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Neuronal Function
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Neurons are diverse in shape and size. A typical neuron has a cell body (or soma) with fibre-like processes called dendrites and axons emerging from it. The dendrites are branches that leave the cell body and receive information from adjoining neurons. The dendrites have knob-like extensions called dendritic spines. The cell body has an extensive system of rough endoplasmic reticulum containing basophilic granules (Nissl substance), which synthesize proteins. The dendritic spines, dendrites and soma receive information from other cells.
Toxoplasma gondii
Published in Peter D. Walzer, Robert M. Genta, Parasitic Infections in the Compromised Host, 2020
Necrotizing lesions are not dependent on the host's inflammatory response. Severe necrotizing processes may occur with minimal or no inflammation, suggesting that unimpeded proliferation or Toxoplasma causes lysis and destruction of infected cells. In addition to the ability of the organism to infect any cell in the central nervous system (including neurons, glial cells, vascular endothelial cells, pericytes, and astrocytes), nonspecific changes such as vacuolization within neurons and Purkinje cells and loss of Nissl substance may occur (307,318-321).
Cellular Responses to Ischaemic CNS Injury
Published in Martin Berry, Ann Logan, CNS Injuries: Cellular Responses and Pharmacological Strategies, 2019
The description of neurons given above and the comparison with the “dark” cell response discussed previously has been established in the literature for some years.77 However, detailed comparison of the ultrastructure of “dark” neurons and those that have been exposed to high levels of glutamate result in questioning of a direct correlation between the two. For example, ischaemic neurons demonstrate mitochondrial swelling and loss of Nissl substance. Neurons exposed to toxic levels of glutamate do not demonstrate mitochondrial swelling and Nissl substance is still recognisable. Neither is there loss of polysomes (Figure 2.7B). There are also major differences in the fine structure of the chromatin within the nuclei of cells in these two groups (Figure 2.7A).
MiR-125b blocks Bax/Cytochrome C/Caspase-3 apoptotic signaling pathway in rat models of cerebral ischemia-reperfusion injury by targeting p53
Published in Neurological Research, 2018
Yun-Liang Xie, Bo Zhang, Ling Jing
As is shown in Figure 4, compared with Control group and Sham group, which showed no cerebral cortex edema with normal neurons and visible Nissl bodies, there was edema of cerebral cortex neurons, large neuronal necrosis, and irregularly arranged Nissl substance in CIR group. For the CIR + miR-125b group and CIR + PFT-α group, there was partial edema of cerebral cortex neurons, few neuronal necrosis, and increased visible Nissl substance. The statistical analysis results showed that in comparison with CIR + miR-125b group and CIR + PFT-α group, the number of surviving neurons, Nissl-positive cells, and NeuN-positive neurons were significantly increased in Control group and Sham group (all P < 0.05), but CIR group, CIR + miR-NC group and CIR + anti-miR-125b + PFT-α group showed a decrease trend (all P < 0.05).
Brain targeted delivery of mucoadhesive thermosensitive nasal gel of selegiline hydrochloride for treatment of Parkinson's disease
Published in Journal of Drug Targeting, 2018
Vinay Sridhar, Sarika Wairkar, Ram Gaud, Amrita Bajaj, Pramod Meshram
Vacuolation is a cellular response triggered in order to immobilise pathological prion proteins, like α-synuclein associated commonly with PD, having the ability to form channels that compromise cellular membranes [57,58]. Fluid accumulation in the neurophil creating a vacuolated space has been reported to be observed in the initial stages of neurodegeneration (Figure 8(A)). Also, shrunken nuclei can be seen often due to excessive fluid accumulation within the neuron making the nucleus appear shrunken (Figure 8(B)). Furthermore, central chromatolysis was observed in Figure 8(C) in which the nucleus lost its central position becoming eccentric, lying adjacent to the cell membrane due to the neural insult and loss of nuclear suspension. During recovery from the neural insult, the Nissl substance may reaggregate, but from the centre, so that there remains cytoplasmic clarity peripherally leading to peripheral chromatolysis, considered a microscopic indication of early neuronal recovery. Due consideration was given to processing artefacts and such observations were excluded as neuronal damage. The ‘dark neuron’ artefact as reported previously was observed in some slides (Figure 8(D)) [59]. It is a consequence of contraction in perturbed neurons due to mechanically induced polarisation, glucose deprivation, and disruption of neuronal membranous attachments, leading to shrinkage during dehydration for paraffin embedding, and reduced cytoplasmic osmolarity.
Exosomes derived from GIT1-overexpressing bone marrow mesenchymal stem cells promote traumatic spinal cord injury recovery in a rat model
Published in International Journal of Neuroscience, 2021
Yongjun Luo, Tao Xu, Wei Liu, Yuluo Rong, Jiaxing Wang, Jin Fan, Guoyong Yin, Weihua Cai
At the 28th day after injury, Nissl substance in the neurons cytoplasm from acquired spinal cord sections underwent a Cresyl Violet staining (FD Neuro Technologies, USA). The specimens were rinsed in distilled water, and subsequently stained with Cresyl Violet solution for 10 min. Finally, tissues differentiated in 95% ethyl alcohol were cleaned up with xylene and mounted with neutral balsam after rinsing with distilled water. Severely damaged nervous tissue and the blank area of staining were considered as lesion areas. The identified parts in each section were measured via ImageJ software. The volume of lesion tissues was calculated by the sum of all the lesion area multiplied by the distance between the sections (about 200 μm).