bluuebunny/crossref_metadata_2025_split huggingface dataset:
Localization of the pool of G4 acetylcholinesterase characterizing fast muscles and its alteration in murine muscular dystrophy
Authors: Gisiger V. , Stephens H. R. 
Published: January 2005

AbstractThe distributions of acetylcholinesterase and its molecular forms within muscles of normal and dystrophic 129/ReJ mice were established by a concomitant cytochemical and biochemical study performed on 1‐mm serial sections of three predominantly fas muscles, i.e., anterior tibialis, extensor digitorum longus, and sternomastoid, as well as the slow‐twitch soleus. This comparative study showed the following main finding.(1)In every muscle of bothe normal and dystrophic mice (a) the three asymmetric forms were confined to the motor zone where they systematically codistributed with the endplates, and (b) all globular forms, including G4, were concentrated at the motro zone from which they extended over the entrie muscle length along a concentration gradient. (2) In the normal muscles, the perijunctional sarcoplasmic cytochemical reaction exhibited by individual fibers was grouped into a well‐defined conjunctional acetylcholinesterase compartment in which the endplates were embedded. The overall intensity of the cojunctinal cytochemical reaction was either high or low according to whether the muscle was predominantly fast or slow. (3) This conjuncitonal acetylcholinesterase compartment varied in close parallelism with G4 and thus appeared as the cytochemical correlate of the G4 molecules concentrated around the endplates. In particular, as the shape of the motor zone progressively increased in complexity along with the intricacy of the muscle fiber organization, from sternomastoid to extensor digitorum longus to anterior tibialis, so did both the relative volume occupied by the cojunctional acetylcholinesterase compartment and the proportion of G4. (4) The motor zone of the normal fast‐twitch muscles characteristically differed from that of the soleus by the presence of a G4‐rich enviornment around the endplates, which was cooperatively provided by the the surrounding fibers. (5) In dystrophic muscles, this cojunctinal G4‐rich compartment was lost: the cytochemical compartment was no longer discernable, while G4 was reduced to a minimal low level similar to that characteristic of the normal soleus.
Immune response products alter CNS acitivity: Interferon modulates central opioid function
Authors: Dafny N. , Lee J. R. , Dougherty P. M. 
Published: January 2005

AbstractThe presents report provides evidence to support the hypothesis that peptides released during an immune response alter CNS activity and thus may provide a means for the immune system to transmit afferent single into the brain. Specifically, it is demonstrated that recombinant interferon‐alpha (rIFN‐α), a peptide associated with the immune response to viral infection, can alter opiate withdrawal severity in a dose‐dependent manner upon direct injection into brain areas essential for this phenomenon. These results are compared and contrasted with the effect of systemically injected rIEN‐α upon opiate withdrawal. In addition, an electrophysiological investigation into the basis of the interaction of opioids and rIFN‐α in brain structures essential for the expression of opioid activities is also presented. Finallu, the effects of rIFN‐α upon the functions of both the CNS and other systems is discussed in terms of the effects reported for other peptides associated with immune responses.
Neuropeptide Y in the rat nucleus accumbens: Ultrastructural localization in aspiny neurons receiving synaptic input from GABAergic terminals
Authors: Massari V. J. , Chan J. , Chronwall B. M. , O'Donohue T. L. , Oertel W. H. , Pickel V. M. 
Published: January 2005

