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The term “外周神经末梢镇静” (Peripheral Nerve Terminal Sedation) refers to the pharmacological or physiological modulation, suppression, or calming of peripheral nerve terminals, typically to achieve analgesia or reduce pathological sensory transmission. This concept underlies approaches such as local anesthesia, peripheral nerve blocks, and analgesic strategies targeting noxious stimuli transmission at the nerve terminal level. Common clinical contexts include anesthesia for minor surgery, treatment of neuropathic pain, or acute pain from injury or inflammation. However, this is an effect or a functional description—not a discrete molecular entity, receptor, or canonical drug target. Therefore, it should not be used as a structured pharmacological 'target.' Instead, specific molecular targets (e.g., voltage-gated sodium channels, TRPV1 receptors, P2X receptors) should be identified when seeking molecular detail for peripheral nerve terminal modulation.
Drugs inducing "peripheral nerve terminal sedation" typically achieve this effect through mechanisms such as the blockade of voltage-gated sodium channels (e.g., by local anesthetics), desensitization of peripheral nociceptors (pain fibers), inhibition of neurotransmitter release at nerve terminals, modulation of inflammatory mediators at nerve endings, and dampening peripheral input to the central nervous system.
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