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M E Atkinson

Publications and source records attributed to M E Atkinson.

At least 19 recordsLinked to original sources
PubMed1991

A quantitative study of neuropeptide immunoreactive cell bodies of primary afferent sensory neurons following rat sciatic nerve peripheral axotomy.

Following peripheral axotomy, fluoride resistant acid phosphatase (FRAP) and most neuropeptides are depleted in the central terminals of axotomised nerves and reduced in their corresponding cell bodies (DRG) but vasoactive intestinal polypeptide (VIP) increases. The increase in VIP probably results from a change in gene expression in other ganglion cells which do not normally express VIP. A quantitative study was performed to investigate the proportion of DRG cells immunoreactive for different peptides at increasing times after sciatic nerve section. Retrograde fluorescent neuronal labelling of sciatic nerve cell bodies by injection of fast blue into the proximal stump was combined with unlabelled antibody immunohistochemistry for CGRP and VIP. The proportion of cells immunoreactive for these peptides was quantified between two and fourteen days post-axotomy. The number of VIP immunoreactive profiles increased significantly in the first 4 days post-axotomy, followed by a slight decrease before rising again. In contrast, the number of and CGRP-immunoreactive cell profiles declined to zero by 14 days post-axotomy. 4 days post-axotomy 50% of VIP positive cells were also immunoreactive for CGRP. There was neither colocalisation between VIP and FRAP nor between CGRP and FRAP. It is concluded that many peptidergic DRG cell bodies switch their expression of peptide to VIP after injury, whereas non-peptide-containing subpopulations do not.

Acid Phosphatase↗
PubMed1990

Collateral branching innervation of rat molar teeth from trigeminal ganglion cells shown by double labelling with fluorescent retrograde tracers.

Somatotopic projections of each maxillary molar tooth were defined by injecting individual teeth with True blue and plotting the location of fluorescent cells in sections of the trigeminal ganglia. Collateral branching was investigated by injecting True blue and Diamidino yellow into pairs of maxillary molar teeth and examining the ganglia for double labelled cells. Maxillary molar teeth project to the lateral ophthalmomaxillary region of the ipsilateral ganglion with extensive overlap of the projections from individual teeth. Double labelling with both dyes demonstrated considerable collateral branching from single trigeminal ganglion cells to the molar teeth.

Animals↗
PubMed1986

Peripheral axotomy of the rat mandibular trigeminal nerve leads to an increase in VIP and decrease of other primary afferent neuropeptides in the spinal trigeminal nucleus.

In the vasoactive intestinal polypeptide (VIP)-rich lumbosacral spinal cord, VIP increases at the expense of other neuropeptides after primary sensory nerve axotomy. This study was undertaken to ascertain whether similar changes occur in peripherally axotomised cranial sensory nerves. VIP immunoreactivity increased in the terminal region of the mandibular nerve in the trigeminal nucleus caudalis following unilateral section of the sensory root of the mandibular trigeminal nerve at the foramen orale. Other primary afferent neuropeptides (substance P, cholecystokinin and somatostatin) were depleted and fluoride-resistant acid phosphatase activity was abolished in the same circumscribed areas of the nucleus caudalis. The rise in VIP and depletion of other markers began 4 days postoperatively and was maximal by 10 days, these levels remaining unchanged up to 1 year postoperatively. VIP-immunoreactive cell bodies were absent from trigeminal ganglia from the unoperated side but small and medium cells stained intensely in the ganglia of the operated side after axotomy. These observations indicate that increase of VIP in sensory nerve terminals is a general phenomenon occurring in both cranial and spinal sensory terminal areas. The intense VIP immunoreactivity in axotomised trigeminal ganglia suggests that the increased levels of VIP in the nucleus caudalis are of peripheral origin, indicating a change in expression of neuropeptides within primary afferent neurons following peripheral axotomy.

Acid Phosphatase↗
PubMed1986

The origins of the sciatic nerve and changes in neuropeptides after axotomy: a double labelling study using retrograde transport of true blue and vasoactive intestinal polypeptide immunohistochemistry.

