China
Africa
Explore chapters and articles related to this topic
The Dorsal Vagal Complex Forms a Sensory-Motor Lattice: The Circuitry of Gastrointestinal Reflexes
Published in Sue Ritter, Robert C. Ritter, Charles D. Barnes, Neuroanatomy and Physiology of Abdominal Vagal Afferents, 2020
T.L. Powley, H.-R. Berthoud, E.A. Fox, W. Laughton
The hold of the rostral-to-caudal model on thinking in this area can be appreciated by a re-examination of an even more influential paper on dmnX viscerotopy. After reviewing the literature prior to 1955, Mitchell and Warwick50 approached the issue empirically by sectioning the trunks and branches of the vagus at different levels in rhesus monkeys and mapping patterns of chromatolysis in the dmnX. After sectioning the anterior abdominal vagus, the investigators obtained chromatolysis through the longitudinal extent of the dmnX, with a somewhat greater concentration of chromatolytic cells in the rostral pole. Furthermore, unaffected cells were found throughout the longitudinal extent of the dmnX (see their Figure 5). In fact, their results are consistent with the longitudinal columnar patterns of the preganglionics already described, and the points just raised regarding the Molhant, Malone and Vermeulen experiments are again relevant here. Nonetheless, the investigators (we assume at least in part because of the rostral-to-caudal presupposition) construed their results in terms of an inverted viscerotopy. “Incomplete” was adopted as a qualifier in explicit recognition of the fact that cells projecting into the abdomen were found throughout the axial dimension of the nucleus.
The nervous system and the eye
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
James A.R. Nicoll, William Stewart, Fiona Roberts
Central chromatolysis occurs between 5 and 8 days after transection, and is characterized by swelling of the cell body and displacement of the nucleus to the periphery of the cell. The cytoplasm becomes pale and homogeneous and there is dispersion of the Nissl substance – chromatolysis – accompanied by increased synthesis of RNA and protein. This reaction occurs in central and peripheral neurons, but particularly the latter. It may be followed by recovery with or without axonal regeneration, or may proceed to degeneration and ultimate death of the neuron. Effective regeneration is limited to the peripheral nervous system (PNS). In contrast, those neurons with projections lying entirely within the CNS tend to undergo retrograde degeneration and die. However, there is evidence of continuing neurogenesis from a population of stem cells residing in the subventricular zone of the basal ganglia and hippocampi.
Neuropharmacology Of Amphetamines And Related Stimulants
Published in John Caldwell, S. Joseph Mulé, Amphetamines and Related Stimulants: Chemical, Biological, Clinical, and Sociological Aspects, 2019
In spite of this lack of a robust apomorphine activation of end-stage behaviors, there is considerable evidence consistent with a dopamine receptor supersensitivity following chronic intoxication in cats and monkeys. As already stated, amphetamine enhances impulse-related release of dopamine, and it is not unreasonable to suggest that a local circuit overactivity can lead to a hypermetabolic exhaustion of certain catecholamine neurons, resulting in catecholamine depletion and/or chromatolysis. Neuronal chromatolysis, primarily in the catecholamine neuron areas, was demonstrated by Escalante and Ellinwood.94,95 Recently Seiden et al.96 demonstrated that there is a striking depletion of dopamine in the caudate nucleus (70% reduction) and a marked depletion of norepinephrine in the midbrain and frontal cortex 3 to 6 months after cessation of chronic methamphetamine. Thus, there is evidence for chronic depletion establishing the setting for postjunctional supersensitivity. Further support for dopamine receptor supersensitivity has been indicated in recent work by Creese et al.,97 showing increased dopamine receptor binding following 60HDA lesions of the nigrostriatal pathway. Segal et al.98 noted an increased response to direct intraventricular-infused norepinephrine in 60HDA-pretreated animals. Chronic treatment with 5 mg/kg amphetamine, however, did not increase haloperidol binding to postsynaptic receptors whereas chronic treatment with various neuroleptics did.99