AbstractThe ultrastructure, afferent input, and sites of termination of neurons containing neuropeptide Y‐like immunoreactivity (NPY‐LI) were examined in the adult rat nucleus accumbens by using the peroxidase‐anti‐peroxidase (PAP) method. The NPY‐LI was seen in sparsely distributed, spindle‐shaped perikarya having cross‐sectional diameters of 15–20 μm. These perikarya exhibited highly invaginated nuclear membranes and thin rims of cytoplasm containing Golgilamellae, dense‐core vesicles, and other organelles. A few large, principally aspiny, dendrites also showed NPY‐LI. The dendrites received synaptic input from unlabeled terminals forming both symmetric and asymmetric junctions. Immunolabeling for NPY was evident in other processes that were not clearly differentiated as dendrites or axons. These were seen primarily near glial processes and the basal laminae of blood vessels. A few myelinated and many unmyelinated axons and axons terminals also were labeled for NPY. These terminals contained numerous, small (40–60 nm), clear and one or more large (80–100 nm) dense core vesicles. Forty‐seven percent (27 out of 57) of the terminals containing NPY‐LI formed symmetric junctions with unlabeled dendrites or dendritic spines. The remainder lacked recognizable densities within single planes of section. The neurons exhibiting NPY‐LI in the nucleus accumbens were characterized further with respect to their afferent input from terminals labeled for the GABA‐synthesizing enzyme, glutamic acid decarboxylase (GAD). Immunogold labeling of a rabbit antiserum against NPY and PAP labeling for a sheep antiserum to GAD were sequentially applied to the same sections. The GAD‐labeled terminals formed symmetric junctions primarily with the more numerous unlabeled dendrites. However, a few synaptic junctions also were detected between the GAD‐labeled terminals and dendrites showing immunogold labeling for NPY. We conclude (1) that in the rat nucleus accumbens, NPY‐LI is found principally in neurons of the aspiny type and (2) that the output from these presumably intrinsic neurons to other neighboring neurons or blood vessels is at least partially modulated by GABA.
Protective action of calcium channel blockers on Na+, K+ –ATPase in gerbil cerebral cortex following ischemia
Authors: Palmer G. C. , Palmer S. J. , Christie‐Pope B. C. 
Published: January 2005

AbstractThe present study was initiated to determine whether pretreatment of gerbils with calcium channel blockers, flunarizine and verapamil would prevent injury to cerebral ATPases following secondary ischemia consisting of 60‐min bilateral clamping of the carotids followed by 40 min of reperfusion. The sequence of ischemia produced a deficit in Na+, K+ ‐ATPase activity without influencing Ca++, Mg++ ‐or Mn++ ‐sensitive ATPases. Pretreatment with flunarizine significantly prevented the damage to Na+, K+ ‐ATPase while the effect of verapamil was marginal. Verapamil, along with dimethylsulfoxide (DMSO), reduced the mortality rate of gerbils subjected to the paradigm of ischemia. When added directly to the cerebral fractions in vitro the two calcium channel blockers inhibited Na+, K+ ‐ATPase alone. Flunarizine was more potent in vitro than verapamil.
Insulin and insulinlike growth factor receptors regulating neurite formation in cultured human neuroblastoma cells
Authors: Recio‐Pinto E. , Ishii D. N. 
Published: January 2005

AbstractThe functional role of brain insulin and insulinlike growth factor (IGF) receptors is being sought. Recently it has been found that these ligands are members of a newly identified family of neuritogenic polypeptides. We studied the relationship between125I‐insulin and125I‐IGF binding and their capacity to enhance neurite formation in cultured human neuroblastoma SH‐SY5Y cells. The binding of125I‐insulin was temperature‐dependent and heterogeneous. The Scatchard plot and dissociation rate were both consistent with the presence of two types of sites. There appeared to be about 900 high affinity sites per cell with a Kd of about 3 nM. This compared favorably with the half‐maximal concentration of 4 nM for enhancement of neurite formation. The type I IGF sites were also present. Physiology concentrations of insulin clearly enhanced neurite formation through the insulin sites, whereas physiology concentrations of IGF‐I and IGF‐II enhanced through the IGF sites. Cross‐occupancy of sites was observed at supraphysiologic concentrations, providing a reasonable explanation for the broad dose‐response curves for these ligands. These results support the suggestion that one function of insulin and IGF receptors in neural tissues may be to modulate neurite formation.
The complete nuleotide sequence and structure of the gene encoding bovine phenylethanolamine N‐methyltransferase
Authors: Batter D. K. , D'Mello S. R. , Turzai L. M. , Hughes H. B. , Gioio A. E. , Kaplan B. B. 
Published: January 2005

