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PubMed1990

Neurophysiological concomitants of soman-induced respiratory depression in awake, behaving guinea pigs.

Soman-induced respiratory failure was investigated in awake, behaving guinea pigs chronically instrumented to allow concurrent recordings of medullary respiratory-related unit (RRU) activity, diaphragm electromyogram (DEMG), and electrocorticogram. Responses to soman typically began with hyperpnea. Loss of consciousness, as indicated by the development of seizure activities, took place shortly after the onset of hyperpnea. This was followed by dyspnea, hypopnea, and finally, respiratory failure. The most profound respiratory dysfunctions were seen during the development of dyspnea characterized by a progressively degenerative RRU-DEMG phase relationship (phase anomalies) and mixed patterns of ataxic breathing. Electrophysiographic records indicated that the anomalous RRU-DEMG phase phenomenon is attributable to a state of functional dissociation in some brainstem mechanisms that are normally involved in the orchestration of a synchronous respiratory drive. The failure of bulbar rhythmogenic mechanisms to maintain an orderly and synchronous recruitment of respiratory drive, which led to untimely and chaotic activations of respiratory muscles, was apparently the underlying cause of various ataxic breathing patterns and a reduced ventilatory efficiency. Spectral analyses of DEMG activities showed that, despite episodic muscle fasciculations and signs of fatigue, the functional integrity of the diaphragm was not significantly compromised by soman at a dose sufficient to produce respiratory failure. These findings not only support the notion of a relatively more important involvement of central respiratory mechanisms in soman-induced respiratory failure, but also identify a state of functional dissociation of central respiratory timing mechanisms as being a significant component in soman intoxication.

Animals↗
PubMed1992

Protection of rhesus monkeys against soman and prevention of performance decrement by pretreatment with acetylcholinesterase.

The ability of acetylcholinesterase from fetal bovine serum (FBS AChE) to protect against soman, a highly toxic organophosphorus (OP) compound, was tested in rhesus monkeys. Intravenous administration of FBS AChE produced a minimal behavioral effect on the serial probe recognition task, a sensitive test of cognitive function and short-term memory. Pharmacokinetic studies of injected FBS AChE indicated a plasma half-life of 40 hr for FBS AChE in monkeys. Both in vitro and in vivo titration of FBS AChE with soman produced a 1:1 stoichiometry between organophosphate-inhibited FBS AChE and the cumulative dose of the toxic stereoisomers of soman. Administration of FBS AChE protected monkeys against the lethal effects of up to 2.7 LD50 of soman and prevented any signs of organophosphate intoxication, e.g., excessive secretions, respiratory depression, muscle fasciculations, or convulsions. In addition, monkeys pretreated with FBS AChE were devoid of any behavioral incapacitation after soman challenge, as measured by the serial probe recognition task. Compared to the current multicomponent drug treatment against soman, which does not prevent the signs or the behavioral deficits resulting from OP intoxication, use of FBS AChE as a single pretreatment drug provides significantly effective protection against both the lethal and the behavioral effects of soman.

Acetylcholinesterase↗
PubMed1993

GABA-immunoreactive profiles provide synaptic input to the soma, axon hillock, and axon initial segment of ganglion cells in primate retina.

GABA-immunoreactive displaced amacrines were previously shown to make synapses onto neuronal profiles in the ganglion cell layer (GCL) of macaque monkey retina [Koontz, Hendrickson and Ryan (1989) Visual Neuroscience, 2, 19-25]. These postsynaptic elements have been investigated further using postembedding immunogold methods for electron microscopy. This paper provides ultrastructural evidence that GABA-immunoreactive profiles are presynaptic to the ganglion cell soma, axon hillock, and axon initial segment in the GCL and its border with the nerve fiber layer (NFL). Some axonal profiles have a dense undercoat and fasciculated microtubules, features that are characteristic of the axon initial segment in many neurons of both central and peripheral nervous systems. These features are confined to small- and medium-diameter (0.2-0.6 microns) axon profiles located near the GCL/NFL border and are not found on axonal profiles lying deep in the NFL, suggesting that the dense-coated region does not extend far along the axon and that the dense-coated region may be narrower than the distal part of the axon. The dense-coated region may correspond to the ganglion cell "narrow segment" recently described in a variety of species using light microscopic methods. The results presented here strengthen our previous hypothesis that GABA-immunoreactive neurons in the GCL provide direct synaptic input to ganglion cells near the site of action potential initiation.

Aged↗
PubMed1988

Antibodies against acetylcholinesterase and low levels of cholinesterases in a patient with an atypical neuromuscular disorder.

