ACh now begins to destimulate the muscle fiber. The Ca2+ ions that bound to the Troponin molecules are now removed and pumped back into the Sarcoplasmic Reticulum via active transport utilizing ATP molecules produced from cellular respiration. The Troponin will now return to its original shape,breaking the connections between Actin and Myosin as well. Once the Ca2+ ions are no longer bound to the Troponin, Tropomyosin blocks the Myosin binding sites again. This ends the muscle contraction and the muscle fiber relaxes.
The adrenal medulla, which is in the autonomic nervous system, will then secrete, once action potential is reached, epinephrine (Adrenaline) into the blood. Epinephrine brings its effects to target receptors, which will in turn cause changes in the body. Adrenaline leads the Sympathetic Nervous System to become more prominent and inhibit the action of the Parasympathetic system in the body. Thus, the body focuses less on housekeeping and more on fighting or fleeing. It increases the amount of oxygen the lungs intake and the level of blood glucose.
To further complicate Johnson's perception, Sacks states "Yet the brain remains capable of making radical shifts in response to sensory deprivation"(Sacks,331). Making radical shifts gives us an indication that the brain could be termed as a pacemaker within us, as it controls what we do. Furthermore, genes and the brain have quite similar functions to carry out, which is giving out instructions to us, so in that regard both could be termed as pacemakers. The term pacemaker is indeed a very complex term and not as simple as it
They exert a wide range of functions in neuronal/glial proliferation, differentiation and apoptosis, as well as in maintaining the membrane permeability to ions and in the stabilization of synaptic transporters and receptors, the latest processes relevant to the generation and propagation of the nervous impulse and synaptic transmission.20,39,40 Moreover, cell and animal models underscore the key function of sphingolipids in the neurite growth and myelination of the cerebellum and forebrain, among other brain regions.41,42 Deficiency of ceramide synthase-2 that generates sphingolipids with C22-C24 fatty acyl chains results in 50% loss of compacted myelin and 80% loss of CNS myelin basic protein.42 Similarly, a 60% reduction of myelin-associated glycoprotein in the cerebellum and forebrain characterizes mice deficient in ceramide synthase-1, the enzyme that generates C18:0 sphingolipids.41 Interestingly, mice deficient of ceramide synthase -6, which generates C16:0 sphingolipids, as well as mice deficient of GM3 synthase that is responsible for one of the first steps in the production of gangliosides, both present hyperactive behavior and have been postulated as suitable animal models for
An important function of the dendrite is the integration of various input signals. Synapses are the gaps between the axons of transmitting neurons and the dendrites of receptor neurons. Electrochemical signals are carried across the gap by neurotransmitter molecules. These end up at the receptor proteins located in the ends of dendrites. There are various neurotransmitter chemicals.
Acetylcholine, Ach is the ganglionic neurotransmitter. Ach release from preganglionic synapse binds to nicotinic Ach receptors on the postganglionic cell. Postganglionic neuron is depolarized by Ach binding generating an action potential that elicits a response by traveling to the target
Some scholars, however, argue that ADC is caused by a macrophage-initiated cascade of events that leads to the degeneration and dysfunction of the brain (McGuire, 2003). To this school of thought, this macrophage-initiated cascade is not influenced by the quantity of viruses in the brain. This second hypothesis is informed by the fact that activated macrophages can produce neurotoxins that trigger the production of pro-inflammatory cytokines and oxygen free radicals. As highlighted by McGuire (2003), various in-vitro studies have indicated that these factors can kill human brain cells. In line with this discourse, Pulliam, Gascon, Stubblebine, McGuire, and McGrath (1997) reported significantly higher amounts of a specific subtype of macrophages among patients with ADC as compared to their
Amiodarone is a group three antiarrhythmic drug which means that it works by blocking the potassium channels which then slows down the cells ability to repolarize but it has properties of all four type of antiarrhythmic. Group one of antiarrhythmic blocks the sodium channels in the heart which then slows down the electrical conduction of
It is secreted by type II alveolar cells, which secrete alveolar fluid (surfactant is a component of alveolar fluid). Surfactant is a mixture of phospholipids and lipoproteins, which serves to lower the surface tension of alveolar fluid, 30 preventing collapse of alveoli and maintaining their patency 8. Meconium, when aspirated into the lungs, deactivates surfactant. Research has also shown that meconium disturbs surfactant synthesis, with a study concluding that surfactant phosphatidylcholine (a phospholipoprotein which forms about 85% of the lipid component in surfactant) concentrations are low in infants with meconium aspiration syndrome 14. In addition, another study has demonstrated the surfactant-stripping effect of meconium, due to the high minimum surface tensions of the major free fatty acids of meconium (palmitic, stearic, and oleic acids) 15,16.