At the neuromuscular junction, motor neurons release acetylcholine which binds to nicotinic acetylcholine receptors on the muscle. These receptors are ligand-gated ion channels that are permeable to small cations.
Opening these channels depolarizes the muscle cell membrane, which causes the opening of calcium channels, primarily on the sarcoplasmic reticulum (SR) for skeletal muscle. The key channel is called the ryanodine receptor and is either mechanically coupled to a voltage-gated calcium channel (skeletal muscle) or activated by calcium released from voltage-gated calcium channels (smooth & cardiac muscle), but in both cases the change in voltage is the initial signal.
Calcium concentrations are very low in the muscle cell at rest, but high within the sarcoplasmic reticulum so calcium rushes through and some of it binds with troponin (not tropomyosin itself, but they are associated/attached with one another), which releases the hold of tropomyosin on the actin filament.
The calcium-bound tropomyosin doesn't go anywhere, but as calcium is quickly pumped into the SR or buffered up by calcium-binding proteins, troponin is no longer bound to calcium, allowing tropomyosin to block the myosin binding sites.
The increase in calcium concentration is transient, and travels in a wave down the muscle. If there are no further action potentials, the muscle will relax. Constant contraction requires a constant train of action potentials, and the overall strength of the contraction can be regulated by the firing rate of the motor neuron.
The Wikipedia pages for muscle contraction, tropomyosin, voltage-gated calcium channel, and ryanodine receptor can all be helpful. I'd also recommend a basic textbook on neuroscience, which typically covers neuron effects on muscles and some of the mechanics of muscle contraction. I typically recommend Purves, see https://neuroscience5e.sinauer.com/ or a library or anyplace you get books from (any edition is fine).