Antibodies against acetylcholinesterase were found in the serum of a patient presenting dyspnea, generalized muscle paresis, diminished tendon reflexes, and fasciculations. Electrodiagnostic studies showed a decremental response, an incomplete interference pattern, and reduced motor nerve conduction velocity. Edrophonium administration resulted in extreme cholinergic crisis. Biopsies displayed muscle atrophy and nervous tissue degeneration. Recurrent acute respiratory failure ended in death. The patient's serum pseudocholinesterase and red blood cells acetylcholinesterase levels were generally very low, with periodical fluctuations. Minute quantities of the patient's serum inhibited the activity of cholinesterases from normal human serum and from various fetal tissues. Enzyme inhibition was abolished following preadsorption of the serum immunoglobulins with goat antihuman Fab, and radioiodinated acetylcholinesterase from human erythrocytes was precipitated by the patient's serum, confirming that anticholinesterase antibodies were present. Acetylcholinesterase extracted from fetal striated muscle with detergent and salt was inhibited to a larger extent than the enzymes similarly prepared from other fetal tissues and more efficiently than buffer-soluble muscle enzyme. These findings suggest that the patient's serum contained antibodies which interacted preferentially with the membrane-associated forms of muscle acetylcholinesterase and indicate that autoantibodies against acetylcholinesterase could play a role in the pathogenesis of the disease.

Acetylcholinesterase↗
PubMed1996

Unilateral tongue atrophy due to an enlarged emissary vein in the hypoglossal canal.

A 16-year-old girl presented to our clinic with right-sided tongue atrophy and fasciculations of 1-year duration. Enlargement of the outer opening of the hypoglossal canal was reveal by conventional and computed tomography of the skull. Magnetic resonance imaging disclosed an enlarged venous system extending from the jugular vein to the internal jugular vein on the right, with low signal density suggestive of a flow void. A right-sided occipital craniotomy was performed. When the hypoglossal canal was opened, an enlarged emissary vein compressing the hypoglossal nerve was identified. This is the first reported case of unilateral tongue atrophy and an enlarged hypoglossal canal due to an enlarged emissary vein.

Adolescent↗
PubMed1987

Expression of fasciclin I and II glycoproteins on subsets of axon pathways during neuronal development in the grasshopper.

The "labeled pathways" hypothesis predicts that axon fascicles in the embryonic neuropil are differentially labeled by surface recognition molecules used for growth cone guidance. To identify candidates for such recognition molecules, we generated monoclonal antibodies (MAbs) that recognize surface antigens expressed on subsets of axon fascicles in the grasshopper embryo. The 3B11 and 8C6 MAbs immunoprecipitate 70- and 95-kd membrane glycoproteins called fasciclin I and II, respectively, which are expressed on different subsets of axon fascicles during development. These two glycoproteins are expressed regionally on particular portions of embryonic axons in correlation with their patterns of fasciculation, dynamically during the period of axon outgrowth in a manner consistent with a role in growth cone guidance, and at other times and places during embryogenesis, suggesting multiple developmental roles.

Animals↗
PubMed1989

Drosophila neuroglian: a member of the immunoglobulin superfamily with extensive homology to the vertebrate neural adhesion molecule L1.

Drosophila neuroglian is an integral membrane glycoprotein that is expressed on a variety of cell types in the Drosophila embryo, including expression on a large subset of glial and neuronal cell bodies in the central and peripheral nervous systems and on the fasciculating axons that extend along them. Neuroglian cDNA clones were isolated by expression cloning. cDNA sequence analysis reveals that neuroglian is a member of the immunoglobulin superfamily. The extracellular portion of the protein consists of six immunoglobulin C2-type domains followed by five fibronectin type III domains. Neuroglian is closely related to the immunoglobulin-like vertebrate neural adhesion molecules and, among them, shows most extensive homology to mouse L1. Its homology to L1 and its embryonic localization suggest that neuroglian may play a role in neural and glial cell adhesion in the developing Drosophila embryo. We report here on the identification of a lethal mutation in the neuroglian gene.

Amino Acid Sequence↗
PubMed1990

Genetic analysis of a Drosophila neural cell adhesion molecule: interaction of fasciclin I and Abelson tyrosine kinase mutations.

