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Biomedical subjects

F J Seil

Publications and source records attributed to F J Seil.

At least 73 records · Page 4Linked to original sources
PubMed1982

Choline acetyltransferase activity in mouse cerebellar cultures.

The finding of the acetylcholine synthetic enzyme, choline acetyltransferase, has been reported in mouse cerebellar cultures, and it has been used as an index of neuronal survival and maturation. These results are curious in light of immunocytochemical studies which show that this enzyme is localized within mossy fiber terminals in glomerular structures of the cerebellar cortex. Since most mossy fibers are of extracerebellar origin, a significant population of mossy fiber terminals would not be expected to be present in cerebellar cultures. The origin of this acetylcholine synthetic activity has been examined in mouse cerebellar cultures. Two groups of explants, one with and the other without incorporated dorsal pontine tissue, were cultivated. Only cultures that included pons showed well developed glomerular structures with mossy fiber rosettes. Homogenates of the cultures were assayed for their ability to synthesize acetylcholine, and the synthesis was shown to be due to choline acetyltransferase by use of the specific inhibitor, (naphthylvinyl)pyridine. Cultures lacking dorsal pontine tissue had only low levels of enzyme activity, whereas those which included pons had 20-60 times greater synthetic activity. These results indicate that the choline acetyltransferase activity arises from pontine tissue in cerebellar cultures and are consistent with mossy fibers being the source of this enzyme.

Acetylcholine↗
PubMed1982

Phenytoin neurotoxicity in developing mouse cerebellum in tissue culture.

Phenytoin applied to developing neonatal mouse cerebellar cultures at concentrations of 9-46 micrograms/ml of nutrient medium from the day of explantation to 16 days in vitro induced cerebellar cortical degeneration. The degree of neurotoxicity correlated with drug concentration. Purkinje cells were the most susceptible of the cerebellar elements, and intracerebellar nucleus neurons were the most resistant. In contrast, mature mouse cerebellar explants were resistant to chronic exposure to high concentrations of phenytoin.

Animals↗
PubMed1982

An ultrastructural study of cortical remodeling in cytosine arabinoside induced granuloprival cerebellum in tissue culture.

Mouse-derived cerebellar explants were exposed for 5 days to cytosine arabinoside, an inhibitor of deoxyribonucleic acid synthesis. They were then maintained in normal nutrient medium until fixation for electron microscopy at 15-20 days in vitro. The cerebellar cortex lacked granule cells, but Purkinje cells, Golgi neurons and a few basket and stellate cells survived. Astrocytes and oligodendrocytes were diminished in number and myelination was absent. Purkinje cell recurrent axon collaterals increased in number and formed synapses with the surviving cortical neurons and their processes. The ultrastructural alterations that occurred in the cytosine arabinoside-treated cultures were consistent with an interpretation of cortical remodeling in which Purkinje cell axon collaterals were the dominant inhibitory elements.

Animals↗
PubMed1981

A comparison of demyelinating and myelination-inhibiting factor induction by whole peripheral nerve tissue and P2 protein.

Sera from rabbits sensitized with whole bovine spinal roots demyelinated and inhibited myelination in both peripheral and central nervous system tissue cultures. Antisera directed against the peripheral nerve myelin basic protein, P2, demonstrated no antimyelin activity in vitro. These results suggest that demyelinating and myelination-inhibiting factors are directed against some peripheral nerve component(s) other than the P2 protein.

Animals↗
PubMed1981

Immunization with purified myelin-associated glycoprotein does not evoke myelination-inhibiting or demyelinating antibodies.

Antisera produced in rabbits against purified myelin-associated glycoprotein did not inhibit myelin formation in cerebellar tissue cultures or demyelinate centrally or peripherally myelinated fibers in spinal cord-dorsal root ganglia cultures. These results suggest that antibodies directed against other myelin components are responsible for the myelination-inhibition and demyelination produced by anti-central nervous system (CNS) and anti-myelin antisera in vitro.

Animals↗
PubMed1980

Kainic acid neurotoxiocity in granuloprival cerebellar cultures.

