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D Dahl

Publications and source records attributed to D Dahl.

At least 55 records · Page 3Linked to original sources

NMDA receptor antagonists reduce medial, but not lateral, perforant path-evoked EPSPs in dentate gyrus of rat hippocampal slice.

NMDA receptor antagonists produced differential effects on medial and lateral perforant path-evoked excitatory postsynaptic potentials (EPSPs) recorded in the dentate gyrus molecular layer of hippocampal slices. D-(-)-2-amino-5-phosphonovaleric acid (D(-)-APV) and 3[(+/-)-2-carboxypiperazin-4-yl]-propyl-1-phosphonic acid (CPP) significantly reduced the peak amplitude and total area, but not the initial negative slope, of the medial perforant path-evoked EPSP. Neither antagonist affected any component of the lateral perforant path-evoked EPSP. In contrast, population spikes evoked by stimulation of either pathway were depressed.

2-Amino-5-phosphonovalerate↗

Neuronal markers in the rodent pineal gland--an immunohistochemical investigation.

Although some embryological and morphological features speak in favour of a neuronal character of rodent pinealocytes, histochemistry and ultrastructure let this issue appear controversial. Using antibodies to different neurofilaments, the neural adhesion molecule L1, synaptophysin and tubulin as neuronal markers, the pineal glands of rat and guinea-pig were studied by means of immunofluorescence. Neurofilament-immunoreactivity was present in some rat pineal nerve fibers and in the majority of guinea-pig pinealocytes, L1 decorated rat intrapineal nerve fibers, synaptophysin was almost ubiquitously distributed in the pineal of both species, while tubulin-immunofluorescence was seen in nerve fibers of rat and guinea-pig pineal and in some pinealocytes of the latter. These findings speak in favour of the neuronal character of guinea-pig pinealocytes. The lack of neurofilament- and tubulin-immunoreactivity in rat pinealocytes might be attributable to very low concentrations of these proteins or species differences as to their expression. Further studies including in situ-hybridisation of relevant mRNAs will be necessary to answer these questions definitely.

Animals↗

Involvement of capsaicin-sensitive nerves of the rat urinary bladder in acrylamide neuropathy.

Acrylamide monomer is neurotoxic in man and experimental animals, producing a sensorimotor distal axonopathy. In spite of remarkable effect of acrylamide on micturition, resulting in urine retention in both man and rat, bladder autonomic innervation has been little studied. This study focused on the effect of acrylamide on capsaicin-sensitive nerves of the rat bladder, because of the role played by these fibres in regulating the afferent arm of reflex micturition.

Acrylamide↗

Neurofilament protein-triplet immunoreactivity in distinct subpopulations of peptide-containing neurons in the guinea-pig coeliac ganglion.

A battery of polyclonal and monoclonal antibodies raised against the triplet of identified neurofilament protein subunits was used to investigate neurofilament protein immunoreactivity in neurons of the guinea-pig coeliac ganglion. Using optimal conditions of fixation and tissue processing for each antibody we found that only 20% of the postganglionic sympathetic neurons in the guinea-pig coeliac ganglion contain neurofilament protein-triplet immunoreactivity. Double labelling with neurofilament protein-triplet antibodies raised in different species demonstrated that all of these antibodies labelled the same population of neurons. Double labelling using mouse monoclonal antibodies against neurofilament proteins in combination with rabbit polyclonals to neuronal markers showed that neurofilament protein-triplet immunoreactivity is restricted to specific chemically coded subpopulations of noradrenergic neurons. Approximately 52% of neurons in the ganglion contain neuropeptide Y and are presumed vasomotor neurons projecting to blood vessels in the submucosa of the small intestine. Virtually none of the neuropeptide Y-containing neurons were labelled with neurofilament protein-triplet antibodies. Neurons that contain somatostatin (21%) project to the submucous ganglia of the small intestine. Approximately two-thirds of neurons containing somatostatin are immunoreactive for the neurofilament protein-triplet. The other postganglionic neurons in the ganglion (27%) project to the myenteric plexus of the small intestine and do not contain either neuropeptide Y or somatostatin. Approximately a quarter of these neurons were labelled with neurofilament protein-triplet antibodies. These results suggest that the neurofilament protein-triplet may not be an intrinsic component of the cytoskeleton of all neurons. Furthermore the idea of a chemical coding of neurons should be extended to cytoskeletal proteins. The finding that these neurofilament proteins are confined to specific neuronal subpopulations has important implications for the search for a role of the neurofilament protein-triplet in neurons, for the interpretation of classical neurohistological silver impregnation techniques which appear to stain only neurofilament protein-triplet-containing neurons, as well as for neuropathological conditions that may involve these proteins in disease processes.