Drosophila fasciclin I is a homophilic cell adhesion molecule expressed in the developing embryo on the surface of a subset of fasciculating CNS axons, all PNS axons, and some nonneuronal cells. We have identified protein-null mutations in the fasciclin I (fas I) gene, and show that these mutants are viable and do not display gross defects in nervous system morphogenesis. The Drosophila Abelson (abl) proto-oncogene homolog encodes a cytoplasmic tyrosine kinase that is expressed during embryogenesis primarily in developing CNS axons; abl mutants show no gross defects in CNS morphogenesis. However, embryos doubly mutant for fas I and abl display major defects in CNS axon pathways, particularly in the commissural tracts where expression of these two proteins normally overlaps. The double mutant shows a clear defect in growth cone guidance; for example, the RP1 growth cone (normally fas I positive) does not follow its normal path across the commissure.

Alleles↗
PubMed1984

The neuronal adhesion protein D2 in differentiating aggregates of brain cells.

The D2-protein is a high molecular weight protein involved in interneuronal adhesion. The concentration of D2-protein was measured both in aggregates of fetal rat telencephalic cells cultured in a chemically defined medium and in developing forebrain. Both the concentration of the D2-protein and the degree of sialylation were changed in the cultures in parallel with the corresponding values obtained from postnatal forebrain. In the cultures the highest specific concentration of D2-protein was observed after 12 days in culture. This value was 2.7 times higher than the average value of adult rat forebrain. Antibodies to D2-protein have previously been shown to inhibit fasciculation of neuritic fibers extending from cultured explants of sympathetic ganglia. We investigated the effect of such antibodies on the differentiation of aggregating telencephalic cells. By adding surplus antibodies to the cultures from day 11 to day 16 we were able to decrease the specific concentration of D2-protein on the neurons by 53% measured at day 19. The decrease was not compensated fully even after further 10 days in the culture. Although the concentration of D2-protein was decreased during the period of synaptogenesis no change was found in the specific concentration of a marker of mature synapses, the D3-protein. Thus, in this culture system synaptogenesis could proceed to an unimpaired extent in the presence of a decreased concentration of a putatively involved adhesion molecule. However, the specific concentration of two markers of myelination, 2',3'-cyclic nucleotide 3'-phosphodiesterase and myelin basic protein, were both increased, suggesting an antibody-induced stimulation of myelination in the cultured aggregates.

Animals↗
PubMed1986

Retinotectal projection in reeler mutant mice: relationships among axon trajectories, arborization patterns and cytoarchitecture.

The distribution of axons in the midbrain and thalamus of homozygous reeler mutant mice is anomalous. The cytoarchitecture of these regions is normal. In the normal mouse SC there is a distinct SO in which fascicles of retinotectal axons pass caudally before terminating in the overlying SGS. In reeler, by contrast, fascicles of retinotectal axons are distributed through the entire thickness of SGS as well as through SO. There are also abnormalities of fiber pattern in the thalamus, most notably in the region of the dorsal nucleus of the LGd. Retinotectal axon trajectory and patterns of terminal arborization in reeler and normal animals were compared by single-fiber HRP axonography. In normal mice, two distinct morphological classes of retinotectal axons form focal terminal arborizations at different radial levels in the superficial layers of the SC. Class U axons are of relatively small diameter and terminate in upper portions of SGS. Class L1 axons are of larger diameter and form terminal arbors which are confined to SO and deeper regions of SGS. Axons of both classes ascend to their terminal zones from parent axons which course through SO. Similarly, in reeler mice axons of both large and small diameter can be distinguished. However, many axons of both classes pass caudally in anomalous fascicles distributed through the full thickness of SGS and descend to terminate. Other axons pass in normal fashion in SO and ascend to terminate in SGS. Regardless of their trajectories, the small axons terminate superficially in SGS while the thick axons terminate deeper in SGS and/or SO, as in normal mice. These findings suggest that the ingrowth of afferents and the formation of terminal arbors are regulated by different mechanisms and that fiber architecture and cytoarchitecture are regulated by different mechanisms. It is not known if the anomalous fiber pattern in reeler adults arises in development through a defect in initial patterns of axon fasciculation or from a failure of axon elimination.

Animals↗
PubMed1986

Influence of thyroid hormones on rat cerebellar cell aggregation and survival in culture.