The effect of pulsed radiofrequency application on nerve healing after sciatic nerve anastomosis in rats
Published in Ultrastructural Pathology, 2022
Uğur Ö. Bayır, Recep Aksu, Özlem Öz Gergin, Gozde Ozge Onder, Leman Sencar, Eray Günay, Arzu H. Yay, İbrahim Karaman, Cihangir Bicer, Sait Polat
Peripheral nerve damage is observed in approximately 2.8% of trauma patients.1 In the first few hours after the peripheral nerve damage, the cell cytoplasm and nucleus develop swelling and chromatolysis. Edema and swelling in the axonal root continue for a few days. Axonal and myelin disintegration, called Wallerian degeneration (WD), occurs in anterograde and retrograde directions within three days.1,2 Anterograde WD proceeds with Schwann cell and macrophage infiltration.1–3 Macrophage infiltration is increased by reactive Schwann cells.4 Only the baseline membrane remains within 3–6 weeks. Schwann cells proliferate to conjoin the baseline membranes of the two nerve endings. Nerve regeneration continues on the body (Bunger band) formed by Schwann cells.1–3 Schwann cells reaches multiplication three days after the lesion. Regenerative axons progress to the distal nerve concerning Schwann cells and baseline lamina in the endoneurial tube, forming the regenerative unit.3 The growth reaches up to 1–3 mm/day. This slow recovery rate of nerve tissue prolongs the time for the formation of neurotrophic factors in the distal segment of the nerve and thus prevents rapid regeneration.2
Effects of Theranekron and alpha-lipoic acid combined treatment on GAP-43 and Krox-20 gene expressions and inflammation markers in peripheral nerve injury
Published in Ultrastructural Pathology, 2021
Leman Sencar, Gülfidan Coşkun, Dilek Şaker, Tuğçe Sapmaz, Samet Kara, Alper Çelenk, Sema Polat, Derviş Mansuri Yılmaz, Y. Kenan Dağlıoğlu, Sait Polat
Following injury, serious histological changes are observed in the distal and proximal part of the peripheral nerve. It is known that during the first 6 hours, the nucleus migrates to the periphery and the Nissl bodies undergo chromatolysis in the neuron cell body. Distal occurs to the damaged area in the axonal cytoskeleton and myelin sheath, and Wallerian degeneration occurs as a result of fragmentation and degeneration.5,9 As a result, in the first 48–96 hours it was determined that the axon continuity disrupted and impulse transmission was impaired. The regeneration process begins after phagocytosis of myelin sheath and axon debris by Schwann cells and macrophages.4,7 As Schwann cells form the Büngner bands that guide the formed axon sprouts, the axon starts growing at a rate of 1–3 mm per day in the neurilemma tube.6 Furthermore, significant structural changes are also observed in the proximal segment of the nerve close to the damaged area.4
Systemic angiopathy and axonopathy in hereditary transthyretin amyloidosis with Ala97Gly (p. Ala117Gly) mutation: a post-mortem analysis
Published in Amyloid, 2018
Haruki Koike, Takeshi Yasuda, Ryoji Nishi, Shohei Ikeda, Yuichi Kawagashira, Masahiro Iijima, Gen Sobue, Masahisa Katsuno
In the spinal cord, parenchyma was intact in terms of amyloid deposition at any levels. Although amyloid deposition was found in the leptomeningeal small vessels, it was mild compared to other visceral organs. Central chromatolysis was observed in spinal motor neurons; however, the numbers of neurons in the anterior horns and Clarke’s columns were well preserved. In the ventral and dorsal spinal roots, amyloid deposition was not apparent and myelinated fibres were preserved. Massive amyloid deposits were seen around the dorsal root ganglia and thoracic sympathetic ganglia but minimal deposits in the parenchyma of these ganglia. The extent of neuronal loss was also minimal in these ganglia (Figure 1(F)). Myelinated fibres were depleted even in the proximal portions of the sciatic/tibial and median nerves (Figure 1(G)). Perineural amyloid deposition was prominent throughout the length of these nerves, whereas it was mild to moderate in the endoneurium (Figure 1(H)).