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Occupational toxicology of the nervous system
Published in Chris Winder, Neill Stacey, Occupational Toxicology, 2004
OPIDN is caused when the organophosphate molecule binds with neurotoxic esterases in the long processes of the nerves (the axons). The enzymes have functions related to transport of nutrients and energy molecules from the cell body to the end of the nerves. Phosphorylation of such proteins results in localised disruption of axoplasmic transport. If prolonged, these effects are followed by swelling of the axon, followed by degeneration from the site of the damage to the end of the axon. If exposure continues, this process can continue up the axon by the phosphorylation of more proteins. Lesions are characterised by degeneration of axons followed by degeneration of the cells that surround (and contribute to the insulation of the fibres) the myelin containing support cells (Abou-Donia 1981). This effect can occur in sensory or motor nerves in either the central or peripheral nervous systems (Marrs 1993). Initially, the condition arises as a distal symmetrical sensorimotor mixed peripheral neuropathy mainly affecting the lower limbs with tingling sensations, burning sensations, numbness and weakness. In severe cases paralysis may develop (Lotti et al. 1984). Longer nerves are affected more, probably because or their requirements for active nutrient supply (shorter nerves may continue to get supplied through passive mechanisms, such as diffusion). Regeneration is possible if exposure ceases and damage is not too extensive (IPCS 1986; Lotti 1992).
Chapter 10: The Use of Microspheres in the Study of cell Motility
Published in Alan Rembaum, Zoltán A. Tökés, Micro spheres: Medical and Biological Applications, 2017
Cytoplasmic organelles (membrane-limited) are rapidly moved within the cytoplasm of invertebrate and vertebrate axons in both the anterograde (away from the cell body) and retrograde (toward the cell body) directions and these movements are thought to constitute rapid axoplasmic transport;120 these movements have been reactivated in permeabilized axons.121,152 Adams and Bray122 injected a variety of particulate objects, including polystyrene microspheres derivatized in various ways, poly acrolein beads, paraffin oil, and glass fragments, into the giant axons of the shore crab. In many cases, these objects were observed to move uniformly in the anterograde direction (away from the cell body) with a velocity distribution profile very similar to that of the endogenous organelles. The authors argue that there are few restrictions on the chemical nature of particles that will move in axons although the presence of negative charges appears to be essential (perhaps in order to bind a protein component present in the axoplasm that is essential for expression of motility). These observations are interesting in light of the fact that a nonmembrane bounded object can interact with the motor for organelle transport within the axon. Katz et al.123 demonstrated that rhodamine-labeled acrylic microspheres (negatively charged; 0.02 to 0.20 μm in diameter) were taken up at axonal endings and retrogradely transported through the axonal cytoplasm to the cell body. No anterograde axoplasmic transport was observed; polystyrene microspheres of comparable size and acrylic microspheres greater than 0.2 μm in diameter were not transported. Although the mechanism by which these microspheres were taken up into the cell and transported along the axon is unknown, the authors hypothesize that they are taken up by endocytosis and the membrane-enclosed microspheres are transported by rapid axoplasmic transport. This hypothesis derives, in part, from the observation of Adams and Bray122 that negatively charged polystyrene microspheres (0.37 to 0.50 μm diameter) move only in the anterograde direction when injected directly into axons. They observed that these microsphere movements were ATP-dependent and exhibited velocities in the range of 0.4 to 0.6 μm/sec. Allen and coworkers125 were the first to show that cytoplasm extruded from the squid giant axon exhibited ATP-dependent movement of axonal organelles along microtubules and gliding-type movements of microtubules along a glass surface.125 Gilbert and Sloboda128 isolated a population of small membrane-bounded organelles from the axoplasm, labeled these organelles with a fluorescent lipid probe, and demonstrated that they were actively transported after being injected back into extruded squid axoplasm; this motility was abolished if the organelles were protease treated prior to injection into the axoplasm. Allen et al.125 added fluorescent polystyrene microspheres (0.537 μm in diameter) to extruded squid axoplasm and observed linear movements at 0.135 μm/sec using the fluorescence microscope.
