fetal calf serum. We report here that in the presence of horse serum alone the proliferative rate of neuroblasts is strongly reduced. A high proliferative rate is restored upon the addition of bovine transferrin and to a lesser extent with added FeSO4or hemin. These findings suggest that the transferrin of horse serum cannot be used by chick neuroblasts in vitro, while bovine transferrin exogenously added is active in promoting cell proliferation. We propose that the stimulatory activity of the fetal calf serum is due to bovine transferrin, since when this serum is fractionated by gel filtration, the fractions that stimulate the proliferation of neuroblasts grown in the presence of horse serum are located in the molecular weight area of transferrin, and they do contain transferrin as seen by immunoblotting with a specific anti‐transferrin ant

ISSN:0360-4012    

DOI:10.1002/jnr.490280311

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1991

数据来源: WILEY