Animals↗

Patterns of neurofilament stain in the spiral ganglion of the developing and adult mouse.

The objective of the study was to identify neurofilament-positive cells and their projections in the intact spiral ganglia of the mouse. One polyclonal and three monoclonal antibodies against neurofilament triplet subunits NF 68 K, 160 K and 200 K were used. In the newborn mouse most of the spiral neurons and their processes stain positively, although the perikaryal stain is very light. During early postnatal development, some cells show a selective intense stain. The progressive myelination of the neuronal processes further restricts the stain to a small neuronal population of positive perikarya and to their nonmyelinated fibers. This pattern of stainability implies that the neurofilament-positive cells are compatible with the type II spiral neurons. The stain reveals two populations of spiral neurons: 1) the cells which are scattered within the ganglion and show a bipolar distribution of fibers; and 2) the cells that form an interrupted chain along the intraganglionic bundle. The latter cells are also bipolar, but their peripheral processes join the intraganglionic bundle for varying distances before reaching the radial bundles. The identification of selective groupings of filamentous nonmyelinated cells in the corresponding location in different mammals is discussed. In conclusion, the use of neurofilament antibodies in staining of the intact spiral neurons permitted us to identify a distinct cell population of neurofilament-positive nonmyelinated nerve cells located along and projecting (at least partly) into the intraganglionic bundle.

Aging↗

The c-myc-regulated gene mrl encodes plasminogen activator inhibitor 1.

The DNA sequence of the c-myc-regulated gene mrl (G. C. Prendergast and M. D. Cole, Mol. Cell. Biol. 9:124-134, 1989) reveals that it encodes plasminogen activator inhibitor 1 (PAI-1), a regulator of extracellular proteolysis. Comparison of the human and mouse PAI-1 promoters and cDNA 3' noncoding regions revealed several highly conserved sequence domains, potential targets for c-myc and other factors influencing PAI-1 expression. We discuss possible roles for PAI-1 in normal and neoplastic cell growth control.

Animals↗

A retrospective clinical and neuroimmunohistochemical study of rheumatoid arthritic patients with atlanto-axial subluxation.

In a retrospective study of 87 RA patients with radiographically documented anterior atlanto-axial subluxation (AAS) in flexion-extension radiographs, 40 had been studied radiographically before they developed AAS. Of these 40 patients, 34 had had occipitocervical pain already before the subluxation. This shows that pain early in the course of the rheumatoid cervical spine is not caused by or associated with AAS itself. In a separate operatively treated group of 5 patients, ligament neuroanatomy in AAS was more closely studied, using specific heteroantisera to cytoskeletal neurofilaments and various transmitter neuropeptides as neural markers and the highly sensitive avidin-biotin-peroxidase complex (ABC) immunohistochemical staining procedure. These specimens were obtained from the ligamentous structures between the posterior arch of the atlas and the spinous process of C2, corresponding to the C1-C2 interspinal non-inflammatory ligament, during atlanto-axial stabilizing operations. This ligamentous tissue contained, in addition to focal inflammatory cell infiltrates, neurofilament and/or neuropeptide immunoreactive neural elements. This finding may suggest that pain early in anterior AAS could be caused not only by synovitis, for example, but also by local ligamentary involvement leading to irritation of local neural elements. This phenomenon may have contributed to the local occipitocervical pain experienced by 34/40 patients who later developed AAS.

Arthritis, Rheumatoid↗

Early neuronal development in the spinal cord of a reptile assessed by neurofilament protein immunoreactivity.

The neural tube in the Gallotia galloti Stage 22 (S.22) embryo is already closed at the level of the cervical flexure, while caudal closure does not end until S.23. Cell proliferation begins shortly after the final neural tube closure, being rapid and giving rise, by S.26, to a thick ventricular zone. Cell migration does not start until S.28, initially in the basal plate, and forming putative motoneurons. Migration in the alar plate does not start until S.33. The appearance of the first neurofilament protein-positive perikarya coincides with the structural and ultrastructural identification of the neuron, although neurofilament-immunoreactive cells can already be identified inside the ventricular zone. Finally, from S.35 onwards, after major cell migration has already occurred, neuronal maturation continues in situ.