Ameliorative effect of vitamin E and selenium against bisphenol A-induced toxicity in spinal cord and submandibular salivary glands of adult male albino rats
Published in International Journal of Environmental Health Research, 2023
Dina W. Bashir, Yasmine H. Ahmed, Mohamed A. El-Sakhawy
Partial recovery was observed in the myelinated nerve fibers of the SC white matter in Group III rats, as some of these fibers demonstrated regular and intact myelin sheaths, while others remained dispersed. The axoplasm appeared degenerated in some axons and normal in others. The structure and shape of the mitochondria were normal in some axons, while degenerated in others and with the empty appearance observed in Group II. In some cases, part of an axon reflected areas with normal axoplasm, while other parts had degenerated axoplasm; likewise, both normal and degenerated mitochondria could be observed in the same axon (Figure 2(d)).
Biological function simulation in neuromorphic devices: from synapse and neuron to behavior
Published in Science and Technology of Advanced Materials, 2023
Hui Chen, Huilin Li, Ting Ma, Shuangshuang Han, Qiuping Zhao
Electrical synapse is the gap junction, a special way of cell-to-cell linkage, which makes the action potential direct transmission between cells (Figure 1(c-i)). For this synapse, the synaptic cleft is very small, only several nanometers. In the presynaptic and postsynaptic membrane, there are some connexons that are made up of connexins. Two connexons form a gap junction channel, a non-gate control channel, which allows some small molecules of water-soluble substances and ions to pass through. When the action potential is generated in a neuron, the local current based on ionic current can be directly stimulated and transmitted to another neuron through the gap junction channel. By this way, the action potential is propagated from neuron to neuron. From this, the electrical synapse has lots of outstanding features, such as low resistive, rapid and bidirectional propagation. Different from electrical synapse, chemical synapse depends on the neurotransmitters to accomplish the information transfer from neuron to neuron (Figure 1(c-ii)). In chemical synapse, there are more mitochondria and a large number of vesicles, in which the latter is also called synaptic vesicle with 20–80 nm diameter and high contains concentrations of neurotransmitters such as acetylcholine or amino acid transmitters, catecholamine transmitters and neuropeptide transmitters. When the action potential is transmitted to the presynaptic terminal of a neuron, the presynaptic membrane depolarizes. After the depolarization exceeds the threshold value, Ca2+ channel is activated and Ca2+ enters into the axoplasm of the terminal from the outside of the cell. The increase of Ca2+ can trigger the efflux of synaptic vesicles and cause the quantized release of neurotransmitters. Meanwhile, excess Ca2+ in the axoplasm is transported outside through Na+-Ca2+ reverse transporter in order to its normal concentration in the presynaptic terminal. Once the neurotransmitters are released, they can enter into the synaptic cleft and reach the postsynaptic membrane by diffusion. Ultimately, these neurotransmitters can act on the ionotropic receptor and control the permeability of certain ions. When certain ions enter the postsynaptic terminal, if the terminal occurs depolarization, the signal is called excitatory postsynaptic potential (EPSP). In this process, the excitatory neurotransmitters act on the ionotropic receptors in the postsynaptic terminal to open the specific ion channels (Na+ and K+). The net inward current is generated because Na+ influx of is greater than K+ outflow, in turn, lead to the depolarization of the postsynaptic terminal. On the contrary, inhibitory neurotransmitters are released from the presynaptic terminal to act on the ionotropic receptors, and then open the Cl- channel to generate the outward current that hyperpolarizes the postsynaptic membrane. In this case, it is called inhibitory postsynaptic potential (IPSP). By this way, the information is transmitted to the next neuron by releasing neurotransmitters. The distinguishing between electrical and chemical synapses is listed in Table 1. However, the chemical synapse is the majority of synapses in the human brain.