A neuromuscular junction (or myoneural junction) is a chemical synapse formed by the contact between a motor neuron and a muscle fiber.[1] It is at the neuromuscular junction that a motor neuron is able to transmit a signal to the muscle fiber, causing muscle contraction.
Muscles require innervation to function—and even just to maintain muscle tone, avoiding atrophy. Synaptic transmission at the neuromuscular junction begins when an action potential reaches the presynaptic terminal of a motor neuron, which activates voltage-dependent calcium channels to allow calcium ions to enter the neuron. Calcium ions bind to sensor proteins (synaptotagmin) on synaptic vesicles, triggering vesicle fusion with the cell membrane and subsequent neurotransmitter release from the motor neuron into the synaptic cleft. In vertebrates, motor neurons release acetylcholine (ACh), a small molecule neurotransmitter, which diffuses across the synaptic cleft and binds to nicotinic acetylcholine receptors (nAChRs) on the cell membrane of the muscle fiber, also known as the sarcolemma. nAChRs are ionotropic receptors, meaning they serve as ligand-gated ion channels. The binding of ACh to the receptor can depolarize the muscle fiber, causing a cascade that eventually results in muscle contraction.
Neuromuscular junction diseases can be of genetic and autoimmune origin. Genetic disorders, such as Duchenne muscular dystrophy, can arise from mutated structural proteins that comprise the neuromuscular junction, whereas autoimmune diseases, such as myasthenia gravis, occur when antibodies are produced against nicotinic acetylcholine receptors on the sarcolemma.
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Answer:
The answer is (d) (iv) and (v).
Explanation:
Soil bacterium Bacillus thruingiensis (Bt) produces proteins that kill certain insects like lepidopterans (tobacco dudworm, armyworm), coleopterans (beetles) and dipterans (flies, mosquitoes). Bacillus thuringinesis forms some intracellular protein crystals. These crystals contain a toxic insecticidal protein. The Bt toxin protein exists as an inactive toxin and is converted into an active form due to the alkaline pH of the alimentary canal that solubilities the crystals. The activated toxin binds to the surface of midgut epithelial cells and creates pores which cause cell swelling and lysis and finally cause the death of the insect.
So, the correct answer is '(iv) and (v)'.
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