One month after sciatic nerve section, only dorsal root ganglion cells which take up True blue applied to the cut end of the nerve show vasoactive intestinal polypeptide immunoreactivity. This indicates that VIP expression is only in cells with damaged axons. Motor axons with True blue-positive perikarya in the ventral horn originate from the fourth to sixth lumbar segments whereas unmyelinated and small myelinated sensory nerves terminate in the third to fifth lumbar segments of the spinal cord.

Animals↗
PubMed1986

Vasoactive intestinal polypeptide (VIP) increases in the spinal cord after peripheral axotomy of the sciatic nerve originate from primary afferent neurons.

Following sciatic nerve axotomy, vasoactive intestinal polypeptide (VIP) immunoreactivity increases dramatically in the central terminal areas of the nerve whereas other primary afferent neuropeptides are depleted. The contribution of the peripheral nerve to VIP increases in the spinal cord was investigated by performing sciatic nerve section alone, dorsal rhizotomy of the lumbar roots, axotomy and rhizotomy in combination or section of other peripheral nerves terminating in the same segments as the sciatic nerve. VIP, and for comparison, substance P (SP), cholecystokinin (CCK), somatostatin (SOM), were localized in the lumbar spinal cord and corresponding sensory ganglia using unlabeled antibody immunohistochemistry. After sciatic nerve section, SP, CCK and SOM were depleted in the lumbar dorsal horn whereas VIP increased. After rhizotomy alone all neuropeptide staining including VIP was depleted; axotomy followed by rhizotomy produced the same result. Axotomy of other peripheral nerves terminating in the lumbar cord increased the area of neuropeptide depletion but correspondingly increased the area of VIP staining. A large proportion of small and medium diameter dorsal root ganglion cells were stained for VIP after nerve section or axotomy but not after rhizotomy alone. A radical change in neuropeptide metabolism of dorsal root ganglion cells occurs after peripheral axotomy, in the form of a marked increase in VIP synthesis. An intact dorsal root is necessary for increases in VIP in the spinal cord indicating the primary afferent origin of the response.

Animals↗
PubMed1986

Vasoactive intestinal polypeptide increases in areas of the dorsal horn of the spinal cord from which other neuropeptides are depleted following peripheral axotomy.

Peripheral nerve section or local capsaicin application produces depletion of substance P and an enzymatic marker, fluoride-resistant acid phosphatase (FRAP), from circumscribed regions of the terminal areas in the spinal cord. We have made use of this phenomenon to map the extent of central termination of subpopulations of primary afferent neurons containing substance P (SP), somatostatin (SOM), cholecystokinin (CCK), vasoactive intestinal polypeptide (VIP) and FRAP in the rat lumbar spinal cord following sciatic nerve section at midthigh level under ether anaesthesia. Between 2 days and 1 year postoperatively, the animals were perfused transcardially and SP, CCK, VIP and SOM were localised in frozen transverse sections of spinal cord segments L1 to S2 and their corresponding ganglia using unlabelled antibody immunohistochemistry. FRAP was localised using a modified Gomori method. SP, SOM, CCK and FRAP were maximally depleted from identical restricted areas of the dorsal horn of the third, fourth and fifth lumbar segments fifteen days after nerve section and remained so for a year. In contrast, VIP staining increased dramatically in the areas from which the other markers were depleted and showed the same time course. Moreover, a large number of neurons in the corresponding ganglia showed positive VIP immunoreactivity after axotomy but were absent from the unoperated side.

Acid Phosphatase↗
PubMed1979

Ultrastructural morphometry of blastogenesis I: transformation of small lymphocytes stimulated in vivo with dinitrochlorobenzene.

Changes in the volumes and surfaces of subcellular compartments of unstimulated small lymphocytes and immunoblasts in mouse axillary lymph nodes have been established using stereological techniques. Blast transformation was induced in vivo with dinitrochlorobenzene (DNCB). Cell samples were obtained by random sampling regimes applied at light and electron microscopic levels. From electron micrographs the volume densities of euchromatin, heterochromatin, nucleoli, mitochondria, Golgi apparatus and rough endoplasmic reticulum were determined. Cell surface/volume ratios were also computed. By estimating mean nuclear volumes using light microscopy, it was possible to calculate absolute compartmental volumes and to evaluate the plasma membrane surface areas of average cells. Transformation in this model was characterized by a considerable cellular hypertrophy and a substantial increase in plasmalemma surface. Hypertrophy was the consequence of increases in the volumes of all measured intracellular compartments, notably euchromatin and "residual cytoplasm" (including ground cytoplasm and free ribosomes). These changes are discussed in the context of the altered metabolic status of cells.