Animals↗

Neurofilament phosphorylation in neuronal perikarya following axotomy: a study of rat spinal cord with ventral and dorsal root transection.

Rat spinal cord was stained by indirect immunofluorescence with 11 neurofilament monoclonal antibodies that recognize phosphorylated epitopes. All monoclonals were axon-specific in this location. The large motoneurons containing bundles of neurofilaments did not stain and the pattern remained unchanged after transection of the sciatic nerve in the thigh. With nine monoclonals, stained motoneurons were observed in the ventral horns 3 days, 5 days, 1 week, and 2 weeks after transection of the ventral roots close to the spinal cord. The abnormal motoneurons were typically scattered among normal (i.e., nonstained) cells. Even in animals showing the most severe reaction, the whole motoneuron population at the site of rhizotomy was not affected, stained and nonstained perikarya often coexisting side by side. Stained motoneurons were no longer observed 3 weeks after ventral root transection. Changes in neuronal immunoreactivity were also observed after dorsal root transection. However, a different population was affected, i.e., middle-sized neurons in dorsal horns and at the base of ventral horns. With two monoclonals (A9 and D21), cell bodies remained negative following all operations. It is concluded that axotomy in proximity of the cell body may induce certain neurofilament phosphorylation events in motor neuron perikarya, whereas other phosphorylation events remain confined to the axons under these experimental conditions. The absence of changes after transection of the sciatic nerve in the thigh suggests that neurofilament phosphorylation is a reaction to cell injury rather than a cellular event related to nerve regeneration.

Animals↗

Isolation and partial characterization of a glial hyaluronate-binding protein.

A glial hyaluronate-binding protein (GHAP) with an isoelectric point of 4.3-4.4 was isolated from human brain white matter. The 60-kDa glycoprotein appeared to be quite resistant to proteolysis, and comparison with GHAP from a viable glioma removed at surgery showed that the protein isolated from autopsy material was not a degradation product resulting from postmortem autolysis. The protein was localized immunohistochemically with mouse monoclonal and rabbit polyclonal antibodies in cerebral white matter. Only small amounts could be found in the gray matter. After enzymatic deglycosylation, an immunoreactive 47-kDa polypeptide was obtained. Two amino acid sequences of GHAP showed a striking similarity (up to 89%) with a highly conserved region of cartilage proteins (bovine nasal cartilage proteoglycan and rat and chicken link protein). However, the amino acid composition and other amino acid sequences suggested that there are also differences between brain-specific GHAP and cartilage proteins.

Amino Acid Sequence↗

Expression of neurofilament immunoreactivity in developing rat cerebellum in vitro and in vivo.

The developmental expression of neurofilaments immunoreactivity was examined in frozen sections and in primary cultures of rat cerebellum by immunocytochemistry with a series of monoclonal antibodies and with a polyclonal antibody. In tissue sections immunocytochemical staining with all the antibodies used was observed in basket cells where adult-like appearance could be detected by 14 days of age and adult-level intensity was achieved by about 25 days. Granule cells remained unstained. Intense staining appeared in cerebellar white matter as early as 7 days after birth. In contrast, neurofilaments immunoreactivity was detected in cultured granule cells from 7-day-old cerebellum. Only polyclonal antibodies reacting with the highly conserved middle alpha-helical domain of the neurofilament subunits were reactive in culture. Staining could be detected in the nerve cell bodies from the first day after plating; thereafter staining intensity increased and was also distributed in neurite extensions. We conclude that unlike their counterparts in vivo cultured embryonic granule cells can express certain neurofilaments immunoreactivity.

Animals↗

Glial hyaluronate-binding protein in Wallerian degeneration of dog spinal cord.

Wallerian degeneration of spinal cord dorsal columns was produced in three dogs by unilateral extradural dorsal rhizotomy at the lower thoracic level. The spinal cord was studied 1 month, 2 months, and 3 months after surgery. Transverse cryostat sections at the site rhizotomy and at the mid-thoracic level were stained by indirect immunofluorescence with antibodies to the glial fibrillary acidic protein (GFAP) and to the glial hyaluronate-binding protein (GHAP). GHAP immunoreactivity was almost unchanged in the degenerated dorsal column 1 month after rhizotomy. After 2 and 3 months, staining with GHAP antibodies was markedly decreased in the gliosed dorsal column at the site of rhizotomy, but it still persisted at the mid-thoracic level. It is concluded that GHAP persists for long periods of time in dorsal columns undergoing Wallerian degeneration, a finding consistent with its putative role as a nonpermissive substrate preventing nerve regeneration in CNS white matter.