Granuloprival cerebellar cultures devoid of cortical presynaptic glutamatergic fibers were exposed to nutrient medium incorporating either 10(-3) M D-glutamic acid or 10(-4) M kainic acid. No changes were evident in cultures exposed to the former, while cortical neurons were destroyed in kainate-treated explants. These results suggest that kainic acid neurotoxic effects can be manifested in the absence of glutamatergic afferent fibers.

Afferent Pathways↗
PubMed1980

Cytosine arabinoside effects on developing cerebellum in tissue culture.

Cerebellar explants derived from neonatal mice were exposed to cytosine arabinoside, an inhibitor of DNA synthesis. Following such exposure, the cortical regions of the explants contained numerous closely packed large neurons with few intervening elements and without lamination. The surviving large cortical neurons included Golgi cells and Purkinje cells, the latter with persistent dendritic spines in the absence of granule cells. A marked increase in density of subcortical and intracortical neurites was evident in fiber stains. The neurites were identified as Purkinje cell axons and axon collaterals by fiber tracing. Myelin failed to form around the axonal elements. Both regular and phasic spontaneous discharges were recorded electrophysiologically. Trains of cortical stimuli elicited both excitatory and inhibitory responses in the absence of parallel fibers. Antidromic stimulation of Purkinje cell axons evoked inhibition of spontaneous cortical discharges. By contrast, antidromic activation of Purkinje cell axons in control cultures had no effect on spontaneous cortical discharges, or provoked a transient increase in discharge rate. These responses were interpreted as consistent with a cortical remodeling in granuloprival cerebellar cultures in which basket-stellate cell inhibition of Purkinje cells was preempted by Purkinje cell recurrent axon collateral inhibition.

Animals↗
PubMed1979

Toxic effects of kainic acid on mouse cerebellum in tissue culture.

Cultures of mouse cerebellum were exposed for various intervals after explantation to kainic acid, a glutamic acid analog. Purkinje cells and intracerebellar nucleus neurons were destroyed and cortical laminar formation was inhibited by exposure to kainic acid, while granule cells were relatively spared. Prolonged kainate treatment also reduced the granule cell population. The destructive effects of kainic acid were evident upon exposure of Purkinje cells prior to the development of parallel fiber-Purkinje cell synapses, the neurotransmitter for which is believed to be glutamic acid. Glutamate application to intracerebellar nucleus neurons in vitro did not evoke extracellularly recorded excitatory effects, suggesting that these kainate-sensitive neurons do not have significant numbers of glutamate receptors. The combination of these observations suggests that neuronal toxic effects of kainic acid are not exclusively mediated by action on glutamate receptors, but involve other, less specific mechanisms as well.

Animals↗
PubMed1977

Synthetic galactocerebrosides evoke myelination-inhibiting antibodies.

Synthetic galactodihydrocerebrosides with widely different fatty acid components can evoke myelination-inhibiting antibodies in rabbits. Whether these are the only such haptens involved in experimental immunizations of other species or in spontaneous human diseases is not yet known.

Animals↗
PubMed1977

Tissue culture studies of demyelinating disease: a critical review.

Tissue culture studies of human and experimental demyelinating diseases have demonstrated that sera from patients with multiple sclerosis reversibly demyelinate central nervous system cultures. Similar changes are evoked by sera from animals with experimental allergic encephalomyelitis induced by inoculation with whole central nervous system tissue but not by encephalitogenic myelin basic protein. Sera and buffy coat or lymph node cells from humans with idiopathic polyneuritis and animals with experimental allergic neuritis demyelinate cultures of peripheral nervous system tissue. While these studies have contributed to speculations about pathogenetic mechanisms of demyelinating diseases, including the role of both circulating antibodies and delayed hypersensitivity factors, a number of important questions remain unanswered. Among these are the identity of the antigens that evoke antimyelin antibodies and the precise relationship of serum or cellular antimyelin factors to the pathogenesis or clinical course of the demyelinating diseases. Further studies with this technique may provide more complete information about the role of immunological events in induction of disease.

Animals↗