AbstractA cDNA clone for bovine adrenal phenylethanolamine N‐methyltransferase (PNMT) was used to screen a Charon 28 genomic library. One phage was identified, designated λP1, which included the entire PNMT gene. Construction of a restriction map, with subsequent Southern bloty analysis, allowed the identification of exon‐containing fragments. Dideoxy sequence analysis of these fragments, and several more further upstream, indicates that the bovine PNMT gene is 1,594 base pairs in length, consisting of three exons and two introns. The transcription initiation site was identified by two independent methods and is located iapproximately 12 base pirs upstream ffrom the ATG translation start site. The 3′ untranslted region is 88 base pairs in length and contains the expected poly‐adenylation signal (AATAAA). A putative promoter sequence (TATA box) is located about 25 base pairs upstream from the transcription initiation site. Computer comparison of the nucleotide sequence data with the consensus sequences of known regulatory elements revealed potential binding sites for glucocorticoid receptors and the Sp1 regulatory protein in the 5′ flanking region of the gene. Additionally, comparison of the sequence of the exons of the PNMT gene with cDNA sequences for other enzymes involved in biogenic amine synthesis revealed no significant homology, indicating that PNMT is not a member of a multigene family of catecholamine biosnthetic enzymes.
Localization of corticotropin‐releasing factor, somatostatin, and vasoactive intestinal polypeptide in the parabrachial nuclei of the human brain
Authors: Pammer Csilla , Fodor M. , Palkovits M. 
Published: January 2005

AbstractThe immunocytochemical localizations of corticotropin‐releasing factor (CRF), somatostatin (SRIF), and vasoactive intestinal polypeptide (VIP) were studied in the human parabrachial nuclei (PBN) using the avidin‐biotin complex (ABC) technique. The brains were obtained from seven adult male human subjects of 38–74 years. In three cases, the brains were fixed within 2 hr, in four cases within 5 hr, postmortem. All of these peptides were detected in fibers through the orocaudal extent of the lateral PBN, whereas the medial nucleus contained only CRF immunoreactive fibers. Immunoreactive fibers were distributed unevenly within the lateral nucleus with the highest density in the dorsal and much fewer in the ventral part of the lateral subdivision. The highest to lowest density of immunostained processes were detected using CRF, SRIF, and VIP antisera, respectively. Since NPB is known as an important relay nucleus for the central autonomic pathway, the presence of the above noted neuropeptides in nerve fibers in this area may suggest a neurotransmitter or neuromodulatory role of CRF, somatostatin, and VIP in certain autonomic nervous mechanism of the human brain.
Effects of inhibitors of glycoprotein processing on oligodendroglial differentiation in primary cultures of embryonic rat brain cells
Authors: Bhat Narayan R. 
Published: January 2005

AbstractThe effects of N‐linked oligosaccharide processing inhibitors on oligodendroglial differentiation were examined in cultures of embryonic rat brain cells. The glucosidase inhibitors, 1‐deoxynojirimycin (dNM) and castanospermine, were found to have marked inhibitory effects on the developmental expression of oligodendroglial properties, i.e., sulfogalactolipid synthesis and 2′3′‐cyclic nucleotide 3′‐phosphohydrolase (CNP). On the other hand, the mannosidase inhibitors, 1‐deoxymannojirimycin (dMM) and swainsonine, had relatively little effects. Since both classes of inhibitors block the formation of complex‐type oligosaccharide chains as revealed by concanavalin A‐Sepharose affinity chromatography of the glycopeptides, complex oligosaccharides oligosaccharides do not seem to play a role in oligodendroglial differentiation. The results indicate instead that the early trimming reactions involving the removal of glucose residues by processing glucosidases may be critical for the functioning of specific glycoprotein(s) essential to oligodendroglial differentiation.
Glycerol oxidation in discrete areas of rat brain from young, adolescent, and adult rats
Authors: McKenna Mary C. , Tildon J. Tyson , Bezold L. I. 
Published: January 2005