Animals↗

Human fetal spinal cord xenografts survive in the eye of athymic nude rat hosts.

Human fetal spinal cord tissue was recovered from elective abortions and grafted to the anterior chamber of the eye of adult athymic nude rats. The transplants slowly became vascularized from the host iris during the first months. There was a clear cut stage-dependent survival and growth along a more "human" time-table. Fetal spinal cord tissue from embryos younger than gestational week 8 showed a much better survival and growth than tissue from older stages. Using laminin immunohistochemistry blood vessels could be visualized in the grafts. The pattern of vascularization was, however, clearly abnormal; there were fewer vessels which had abnormally thick walls as compared to those in the normal spinal cord. Similar to rat spinal cord allografts the human spinal cord xenografts displayed a relative gliosis and were surrounded by a glial layer visualized with antibodies against glial fibrillary acidic protein. Neurofilament-immunoreactive fibres were found inside the glial layer. A variety of neurons were found including large polygonal motoneuron-shaped cells, albeit with CGRP and AChE negative cell bodies. Both Substance P and enkephalin-immunoreactive cells and fibres were found. It is concluded that xenografted fetal human spinal cord survives, grows and may provide a useful model for experimental studies of human spinal cord development and connectivity.

Animals↗

Axonal regeneration in old multiple sclerosis plaques. Immunohistochemical study with monoclonal antibodies to phosphorylated and non-phosphorylated neurofilament proteins.

Cryostat sections of two old plaques removed at autopsy from the spinal cord of a 62-year-old man with multiple sclerosis of 24-year duration were studied by indirect immunofluorescence with antibodies to neurofilament proteins, glial fibrillary acidic protein (GFAP), glial hyaluronate-binding protein (GHAP), vimentin and laminin. The neurofilament monoclonal antibodies used in this study reacted with phosphorylated epitopes of the two large polypeptides of the neurofilament triplet (NF 150K, NF 200K). As previously reported [Dahl D, Labkovsky B, Bignami A (1989) Brain Res Bull 22:225-232], the neurofilament antibodies either stained axons in the distal stump of transected sciatic nerve in the early stages of regeneration or late in the process, i.e., after regenerating axons had reached the distal stump of the transected sciatic nerve. Both multiple sclerosis plaques were positive for GFAP and vimentin, but negative for GHAP, while astrocytes in myelinated spinal cord white matter stained with both GFAP and GHAP antibodies. Laminin immunoreactivity in the plaques and normal spinal cord was confined to blood vessels. One plaque was almost devoid of axons as evidenced by indirect immunofluorescence with neurofilament antibodies. Another plaque was packed with bundles of thin axons running an irregular course in the densely gliosed tissue. Axons in the plaque only stained with neurofilament antibodies reacting with sciatic nerve in the early stages of regeneration while axons in the surrounding myelinated white matter were decorated by all neurofilament antibodies, regardless of the time of appearance of immunoreactivity in crushed sciatic nerve. It is concluded that reactive astrocytes forming glial scars do not constitute a non-permissible substrate for axonal growth.

Antibodies, Monoclonal↗

Intermediate filament proteins immunologically related to desmin in astrocytes: a study of chicken spinal cord by two-dimensional gel electrophoresis and immunoblotting.

Co-migration experiments by two-dimensional SDS-PAGE using chicken spinal cord extracts and desmin purified from chicken gizzard showed that desmin is not present in spinal cord. However, by the immunoblotting procedure, desmin antibodies recognized 3 spinal cord antigens with different molecular weights and isoelectric points than desmin and the glial fibrillary acidic (GFA) protein. These antigens which also reacted with GFA protein antibodies were not identified in chicken gizzard extracts. The reactivity of the antigens with a monoclonal antibody recognizing an epitope common to most intermediate filament proteins (1) suggests that immunostaining of astrocytes with desmin antibodies (2, 3) is due to the presence of new intermediate filament proteins immunologically related to desmin.

Animals↗

Early posttranslational modifications of the three neurofilament subunits in mouse retinal ganglion cells: neuronal sites and time course in relation to subunit polymerization and axonal transport.

