Retrograde Degeneration; Axon Reaction; Nissl Degeneration; Retrograde Degeneration, Transneuronal. On-line free medical diagnosis assistant. Ranked list of possible diseases from either several symptoms or a full patient history. A similarity measure between symptoms and diseases is provided.

We examined the retinae of two monkeys whose left striate cortex had been removed eight years previously and compared the transneuronally degenerated hemiretina of each eye with the normal hemiretina, and with the retinae of normal monkeys. All retinae were prepared as whole mounts. One from each

TY - JOUR. T1 - Peripheral nerve grafts exert trophic and tropic effects on anterior thalamic neurons. AU - Clatterbuck, Richard E.. AU - Price, Donald L.. AU - Koliatsos, Vassilis E.. PY - 1998/7. Y1 - 1998/7. N2 - Peripheral nerve grafting into the central nervous system (CNS) has been used to study the regenerative capabilities of central neurons given access to a peripheral nervous system (PNS) environment. It is well documented that many CNS neurons regenerate axons along peripheral nerve grafts placed in close proximity to their cell bodies and that these grafts can ameliorate axotomy-induced retrograde degeneration. In the present study, we placed peripheral nerve grafts in proximity to axotomized neurons of the anterior thalamus. Standard histological and retrograde tracing techniques were used to examine these preparations 2 months after grafting. Three effects of these grafts were observed: amelioration of retrograde degeneration of axotomized anterior thalamic neurons, hypertrophy of ...

Results (1) There is a negative correlation between the RNFL thickness and time since onset of injury (n=26; R2=0.2; p=0.03). This equates to a reduction in RNFL thickness of 0.42 μm/year (cf 0.2 μm/year in normal ageing). (2) In 3/7 patients with hemianopia the RNFL thickness began to decrease within 3 months of the acute event and there is a trend to decline further over a year. In patients with homonymous quadrantanopia or scotoma no change in the RNFL thickness has been detected. We have shown previously that retrograde trans-synaptic degeneration can be detected using OCT1. The time course of this can be followed and may be useful as a model of trans-synaptic retrograde degeneration in the human brain. ...

The occurrence of collateral and ultraterminal sprouting by skeletomotor and fusimotor axons is described in teased, silver preparations of normal and de-afferentated hindlimb skeletal muscles. In twelve cat and ten rabbit muscle spindles the proportions of plate-ending fusimotor axons showing sprouting were 30.4 and 34.0 % , respectively. If small end-plates, previously described in the literature as accessory endings, are regarded as young plates newly formed by collateral sprouts, the degree of sprouting in the two spindle samples is increased to 33.9 and 38.3 % , respectively. Sprouting by skeletomotor axons was observed in a variety of cat, rabbit, and rat muscles taken from normal muscles. In a sample of 567 terminal branches examined in muscles from the three animals, 8.1% bore sprouts, or 19.4% if the collaterals forming accessory endings are included as sprouts. Some evidence of retrograde degeneration among the terminal branches of skeletomotor axons innervating normal muscle is ...

To the Editor:. We read with interest the recent article by Zhang et al.1 The authors described secondary degeneration in remote regions after experimental cerebral ischemia, which could provide a target for stroke management. We completely agree that this is an appealing approach. However, the underlying pathology may be different in ischemic rodents and patients with stroke.. Remote areas such as the thalamus connected to the cortical infarct are affected because of delayed retrograde degeneration of afferent connections. This is associated with extensive and complex pathology including inflammatory reactions, β-amyloid (Aβ) accumulation, calcification, and angiogenesis in rats subjected to middle cerebral artery occlusion.2 The Aβ deposition is particularly robust after an ischemic insult, which starts as a diffuse aggregation and over time transforms into dense plaque-like deposits together with calcium in the ventroposterior medial and ventroposterior lateral nuclei.3,4 Altered ...

To form axon fascicles, the research teams manufactured a microdevice in which human neurons derived from induced pluripotent stem cells were injected. What allowed for the formation of the fascicles was the preparation of neural spheroids and a channel narrow enough to align axons, which let them bind to each other.. Spheroids were placed inside the chamber of the device. Axons grew from these spheroids, with some entering the microchannel. Upon this entry, other axons would spontaneously follow, leading to the formation of fascicles that showed properties consistent with those seen in brains. What molecular signaling caused the spontaneous entry remains unexplained, but fascicles were detected in more than 90% of experiments, convincing the researchers the value of the microdevice design.. The device gives us a means to investigate which factors are responsible for the fascicle assembly, says Ikeuchi.. ...

However, one of the most novel findings in the present study is that the apoptotic death of RGC soma in glaucoma 2-4 was robustly prevented in cytNmnat1-Tg mice. This counters the consistent documentation in PNS injury models that Wlds does not protect neuronal cell bodies, 36-38 as well as the conclusions from several studies of CNS injury, including some in retina. In particular, RGC soma were not protected from glaucomatous dropout in the Wlds transgenic rat 39 nor were soma from Wlds mice subjected to optic nerve crush. 35 In contrast, in one of the earliest studies of Wlds retinal phenotypes, retrograde degeneration of Nissl-stained RGC soma was delayed in parallel with that noted for RGC axons following optic nerve transection. 34 And in the double-mutant Wlds.DBA/2J mice carrying the Wlds allele, while soma loss was not prevented in glaucomatous mice exhibiting severe axonal degeneration, the extent to which Nissl-stained RGC soma survived paralleled the extent of axonal sparing. 9 In ...