AbstractWe have reported previously that the oxidation rate of [1,3‐14C] glycerol to 14CO2 is lower in whole brain homogenates from neonatal rats and increases about 30% during the suckling period to adult levels. To determine whether there are developmental changes in glycerol oxidation in discrete regions of brain, we examined the oxidation of glycerol by homogenates of hypothalamus, cerebellum, brain stem, hippocampus, and cerebral cortex of young (4–6 days) and older (18–20 days) pups and adult (>90 day) rats. The oxidation was measured at both low (0.2 mM) and high (2.0 mM) concentrations of glycerol, since the oxidation of glycerol by brain tissue has been shown to exhibit biphasic kinetics. At each age, and with both concentrations of glycerol, there were significant differences among the discrete brain regions. Although the rate of glycerol oxidation increased with age in most areas of brain, each brain region had a distinct developmental profile. In the hypothalamus, the oxidation of glycerol increased significantly between 4–6 days and adult levels at 18–20 days. The oxidation of glycerol was essentially the same in homogenates of cortex from young and older pups, but it was significantly increased in adults. In contrast with other brain regions, the oxidation of glycerol by brain stem was highest at 4–6 days and significantly decreased with age. The developmental profile of glycerol oxidation in hippocampus and cerebellum was particularly complex, since it increased with age at low, but not at high, concentrations of glycerol. This developmental pattern in hippocampus and cerebellum could be related to changes in the biphasic kinetics of glycerol oxidation and suggests that glycerol metabolism is different in these two areas of brain compared with other areas of brain.
GABAA and GABAB sites in bovine adrenal medulla membranes
Authors: Castro E. , Oset‐Gasque M. J. , Cañadas S. , Gimenez G. , González M. P. 
Published: January 2005

AbstractThe effect of several ligands and Ca2+ ions on [3H]GABA binding to bovine adrenal medulla membranes was investigated. Without any blockade, the [3H]GABA binding showed two components, one of low affinity (Kd = 139 ± 22 nM and Bmax = 3.2 ± 0.4 pmol/mg protein) and the other of high affinity (Kd = 41 ± 6 nM and Bmax = 0.35 ± 0.26 pmol/mg protein). Muscimol specifically blocked low‐affinity sites, and ( – )baclofen blocked high‐affinity components. Ca2+ ions were strictly necessary for maximum binding to high‐affinity sites, whereas they did not significantly affect sites of the lower affinity. These results show that the bovine adrenal medulla has a GABAA receptor population of low affinity together with a GABAB receptor of high affinity.
Light‐dependent subcellular movement of photoreceptor proteins
Authors: Whelan J. P. , McGinnis J. F. 
Published: January 2005

AbstractThe intracellular localization of photoreceptor‐specific proteins 33 kd, beta‐transducin, and 48 kd, as determined by immunocytochemistry, is transient and dependent on the lighting environment to which the retina is exposed. Western analysis of the proteins in isolated rod outer segments from mouse retina demonstrates that beta‐transducin actually moves from the outer segment to the inner segement in response to light and that 48 kd moves simultaneously in the opposite direction. The light‐induced movements appear to be initiated by the absorption of light by rhodopsin because red light, which does not bleach rhodopsin, does not produce this redistribution of phototoreceptor proteins. Time course analysis of these movements suggests that the light‐induced shift is detectable at the earliest time examined (30 seconds). The bidirectional movement suggests that the photoreceptor cells have at least two distinct dyneinlike or kinesin‐like translocator molecules that act as microtubule‐based motors. This movement appears to be a basic mechanism by which photoreceptor cells rapidly and radically alter the subcellular concentrations of photoreceptor‐specific proteins, which in turn may affect the rapid changes in membrane potential that occur during phototransduction.
Expression of GD3 ganglioside by developing rat cerebellar purkinje cells in situ
Authors: Reynolds Richard , Wilkin G. P. 
Published: January 2005

AbstractGD3 is a major ganglioside of the immature vertebrate CNS, and its expression is suggested to be characteristic of immature neuroectodermal cells. Using immunocytochemistry on cryostat sections of developing rat cerebellum with a monoclonal antibody specific for GD3, we have found that GD3 begins to be expressed on the plasma membrane of Purkinje cell bodies and dendrites beginning at postnatal day 7. Staining became brighter as the dendritic tree of the cells enlarged. As the Purkinje cells began to mature in different folia, they became GD3+, until by 15 days postnatal all Purkinje cells were GD3+. Positive staining of the dendritic tree was still present in the adult cerebellum. Using a monoclonal antibody 7–8D2, which recognizes cerebellar granule cells and their axons (the parallel fibres), and polyclonal antibodies against a synaptic vesicle component synaptophysin, double‐immunofluorescence staining together with anti‐GD3 antibodies suggested that the appearance of GD3 immunoreactivity did not correlate either with the ingrowth of parallel fibres or the presence of their synapses on Purkinje cell dendrites. However, comparison with earlier morphological studies showed that the appearance of GD3 immunoreactivity correlated well with the formation of climbing fibre synapses on Purkinje cell dendrites and the onset of the rapid expansion of the dendritic tree. These results are in keeping with the idea that elevated GD3 concentrations are found in certain cell types during periods of rapid growth or high metabolic activity but also show that this is not only restricted to immature cells.
Role of arachidonic acid and other free fatty acids in mitochondrial dysfunction in brain ischemia
Authors: Hillered Lars , Chan Pak H. 
Published: January 2005