Animals↗
PubMed1979

Changes in the plasma membrane surface of lymphocytes stimulated in vivo with DNCB.

Stereological principles have been used to evaluate ultrastructural changes which accompany the transformation of lymphocytes stimulated in vivo with dinitrochlorobenzene (DNCB). Whereas unstimulated lymphocytes and blast cells have slightly more than the minimal containing plasmalemmal surface for their volume, stimulated (blast-derived) lymphocytes have an excess surface area in the order of 30%. This observation is discussed in the context of altered cell function and the biosynthesis of additional membrane components.

Animals↗
PubMed1979

On the problem of counting and sizing mitochondria: a general reappraisal based on ultrastructural studies of mammalian lymphocytes.

The authors ask the question whether the parameters "numbers" and "volume" are suitable for the morphometric analysis of mitochondria. In several types of cell, irregularity of mitochondrial shape makes it technically difficult, if not impossible, to obtain reliable stereological estimates of mean organelle volume or number per unit volume. Of more fundamental concern is whether number of mitochondria per cell is of any real value as a structural correlate of respiratory potential and hence as a measure of cell function. Alternative parameters might serve better for this purpose. Though the problem is illustrated by reference to quantitative studies of lymphocytes, it is also pertinent to the investigation of many other cell types.

Animals↗
PubMed1977

An autoradiographic study of experimental odontogenic cyst formation in the mouse.

Proliferative populations of cells within the epithelial lining of developing experimental odontogenic cysts were identified by labeling with 3H-thymidine. Mouse molar teeth extracted from 10-day-old mice were transplanted subcutaneously and host animals were injected with 3H-thymidine 1 h prior to sacrifice. The cysts which developed around the crown of the transplanted teeth were prepared for autoradiographical examination. Labeling indices were high initially but decreased rapidly as the cysts enlarged. The pattern of labeling, however, bore no resemblance to the labeling of the reduced enamel epithelium from which the cysts developed. It was concluded that labeling activity reflects only the state of development and activity of the cyst and not the origin of the cyst.

Animals↗
PubMed1976

A histological study of odontogenic cysts formed following mouse molar tooth transplantation.

The enamel organs of subcutaneously transplanted mouse molar teeth undergo cyst formation and present a model for the study of the pathogenesis of development odontogenic cysts. Maxillary molars extracted from 10-day-old C57B1 mice were grafted subcutaneously into adult mice of the same strain. The grafts were recovered between 2 and 50 days after operation and routinely prepared for histological examination. After initial degeneration, the enamel organ took the form of a squamous epithelium in which after 5 to 6 days squamous hyperplasia took place. Cystic degeneration within the epithelium produced cavities lined with a thick parakeratotic stratified squamous epithelium which resembled the lining of an epidermoid implantation cyst. As the cysts enlarged the lining changed in appearance to a thin squamous non-keratinized epithelium. Similar features have been described in other experimentally produced cysts and in some odontogenic cysts in humans. Their different morphology may arise frominteraction betwen the surrounding connective tissue with epithelium at different stages of development.

Animals↗
PubMed1976

An autoradiographical study of [3H]thymidine incorporation into subcutaneously transplanted mouse molar teeth. Cell proliferation and migration in transplanted teeth.

Mice bearing either allografts or isografts of 10 day old molar teeth were injected with [3H]thymidine to identify proliferating and migrating cells within the graft and surrounding tissues. In isografts proliferating cells were found successively in the area underlying the cervix, in the cervical pulp and the coronal pulp. However, cells did not migrate from the cervical host tissue into the pulp, and it was concluded that donor cells are responsible for reparative processes in tooth isografts. Very few labelled cells were identified at any time in tooth allografts, which were not repaired. It is suggested that allografts are not repaired because allogeneic inhibition prevents the residual donor tissue from proliferating and differentiating. Inhibition of proliferation of residual cells may also account for the absence of a cell-mediated immune response to tooth allografts.

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