In order to study the effect of thyroid hormones on rat cerebellar granule cells, cerebellar perikarya isolated from 5-7-day-old rats were cultured in the presence of normal fetal calf serum, fetal calf serum treated with Dowex-2 ion exchange resin to remove thyroid hormones, or ion exchange-treated serum resupplemented with physiological concentrations of T4 and T3. Granule cells grown under hypothyroid conditions showed abnormal cellular aggregation, neurite fasciculation and cell survival. Cell aggregation, which may be an in vitro correlate of cerebellar granule cell migration to the internal granule layer, was reduced by over 50% under hypothyroid conditions. The rate of protein synthesis in hypothyroid cultures was stimulated by as much as 3-fold compared to thyroid hormone-containing cultures consistent with a proposal that the normal developmental pattern of diminishing protein synthesis specific activity is delayed or prevented under hypothyroid conditions. In addition ultrastructural studies revealed abnormalities in the density of cold-stable microtubules in thyroid hormone-deficient cultures. These results demonstrate that thyroid hormones can influence granule neuron behavior in the absence of Purkinje cells. Furthermore, the observed defects bear numerous similarities to documented abnormalities within the hypothyroid cerebellum, suggesting that this in vitro culture system may serve as a useful model for studying the mechanism of action of thyroid hormones on the cells of the cerebellum.

Animals↗
PubMed1988

Immunohistological localization of cell adhesion molecules L1, J1, N-CAM and their common carbohydrate L2 in the embryonic cortex of normal and reeler mice.

The expression of the cell adhesion molecules L1, J1 and N-CAM and their shared carbohydrate L2 was studied in the embryonic cerebral cortex of normal and reeler mutant mice using light and electron microscopic immunocytochemistry. Apart from a general delay in their appearance in the reeler cortex, the 4 antigens were present with a cellular distribution in both genotypes reflecting the anatomical characteristics of normal and mutant phenotypes. The cell surface glycoprotein L1 was exclusively expressed by neurons, particularly axons, but was never detected at sites of neuron-glia contact. L1 was accumulated in the marginal zone and subplate of the normal cortex and in the homologous layers of the reeler cortex. The secreted glycoprotein J1 was found on glia and neurons. Although initially present in regions of fiber outgrowth, J1 became characteristically excluded from the large fiber tracts at later stages. J1 mapped in the marginal zone and subcortical plate of the normal cortex and in the corresponding layers of the mutant cortex. N-CAM had a more ubiquitous distribution and was present in ventricular zones, particularly at early stages, as well as on glia and neurons and large fiber tracts at later developmental stages. The distribution of the L2 epitope was quite similar to that of the J1 molecule but remained present on large fiber tracts, like N-CAM and L1, also at later developmental stages. These comparative observations in normal and reeler mutant mice lend support to previous suggestions that L1, together with N-CAM, may play a role in the aggregation of neuronal cell bodies after migration and in the fasciculation of developing fiber bundles. They also point to a possible function of the extracellular matrix component J1 in the guidance or support of fiber outgrowth in large fiber tracts.

Animals↗
PubMed1989

HNK-1 marks earliest axonal outgrowth in Xenopus.

In wholemounts of the very early developing nervous system of Xenopus, HNK-1 specifically labeled cell bodies, axons, and growth cones of identifiable CNS neurons during the period of axonal outgrowth. The unique overview provided by these preparations showed that individual growth cones navigate their routes independently rather than by fasciculation and, further, revealed features of the directional and positional choices made by axons of several different but simultaneously developing pathways.

Animals↗
PubMed1990

Aberrant axon growth of the chick embryo retina during normal development.

Axon growth behavior in the optic nerve was examined using a carbocyanine dye, DiI, as a tracer, DiI facilitated clear visualization of the whole growth pattern of the optic nerve, i.e. the initial association of axons, fasciculated growth within the optic fiber layer and flattened growth cones in both living and fixed chick embryo retinae. Retrograde labelling with DiI in fixed retinae revealed that a considerable number of ganglion cells were apparently misdirected, extending their axons toward the periphery of the retina during normal development. The maximum proportion of aberrant ganglion cells reached about 15% of the total upon staining with a single DiI crystal. Misdirection was predominantly observed in retinae prepared from 6- to 8-day-old chick embryos. In embryos more than 9 days old, however, distinction of aberrant ganglion cells from normal ones became difficult, so that any degeneration of misdirected ganglion cells could not be clarified. Almost all of the misdirected ganglion cells were oriented centrifugally to the retinal periphery. These results indicate that misdirection occurs spontaneously during normal development even within the retina.

Animals↗
PubMed1990

Evidence for plasticity in neurotransmitter expression in neuronal cultures derived from 3-day-old chick embryo.