We have characterized stages in the posttranslational processing of the three neurofilament subunits, High (NF-H), Middle (NF-M), and Low (NF-L), in retinal ganglion cells in vivo during the interval between synthesis in cell bodies within the retina and appearance of these polypeptides in axons at the level of the optic nerve (optic axons). Neurofilament proteins pulse-labeled by injecting mice intravitreally with [35S]methionine or [32P]orthophosphate, were isolated from Triton-soluble and Triton-insoluble fractions of the retina or optic axons by immunoprecipitation or immunoaffinity chromatography. Within 2 h after [35S]methionine injection, the retina contained neurofilament-immunoreactive radiolabeled proteins with apparent molecular weights of 160, 139, and 70 kDa, which co-migrated with subunits of axonal neurofilaments that were dephosphorylated in vitro with alkaline phosphatase. The two larger polypeptides were not labeled with [32P]orthophosphate, indicating that they were relatively unmodified forms of NF-H and NF-M. About 75% of the subunits were Triton-insoluble by 2 h after isotope injection, and this percentage increased to 98% by 6 h. Labeled neurofilament polypeptides appeared in optic axons as early as 2 h after injection. These subunits exhibited apparent molecular weights of 160, 139, and 70 kDa and were Triton-insoluble. The time of appearance of fully modified polypeptide forms differed for each subunit (2 h for NF-L, 6-18 h for NF-M, 18-24 h for NF-H) and was preceded by the transient appearance of intermediate forms. The modified radiolabeled subunits in optic axons 3 days after synthesis were heavily labeled with [32P]orthophosphate and exhibited the same apparent molecular weights as subunits of axonal neurofilaments (70 kDa, 145 and 140 kDa, and 195-210 kDa, respectively). Whole mounts of retina immunostained with monoclonal antibodies against NF-H in different states of phosphorylation demonstrated a transition from non-phosphorylated neurofilaments to predominantly phosphorylated ones within a region of the axon between 200 and 1000 microns downstream from the cell body. These experiments demonstrate that the addition of most phosphate groups to NF-M and NF-H takes place within a proximal region of the axon. The rapid appearance of modified forms of NF-L after synthesis may imply that processing of this subunit occurs at least partly in the cell body. The presence of a substantial pool of Triton-insoluble, unmodified subunits early after synthesis indicates that the heaviest incorporation of phosphate occurs after neurofilament proteins are polymerized.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Early and late appearance of neurofilament phosphorylation events in nerve regeneration.

Neurofilament phosphorylation in regenerating rat sciatic nerve was studied by indirect immunofluorescence with monoclonal antibodies reacting with phosphorylated epitopes of the 2 large polypeptides of the neurofilament protein triplet (NF 150K, NF 200K). One group of antibodies decorated axons early in the process. In fact, no differences were seen in double labeled sections between these antibodies and polyclonal neurofilament antibodies as to their reactivity with the distal stump of transected sciatic nerves. Another group stained axons after they had completed their elongation, i.e., after they had reached the distal part of the denervated sciatic nerve. In general, the epitopes recognized by antibodies in this group appeared more sensitive to phosphatase digestion as compared to the first group. Furthermore, there was a good correlation between the thickness of the regenerated axons and staining with these monoclonal antibodies. Thick axons (like those observed in normal nerves) were stained, while bundles of thin axons remained unstained. Monoclonal II32 stained regenerated axons in a remarkable segmental pattern. With this antibody, continuous decoration of the axons was still not observed 7 weeks after transection, the longest follow-up period in this study. We suggest that some neurofilament phosphorylation events may contribute to the stabilization of the axonal cytoskeleton and that abnormalities persist in regenerated axons as to the extent of neurofilament phosphorylation.

Animals↗

Structural similarity of hyaluronate binding proteins in brain and cartilage.

A glial hyaluronate-binding protein (GHAP) was isolated from human brain white matter by affinity chromatography on immobilized hyaluronate. The 60 kDa protein appeared remarkably homogeneous by reversed-phase high pressure liquid chromatography analysis. Four cyanogen bromide peptides and 10 tryptic peptides were characterized by amino acid sequence, a total of 12 sequences since overlaps were found between 2 cyanogen bromide and 2 tryptic peptide sequences. Two sequences of brain GHAP had similarity with rat link protein, a hyaluronate binding protein in cartilage. The region of similarity was contained in the evolutionary conserved COOH-terminal half of link protein which is involved in the binding of hyaluronate. The remaining 10 amino acid sequences of brain GHAP had no similarity with link protein, nor with previously reported protein sequences. The findings suggest that the hyaluronate binding domains of such diverse proteins as brain GHAP and cartilage link protein are similar, probably due to the fact that hyaluronic acid is highly conserved in evolution.

Amino Acid Sequence↗