Acetylcholine

glands. One of the first, and most abundant, neurotransmitters to be discovered is acetylcholine, often abbreviated ACh (Cherry). This was first discovered by a German biologist, Otto Loewi, in 1921 who later won a Nobel Prize for his findings (Boeree). Acetylcholine is present in both inhibitory functions as well as excitatory functions, which means that it can both speed up and slow down nerve signals (“Acetylcholine”). Its role in the central nervous system is excitatory, and plays a role in arousal

Nicotinic acetylcholine receptors (nAChRs) are a family of multi-subunit transmembrane neurotransmitter receptors. They do many functions in the central and peripheral nervous systems. Nicotinic acetylcholine receptors, or nAChRs are receptors that make a response to the neurotransmitter acetylcholine. Nicotinic receptors can respond to some drugs, such as the nicotinic receptor agonist nicotine. So where can we find these receptors? We find these receptors in the central nervous system of humans

people in various populations, affecting mostly women in their 20’s to 30’s and men over the age of 60 (Postevka 2013). Myasthenia gravis is an autoimmune neuromuscular disorder that annihilation the functional acetylcholine receptors at the neuromuscular joints. Normally, acetylcholine is used in signal transmission between nerves and muscles, its goal is to provide muscle contractions. But in this case, the decreasing

INTRODUCTION Within vertebrates, heart rate is established by the sinoatrial (SA) node of the heart. This is achieved through a series of action potentials which drives excitation of cardiac muscles and establishes a rhythmic pace (Fritz et al., 2011). However, there are numerous factors that can affect the SA nodes impact on heart rate, which are primarily related to the autonomic nervous system. The autonomic nervous system is responsible for the regulation of involuntary functions, and is broken

Daphnia and Additives Lab Purpose The purpose of this lab is to test what effect of Nicotine, Acetylcholine, Epinephrine, Caffeine, and Ethanol on an organism’s heart rate. Materials * Microscope * Eye dropper * Pipet * Cotton balls * Depression slide * Beakers * Daphnia * Water * Five additives: Nicotine, Acetylcholine, Epinephrine, Caffeine, Ethanol Procedure 1. Put on safety goggles. 2. Catch a living Daphnia. 3. Transfer to a depression

exocytose; where the vesicles fuse to the cell membrane and prepare to releases the neurontransmitters, acetylcholine, into the synaptic clef. With the botulinum, they would attach to each nerve end acetylcholine, the neurotransmitter, which is responsible for triggering muscle contractions, cannot be released. Then a “series of proteins, vamp, syntaxin, and snap-25, are essential for the release of acetylcholine. Certain botulinum toxin attacks these proteins”

Myasthenia gravis is considered an autoimmune disease because people who have it carry an antibody called polyclonal that destroys the acetylcholine receptors (Neurology, 2013). These antibodies destroy receptor sites in the neuromuscular junction faster than the body can produce them. Usually antibodies protect the body from foreign invaders like bacteria and viruses, but in the case of MG it attacks accessories that are required for muscle movement. In a study conducted by Jon Lindstrom and Seybold

Q1 Muscle contraction can be understood as the consequence of a process of transmission of action potentials from one neuron to another. A chemical called acetylcholine is the neurotransmitter released from the presynaptic neuron. As the postsynaptic cells on the muscle cell membrane receive the acetylcholine, the channels for the cations sodium and potassium are opened. These cations produce a net depolarization of the cell membrane and this electrical signal travels along the muscle fibers. Through

January 2013 my grandmother passed away after battling Alzheimer’s disease. Alzheimer’s disease is a brain disease that is permanent and is affecting more elderly people every day. This horrible disease changes the memory and thinking in the brain. Researchers, for years, have been trying to find a way to stop the progression of Alzheimer’s. Researchers, with the help of doctors have been successful finding a way to slow down the progression, but not completely stop it. Although Alzheimer’s is a

35%, and the mean heart rate decreased by 34% when compared to the amplitude and heart rate with warm saline. When varying concentrations of acetylcholine were put on the heart, there was very little change in the amplitude of heart contraction. Similarly, there was very little change in heart rate when using concentrations of 10-8 to 10-5 M of acetylcholine, but heart rate dropped 20% from 10-5 to 10-4. When d-tubocurarine was used as a blocking agent, heart rate increased 31%. Similar results