Laser irradiation on only the right side in bilaterally inflicted cutaneous wounds enhanced recovery in both sides compared to the nonirradiated control group. The bilateral retrograde degeneration of the motor neurons of the spinal cord expected after the bilateral crush injury of the peripheral nerves was greatly reduced in the laser treated group.

Introduction: Retina Imaging Past and Present.- OCT Technique Past, Present and Future.- Optical Coherence Tomography and Optic Nerve Edema.-OCT and Compressive Optic Neuropathy.- Optical Coherence Tomography (OCT) and Multiple Sclerosis (MS).- OCT and Parkinson s Disease.- Optical Coherence Tomography in Alzheimer s Disease.- Friedreich s Ataxia and More: Optical Coherence Tomography Findings in Rare Neurological Syndromes.- Other Neurological Disorders: Migraine, Neurosarcoidosis, Schizophrenia, Obstructive Sleep Apnea-Hypopnea Syndrome (OSAHS).- Hereditary Optic Neuropathies.- Trans Neuronal Retrograde Degeneration to OCT in Central Nervous System Diseases.- OCT in Toxic and Nutritional Optic Neuropathies.- Animal Models in Neuro Ophthalmology.- Optical Coherence Tomography (OCT) in Glaucoma.- OCT in Amblyopia.- Conclusion: The Exciting Future of OCT Imaging of ...

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TY - JOUR. T1 - Ventral root avulsion. T2 - An experimental model of death of adult motor neurons. AU - Koliatsos, Vassilis E.. AU - Price, William L.. AU - Pardo, Carlos A.. AU - Price, Donald L.. PY - 1994/4/1. Y1 - 1994/4/1. N2 - The present study proposes a reproducible model of experimental degeneration of adult motor neurons in the rat. Avulsion of ventral roots in the adult lumbar cord transects motor axons at the root exit and leads to retrograde cell death of 80% of motor neurons 2 weeks later; this result follows a series of retrograde changes, including chromatolysis, loss of transmitter phenotype, and accumulation of phosphorylated neurofilaments in perikarya. Glial cells recruited at the site of retrograde injury express both microglia‐specific epitopes (as exemplified by OX‐42 immunoreactivity) and macrophage‐specific markers (e.g., ED‐1 immunoreactivity). Macrophage‐specific markers become particularly intense 7 days postaxotomy and provide additional evidence of active ...

Capitalizing on a binary genetic strategy we provide a detailed protocol for neural circuit tracing in mice that express complementary...

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SARM has been reported to associate with mitochondria (Kim et al., 2007; Panneerselvam et al., 2012, 2013); accordingly, we found that GFP-tagged human SARM and endogenous murine SARM associate with neuronal mitochondria. Proteinase K treatment of neuronal mitochondrial fractions reveals that SARM mostly resides on the cytosolic surface of the mitochondria. While the genetic disruption of a previously reported SARM mitochondrial targeting sequence disrupts SARM mitochondrial localization in DRG axons, it does not affect the ability of SARM to promote axon degeneration. These findings suggest that the axonal degradation functions of SARM likely take place within the cytosol and that its association with mitochondria is not essential for this activity.. We have shown that the SAM and TIR domains of SARM are essential for its role in promoting elimination of injured axons. SARM mutants with disrupting mutations in either of these domains fail to restore injury-induced axon degeneration in ...

Viruses have been used as transsynaptic tracers, allowing one to map the inputs and outputs of neuronal populations, due to their ability to replicate in neurons and transmit in vivo only across synaptically connected cells

Traumatic brain injury (TBI) is a leading cause of disability worldwide. Annually, 150 to 200/1,000,000 people become disabled as a result of brain trauma. Axonal degeneration is a critical, early event following TBI of all severities but whether axon degeneration is a driver of TBI remains unclear. Molecular pathways underlying the pathology of TBI have not been defined and there is no efficacious treatment for TBI. Despite this significant societal impact, surprisingly little is known about the molecular mechanisms that actively drive axon degeneration in any context and particularly following TBI. Although severe brain injury may cause immediate disruption of axons (primary axotomy), it is now recognized that the most frequent form of traumatic axonal injury (TAI) is mediated by a cascade of events that ultimately result in secondary axonal disconnection (secondary axotomy) within hours to days. Proposed mechanisms include immediate post-traumatic cytoskeletal destabilization as a direct result of

www.MOLUNA.de Synaptic Plasticity and Transsynaptic Signaling [4174086] - Brain functions are realized by the activity of neuronal networks composed of a huge number of neurons. The efficiency of information transfer within the networks is changeable. Even the networks themselves can change through experience. Information transfer between neurons is performed at the synapse (the site of the neurons contact)