AbstractThe aim of the present investigation was to evaluate the possible role of arachidonic acid and other free fatty acids in ischemia‐induced mitochondrial dysfunction. Respiratory activities were measured in mitochondria isolated from rat brains subjected to 15–30 min of decapitation ischemia. Addition of bovine serum albumin (BSA) to the mitochondria, isolated in BSA‐free media, abolished an ischemia‐induced increase in substrate‐stimulated (state 4) respiration but only partly reversed a marked inhibition of substrate‐, phosphate‐, and ADP‐stimulated (state 3) respiration caused by the ischemia. Individual free fatty acids were measured in aliquots of the same mitochondrial preparations before and after treatment with BSA. There was a significant increase in arachidonic (20:4), stearic (18:0), palmitic (16:0), and docosahexaenoic (22:6) acid during ischemia. BSA treatment removed all 20:4 and reduced the amount of 18:0 and 16:0, but had no significant effect on 22:6. The main conclusions were (1) that 20:4, 18:0, and 16.0 were responsible for the partial uncoupling (increase in state 4 respiration) of mitochondrial respiration during ischemia, (2) that the inhibition of state 3 respiration caused by ischemia could only partly be attributed to an effect of FFAs, and (3) that the ischemia‐induced mitochondrial dysfunction was caused by a combination of factors including 20:4.
Antigen recognized by monoclonal antibodies to mesencephalic neural crest and to ciliary ganglion neurons is involved in the high affinity choline uptake mechanism in these cells
Authors: Barald Kate F. 
Published: January 2005

AbstractHigh‐affinity choline uptake mechanisms are among the characteristics of cholinergic neurons such as the ciliary and choroid subpopulations in the ciliary ganglion (Barald and Berg, 1979).We have produced three monoclonal antibodies (Mabs), two of which were made to 8‐day embryonic chick ciliary ganglion (CG) neurons (CG‐1, CG‐4) (Barald, 1982) and one of which was made to cultured mesencephalic neural crest (NC) cells (CG‐14) removed from the embryo 31 hr after incubation. We have shown that all three Mabs label a common 75 kD antigen present on the cell surface of both CG neurons and NC cells (Barald, 1988).Here we report that the CG‐1 and CG‐4 antibodies, used in the same ratios in which they are synergistically cytotoxic for both the CG and NC cells (Barald, 1988), and Mab CG‐14 alone, have specific effects on the high‐affinity choline uptake mechanism (HACU) of CG neurons and isolated antigen‐positive NC cells in the absence of complement. CG‐1 and CG‐4 in ratios of 8/1 (the same ratios that are used to kill the CG and the NC subpopulation), but neither singly, inhibit the HACU of CG neurons by 40% and that of isolated antigen‐positive NC cells by 75%. However, CG‐14 alone, at 1 μg/ml, inhibits the HACU of both CG neurons and isolated NC cells by 95%.None of the antibodies had an effect on numbers of ouabain binding sites (a measure of the Na+/K+ ATPase) or cell surface acetylcholinesterase (AChE) of CG neurons or NC cells isolated by “no‐flow” fluorescence cytometry with a Meridian Instruments ACAS470 cytometer. CG or NC cells grown in the presence of the antibodies without complement grow and remain healthy for many weeks. They exhibit no difference in morphology, protein content, lactate dehydrogenase activity (LDH), or division time from untreated sister cultures.Therefore, the antigen recognized by all three Mabs may be involved in a high‐affinity choline uptake mechanism, a common characteristic of cholinergic neurons. The Mabs themselves may possibly label some element of the high‐affinity transporter or a proximal membrane component. This implies that such a high‐affinity uptake mechanism is present in the subpopulation of NC cells at early times in development. If these cells in fact are destined to contribute to the avian CG, these characteristics are present in the subpopulation before the NC cells take on a neuronal morphology.