Nerve axon

Mode of Motion. The cyclodienes, like lindane and toxaphene, affect the nerve axon produciag hyperactivity, convulsions, prostration, and death. The biochemical lesion is the competitive inhibition of the y-aminobutyric acid (GABA) neurotransmitter binding site of the nerve axon. Spray workers with lengthy exposure to dieldrin have suffered from prolonged and repeated central nervous system disturbances produciag epileptiform coavulsioas. Similar disturbances occurred ia workers heavily exposed to chlordecoae. 

Phosphonothioate Esters of Phenols. Phosphonates with a single P—C bond are highly toxic and persistent iasecticides but have not been used extensively because some compounds produce delayed neuropathy leading to irreversible paralysis ia higher animals, including humans. Such compounds specifically inhibit an enzyme, neurotoxic esterase, that is responsible for the growth and maintenance of long nerve axons (31,32). 

Figure 6. Transport of material along the nerve axon. Materials such as neurotransmitter peptides are synthesized in the cell body and sequestered in vesicles at the Golgi. Vesicles are then transported down the axon towards the synapse by kinesin motors. Other materials are transported from the synapse to the cell body by dynein motors.

In addition to changes within the nerve, sympathetic afferents become able to activate sensory afferents via as yet poorly characterised a-adrenoceptors. These interactions between adjacent sensory and autonomic nerve axons and between ganglion cells result in excitation spreading between different nerve fibres. These peripheral ectopic impulses can cause spontaneous pain and prime the spinal cord to exhibit enhanced evoked responses to stimuli, which themselves have greater effects due to increased sensitivity of the peripheral nerves. 

Lamina IV is composed of heterogeneous sized cells and is less densely packed than lamina III due to the number of nerve axons passing in this layer. At least three types of neurons have been identified in lamina IV, based on different dendritic projection patterns and these include SCT and PSDC cells. Another cell type has been described which has a dendritic pattern similar to SCT and PSDC, but with local axon terminations. Somas of STT cells are also found in lamina IV. 

The nerve axon sodium channel was studied in detail (in fact, as shown by the power spectrum analysis, there are two sorts of this channel one with fast opening and slow inactivation and the other with opposite properties). It is a glycoprotein consisting of three subunits (Fig. 6.22), the largest (mol. wt. 3.5 X 105) with a pore inside and two smaller ones (mol.wt 3.5 X 104 and 3.3 X 104). The attenuation in the orifice of the pore is a kind of a filter... 

Nerve axons and retinal rod cells depend on the microtubule network to support their distinctive cell morphology... 

Figure 9.8 Simple diagram of mitochondrial H -ion movement and axonal K -ion movement to establish membrane potentials across membranes. Note that H movement from the mitochondrial matrix to the outer surface of the inner membrane requires a specific proton pump that requires energy, which is transferred from electron transfer, whereas the K ion movement occurs via an ion channel with energy provided from the concentration difference of K ions on either side of the membrane (approximately 100-fold). The movement of both the protons and K ions generates a membrane potential. The potential across the membrane of the nerve axon provides the basis for nervous activity (see Chapter 14).

Posterior pituitary Two hormones, vasopressin and oxytocin, are synthesised in the hypothalamus and then transported through nerve axons to the posterior pituitary, where they are stored until released. Vasopressin acts on the kidney to conserve water. Its secretion is stimulated by thirst and a decrease in blood pressure. Secretion of oxytocin initiates uterine contraction for parturition. It also stimulates milk ejection from the mammary glands. 

Figure 13.16 A summary of the control of muscle contraction by the motor neurone. When an electrical impulse arrives at the junction between a nerve axon and a muscle fibre, a small amount of acetylcholine is released. This initiates an action potential which is transmitted throughout the fibre via the T-tubules. This causes the sarcoplasmic reticulum to release Ca ions which initiate contraction of the myofibrils via changes in troponin and tropomyosin. Thus sites on the actin for binding of the myosin cross-bridges are exposed.

The generation of action potentials by nerve axons and muscle fibres was first described by the German physiologist Emil DuBois-Reymond in 1849. 

Experiments on the physiological and biochemical mechanisms of action suggest that bromethalin uncouples oxidative phosphorylation in central nervous system mitocondria(19). This could lead to a decreased production of ATP, a diminished activity of Na /K ATPase, and a subsequent fluid build up manifested by fluid-filled vacuoles between the myelin sheaths. This vacuole formation in turn leads to an increased cerebrospinal fluid pressure and increased pressure on the nerve axons, yielding a decrease in nerve impulse, paralysis, and death. 

The principal cytoskeletal proteins in non-muscle cells are actin, tubulin, and the components of intermediate filaments. Actin can exist either as monomers ( G-actin ) or polymerized into 70 A diameter double filament ( F-actin ). Polymerized actin usually is localized at the margins of the cells, linked by other proteins to the cell membrane. In contrast, tubulin forms hollow filaments, approximately 250 A in diameter, that are distributed within a cell in association, generally, with cell organelles. Stabilized microtubule structures are found in the flagella and cilia of eucaryotic cells however, in other instances - examples being the mitotic apparatus and the cytoskeletal elements arising in directed cell locomotion - the microtubules are temporal entities. Intermediate filaments, which are composed of keratin-like proteins, are approximately 100 A thick and form stable structural elements that impart rigidity, for example, to nerve axons and epithelial cells. 

Nerve axons, 7 Nerve blocks, 16 Nervous conduction, 7 Neuralgia, 85 Neuritis, 85... 

Action potential propagation Local anesthetics, tetrodotoxin,1 saxitoxin2 Nerve axons Block sodium channels block conduction... 

The excitable membrane of nerve axons, like the membrane of cardiac muscle (see Chapter 14) and neuronal cell bodies (see Chapter 21), maintains a resting transmembrane potential of -90 to -60 mV. During excitation, the sodium channels open, and a fast inward sodium current quickly depolarizes the membrane toward the sodium equilibrium potential (+40 mV). As a result of this depolarization process, the sodium channels close (inactivate) and potassium channels open. The outward flow of potassium repolarizes the membrane toward the potassium equilibrium potential (about -95 mV) repolarization returns the sodium channels to the rested state with a characteristic recovery time that determines the refractory period. The transmembrane ionic gradients are maintained by the sodium pump. These ionic fluxes are similar to, but simpler than, those in heart muscle, and local anesthetics have similar effects in both tissues. 

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