Botulinum toxin (Botox) works by blocking the exocytosis of acetylcholine. A number of different medical and cosmetic procedures use this chemical. Injection of small quantities of botulinum toxin (Botox) into specific overactive muscles causes muscle relaxation that smooths the skin and reduces wrinkles. Injection into certain spinal ganglia helps reduce a certain form of chronic pain, and injections into the salivary glands causes the reduction of overactive saliva production. What type of toxin is Botox? Agonist or Antagonist

Botulinum toxin (Botox) works by blocking the exocytosis of acetylcholine. A number of different medical and cosmetic procedures use this chemical. Injection of small quantities of botulinum toxin (Botox) into specific overactive muscles causes muscle relaxation that smooths the skin and reduces wrinkles. Injection into certain spinal ganglia helps reduce a certain form of chronic pain, and injections into the salivary glands causes the reduction of overactive saliva production. What type of toxin is Botox? Agonist or Antagonist

Medical Terminology for Health Professions, Spiral bound Version (MindTap Course List)

8th Edition

ISBN:9781305634350

Author:Ann Ehrlich, Carol L. Schroeder, Laura Ehrlich, Katrina A. Schroeder

Publisher:Ann Ehrlich, Carol L. Schroeder, Laura Ehrlich, Katrina A. Schroeder

Chapter4: The Muscular System

Section: Chapter Questions

Problem 32LE: A _______________ is a drug that causes temporary paralysis by blocking the transmis- sion of nerve...

