Search results for "Axons"
showing 10 items of 101 documents
Multiple sclerosis – candidate mechanisms underlying CNS atrophy
2009
Recently it has become clear that the neuronal compartment plays a more important role than previously thought in the pathology of multiple sclerosis. Apart from demyelination, neuronal pathology is apparently largely responsible for the brain atrophy that can be observed early on and throughout the course of the disease. The loss of axons and their neurons in the course of chronic neuroinflammation is a major factor determining long-term disability in patients. The actual steps leading from immune attack against the myelin sheath to neuronal damage are not yet fully clear. Here we review key findings about direct axonal damage processes, demyelination-related neuronal pathology and cell-bo…
Oligodendrocyte ablation triggers central pain independently of innate or adaptive immune responses in mice.
2014
Mechanisms underlying central neuropathic pain are poorly understood. Although glial dysfunction has been functionally linked with neuropathic pain, very little is known about modulation of pain by oligodendrocytes. Here we report that genetic ablation of oligodendrocytes rapidly triggers a pattern of sensory changes that closely resemble central neuropathic pain, which are manifest before overt demyelination. Primary oligodendrocyte loss is not associated with autoreactive T- and B-cell infiltration in the spinal cord and neither activation of microglia nor reactive astrogliosis contribute functionally to central pain evoked by ablation of oligodendrocytes. Instead, light and electron micr…
Synaptic connectivity of serotonergic axons in the olfactory glomeruli of the rat olfactory bulb.
2010
Although the major mode of transmission for serotonin in the brain is volume transmission, previous anatomical studies have demonstrated that serotonergic axons do form synaptic contacts. The olfactory glomeruli of the olfactory bulb of mammals receive a strong serotonergic innervation from the dorsal and medial raphe nuclei. In the present report, we investigate the synaptic connectivity of these serotonergic axons in the glomerular neuropil of the rat olfactory bulb. Our study shows that serotonergic axons form asymmetrical synaptic contacts on dendrites within the glomerular neuropil. Analyzing the neurochemical nature of the synaptic targets, we have found that 55% of the synapses were …
Bilateral olfactory deprivation reveals a selective noradrenergic regulatory input to the olfactory bulb.
2001
Unilateral olfactory deprivation in the rat induces changes in the catecholaminergic system of the olfactory bulb. Nevertheless, evidence suggests that unilateral deprivation does not fully prevent stimulation of the deprived bulb. The present report analyses the response of the catecholaminergic system of the olfactory bulb in fully deprived rats obtained by bilateral naris occlusion. The complete deprivation produces more rapid and dramatic changes in both the intrinsic and extrinsic catecholaminergic systems of the olfactory bulb. Intrinsic responses involve a rapid decrease in dopamine-containing cells to about 25% of controls, correlated with a decreased Fos expression in juxtaglomerul…
Modelling the spatial and temporal constrains of the GABAergic influence on neuronal excitability
2021
GABA (γ-amino butyric acid) is an inhibitory neurotransmitter in the adult brain that can mediate depolarizing responses during development or after neuropathological insults. Under which conditions GABAergic membrane depolarizations are sufficient to impose excitatory effects is hard to predict, as shunting inhibition and GABAergic effects on spatiotemporal filtering of excitatory inputs must be considered. To evaluate at which reversal potential a net excitatory effect was imposed by GABA (EGABAThr), we performed a detailed in-silico study using simple neuronal topologies and distinct spatiotemporal relations between GABAergic and glutamatergic inputs. These simulations revealed for GABAe…
Late-Onset Globoid Cell Leukodystrophy: Unusual Ultrastructural Pathology and Subtotal β-Galactocerebrosidase Deficiency
1990
An 11-year-old girl was found to have severely reduced β-galactocerebrosidase activity as evidence of late-onset globoid cell leukodystrophy, while her mother had almost normal enzyme activity in circulating white blood cells. Clinically, the patient showed a remitting course marked by seizures, ataxia, white-matter disease on computed tomographic scan, and reduced conduction velocities of peripheral nerves. Symptoms improved somewhat around the age of 10 years. Two sural nerve biopsies, performed 6 years apart, disclosed a demyelinating neuropathy. By electron microscopy, membrane-bound vacuolar lysosomes in Schwann cells of myelinated axons, unlike the typical needlelike inclusions seen …
Neurochemical and morphological studies on demyelination in multiple sclerosis with special reference to etiological aspects.
1972
Light microscopic studies were used as control for neurochemical studies and these showed that some micro plaques could be found also in areas which were normal on visual inspection. Also foreign cell infiltrates were found outside any clear plaque material. The number of these cells did not correlate with other findings like lipid or enzyme chemistry. In electronmicroscopic studies astrocytes demonstrated most lysosomes and phagocytosis of myelin. This increased lysosomal reaction was demonstrated also in biochemical analyses performed on MS biopsy specimens. Occasional nuclear changes like inclusion bodies and protrusion of inner nuclear membrane were observed suggesting some exogenous, p…
Abnormal accumulation of autophagic vesicles correlates with axonal and synaptic pathology in young Alzheimer's mice hippocampus
2012
Dystrophic neurites associated with amyloid plaques precede neuronal death and manifest early in Alzheimer's disease (AD). In this work we have characterized the plaque-associated neuritic pathology in the hippocampus of young (4- to 6-month-old) PS1(M146L)/APP(751SL) mice model, as the initial degenerative process underlying functional disturbance prior to neuronal loss. Neuritic plaques accounted for almost all fibrillar deposits and an axonal origin of the dystrophies was demonstrated. The early induction of autophagy pathology was evidenced by increased protein levels of the autophagosome marker LC3 that was localized in the axonal dystrophies, and by electron microscopic identification…
Neuropathologic and morphometric studies in hereditary motor and sensory neuropathy type II with neurofilament accumulation.
1986
Histological, electron microscopic and morphometric data on sural nerve, muscle, and skin biopsies of three patients affected by autosomal dominant hereditary motor and sensory neuropathy type II with neurofilament accumulation, whose neurological, cardiological and electrophysiological data have been provided in a previous paper disclosed focally enlarged myelinated axons, due to aggregation of neurofilaments in sural nerves of all 3 biopsied patients, as well as densely packed clusters of filaments in occasional non-myelinated axons without axonal enlargement, in several fibroblasts and endothelial cells in muscle and particularly in skin. This accumulation of filaments was less pronounce…
AN ULTRASTRUCTURAL STUDY OF THE RETINA IN HUMAN LATE INFANTILE NEUROAXONAL DYSTROPHY
1993
A case involving a girl who died at 11 years of age and who had developed normally until the age of 18 months, at which time further psychomotor maturation stopped and then regressed, is reported. The patient appeared hypotonic and showed loss of deep tendon reflexes, as well as bulbar signs and increasing immobility. Visual impairment resulted in blindness at the age of 7 years. Her disease was diagnosed as late infantile neuroaxonal dystrophy (LINAD) after examination of sural nerve biopsy samples and after autopsy. Under electron microscopy, retinal axons were filled with tubulocisternal profiles and occasional large lamellar clefts close to or distant from synaptic complexes. These lesi…