We have previously reported the developmental profiles of glutamate decarboxylase (GAD) and choline acetyltransferase (ChAT) bio- and immunocytochemically, assessing GABAergic and cholinergic neuronal phenotypes respectively, in neuroblast-enriched cultures from 3-day-old chick embryo, plated on poly-L-lysine. We have also reported that collagen as culture substrate inhibits neuronal aggregation and neuritic fasciculation in this culture system. In this study we assessed the same parameters for cultures on collagen. In addition, we evaluated the effects of nerve growth factors (NGF) on cholinergic and GABAergic expression on neurons plated either on polylysine or collagen. We found that non-neuronal cells and NGF prolonged the survival of cholinergic and GABAergic neuronal populations and that both markedly stimulated GABAergic expression. In contrast, cholinergic expression was only enhanced by NGF. Immunostaining for GABA and ChAT reflected the biochemical findings. Glutamine synthetase and cyclic nucleotide phosphohydrolase, used as markers for astrocytes and oligodendrocytes respectively, showed very low activity in both substrata and were not related to GAD or ChAT peak activities. Our findings suggest that humoral factors and cell-cell contacts markedly influence neuronal phenotypic expression in culture. Moreover, it appears that during early neuronal differentiation GABAergic neurons are more responsive to microenvironmental regulation compared to cholinergic neurons.

Animals↗
PubMed1994

Developmental expression of N-CAM epitopes in the rat spinal cord during corticospinal tract axon outgrowth and target innervation.

The neural cell adhesion molecule (N-CAM) is an integral membrane glycoprotein which mediates the adhesion of neurons to neurons and to other types of cells. During development, the N-CAM molecule is converted from a microheterogenous, highly sialylated, embryonic form (200-230 kDa) to several distinct, less sialylated but more adhesive, adult forms (120, 140 and 180 kDa). Monoclonal antibodies to epitopes of N-CAM (designated 5A5, 12F8, 5B8, 12F11 and 14E6) were used to investigate the spatial and temporal distribution of these neural cell adhesion molecules during the development of the corticospinal tract (CST) in rat spinal cord, from postnatal day 1 (P1) until adulthood. The light microscopical observations indicate that the embryonic form of N-CAM (200-230 kDa) recognized by 5A5 and 12F8 antibodies, respectively, is probably involved in the process of initial ingrowth of pioneer CST-fibers into the ventralmost part of the dorsal funiculus. The adult forms of N-CAM (120, 140, 180 kDa) recognized by 5B8, 12F11, and 14E6 antibodies, respectively, are present during later stages of CST white matter ingrowth and probably involved in fasciculation of the later arriving CST axons. During the period of CST target innervation (P4-P21), a gradual shift from embryonic (200-230 kDa) to adult (120, 140 and 180 kDa) forms of N-CAM occurs in spinal white matter and in the spinal gray matter adjacent to the ventral most part of the dorsal funiculus. The presence of embryonic N-CAM (200 kDa), with its low adhesive capacity in the CST outgrowth area may allow the CST axons to branch. If this branching is no longer desirable, only the higher affinity forms of N-CAM (120, 140 and 180 kDa) are expressed. The absence of N-CAM on CST target interneurons in the base of the dorsal horn and intermediate spinal gray matter strongly suggest that N-CAM is not involved in CST synapse formation. Together, these results suggest that various forms of N-CAM are involved in CST spinal white matter tract formation and subsequent target innervation, but not in the process of synapse formation.

Aging↗
PubMed1996

Embryonic form of N-CAM and development of the rat corticospinal tract; immuno-electron microscopical localization during spinal white matter ingrowth.

The neural cell adhesion molecule N-CAM has been proposed to function in the guidance of outgrowing axons in the peripheral and central nervous system. Light microscopic observations have shown that the embryonic form of N-CAM (200-230 kDa) is present in the ventralmost part of the dorsal funiculus during corticospinal tract (CST) ingrowth in the first postnatal week (Joosten, Dev. Brain Res., 78 (1994) 226-236). Here, the subcellular localization of the embryonic form of N-CAM (E-NCAM) is determined by pre-embedding staining on vibratome sections and by postembedding immunogold-labelling on Epon embedded spinal cord sections. The electron microscopical observations indicate that E-NCAM is present on the outer membrane of CST growth cones as well as other unmyelinated axons which are present in the ventralmost part of the dorsal funiculus. Furthermore, E-NCAM is localized in an irregular patchy way on the outer side of the axonal membrane of small unmyelinated, later arriving CST axons. From these results it may be deduced that E-NCAM is involved in CST tract formation through guidance of outgrowing pioneer CST growth cones along other unmyelinated axons and through mediation of axon fasciculation of later arriving CST axons.

Age Factors↗