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A patient has been exposed to the organophosphate pesticide malathion,which inactivates acetylcholinesterase. Which of the following symptoms would you predict: blurring of vision, excess tear formation, frequent or involuntary urination, pallor (pale skin), muscle twitching, orcramps? Would atropine be an effective drug to treat the symptoms?(See Clinical Impact 16.2 for the action of atropine.) Explain.
When the neurotransmitter acetylcholine (ACh) binds the acetylcholine receptor (a GPCR) on muscle cells, it causes them to contract. ZIGGY, a chemical analog of ACh, also binds to the same acetylcholine receptor on muscle cells, but instead causes the muscle cells to relax. For this reason, it is sometimes prescribed as a muscle relaxer. Explain in 3-4 sentences how ZIGGY could cause muscle relaxation. How can both ZIGGY and ACh bind the same GPCR? And then how can they have different effects on the cells, despite binding to the same receptor on the same cells?
Flaccid paralysis (resulting from the failure of muscles to contract), induced by the neurotoxin tubocurarine, occurs when this poison blocks the binding of: the inhibitory neurotransmitter melatonin to post-synaptic bicarbonate channels the excitatory neurotransmitter glutamate to post-synaptic calcium channels the excitatory neurotransmitter acetylcholine to post-synaptic sodium channels the inhibitory neurotransmitter glycine to post-synaptic chloride channels the excitatory neurotransmitter serotonin to post-synaptic potassium channels
Lidocaine is an anesthetic that is commonly used in medical and dental practices. After being injected or applied to the skin, lidocaine very quickly causes numbness in that area by affecting nerve transmission. Which option below is a possible mechanism by which lidocaine might work? Mimics the neurotransmitter released by sensory neurons Causes an influx of calcium into the axon bulb of sensory neurons Prevents the opening of sodium channels in the sensory neurons
Multiple sclerosis (MS) is a disorder that causes the destruction of myelin sheaths surrounding neurons. People with MS display many symptoms, including slurred speech, double vision, and poor muscle coordination. What is the direct effect of MS on nerve impulse transmission? Select one: The movement of impulses along neurons is slower than normal. Dendrites cannot be stimulated by acetylcholine, therefore impulses are not generated in neurons. The threshold level of stimulation for neurons is greater than normal. Axons cannot sectete acetylcholine, therefore impulses are not able to travel across synapses. O
Spastic paralysis (resulting from the failure of muscles to relax), induced by the neurotoxin strychnine, occurs when this poison blocks the binding of: the excitatory neurotransmitter acetylcholine to post-synaptic sodium channels the excitatory neurotransmitter glutamate to post-synaptic calcium channels the excitatory neurotransmitter serotonin to post-synaptic potassium channels the inhibitory neurotransmitter glycine to post-synaptic chloride channels the inhibitory neurotransmitter melatonin to post-synaptic bicarbonate channels
In the disease myasthenia gravis, the human body makes—by mistake— antibodies to its own acetylcholine receptor molecules. These antibodies bind to and inactivate acetylcholine receptors on the plasma membrane of muscle cells. The disease leads to a devastating progressive weakening of the people affected. early on, they may have difficulty opening their eyelids, for example, and, in an animal model of the disease, rabbits have difficulty holding their ears up. As the disease progresses, most muscles weaken, and people with myasthenia gravis have difficulty speaking and swallowing. eventually, impaired breathing can cause death. explain which step of muscle function is affected.
Are these true or false? Acetylcholine molecules are actively transported from the axon to their receptors on the muscle membrane by special transport proteins. Receptors on the post-synaptic cell membrane that bind the acetylcholine are voltage-gated channels (channels that open in response to a change in the electrical charge of the membrane). When a muscle cell is not contracting its cell membrane is negative on the inner surface. The effect of a neurotransmitter on the muscle cell membrane is to modify its ion permeability properties temporarily. During depolarization, a small region of the muscle cell's membrane becomes less negative on the inside." Both sodium and potassium are more concentrated in the extracellular fluid than the intracellular fluid. After an action potential passes over a region of the sarcolemma the region remains positively charged throughout the entire muscle contraction. An increase in the calcium ion level in the cytosol causes thin filaments to begin…
Someone goes for a jog first thing in the morning and encounters a squadron of javelinas, causing a release of epinephrine. Some of this circulating epinephrine binds to a G-alpha-s coupled receptor (GPCR) on the surface of muscle cells. Which of the following would occur in the muscle cell as a result of this activation? Nitric oxide synthesis would increase. cyclic AMP (cAMP) activity would increase. Phospholipase C (PLC) would hydrolyze (cut) the molecule PIP2. The levels of adenylate cyclase activity would decrease. The levels of adenylate cyclase activity would decrease. Which ligand is CORRECTLY matched with its characteristic? Group of answer choices Glucagon: stimulates the activation of the mitogen activated protein (MAP) kinase pathway Nitric oxide (NO): must bind to its target protien withn a few seconds because NO degrades rapidly Steroid hormone: produces a response in its target cells within seconds Acetylcholine: hydrophobic molecule that binds to…
are these True or False? Receptors on the post-synaptic cell membrane that bind the acetylcholine are voltage-gated channels (channels that open in response to a change in the electrical charge of the membrane). When a muscle cell is not contracting its cell membrane is negative on the inner surface. The effect of a neurotransmitter on the muscle cell membrane is to modify its ion permeability properties temporarily.
Which of the following statements regarding the motor end plate in the somatic motor division of the nervous system is true? After the activation of voltage-gated calcium channels, the neuron releases ACh onto the muscarinic receptors on the surface of the highly folded area of the muscle fibre. The preganglionic nerve fibre releases ACh onto the postganglionic nerve fibre, which then releases ACh onto the cholinergic receptors of the motor end plate. Chemically gated monovalent cation channels on the motor end plate are activated once the motor neuron releases ACh onto the nicotinic receptors on the surface of the muscle cell. The AChE enzyme enhances the amount of ACh released into the neuromuscular junction
Malathion is an insecticide commonly used in the horticultural industry. Many homeowners apply this chemical to their trees to rid them of infestation by aphids or other insects. Malathion is classified as an organophosphate insecticide. Exposure to malathion is very dangerous to humans and animals because it acts as an irreversible inhibitor of acetylcholinesterase. Predict what might happen to synaptic communication between cholinergic neurons if an individual or animal was poisoned with malathion, and clearly describe the mechanisms at work.