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The "central nervous system neural pathway for tear secretion" refers to the **integrated neural circuits**—primarily parasympathetic, with additional sympathetic and sensory afferent involvement—that control secretion from the lacrimal gland. The principal pathway involves sensory neurons from the ocular surface (especially the cornea), which relay via the trigeminal nerve to central nuclei (notably the superior salivatory nucleus in the brainstem). From there, preganglionic parasympathetic fibers travel via the facial nerve (greater petrosal nerve), synapse in the pterygopalatine (sphenopalatine) ganglion, and postganglionic fibers reach the lacrimal gland to effect tear secretion—primarily via cholinergic (muscarinic) mechanisms[1][2][4][5][6][7]. Disruption or modulation of this pathway can result in dry eye disease or, conversely, be exploited therapeutically with pharmacologic or mechanical neurostimulation[7]. However, this is a system-level target and lacks the precision of a single druggable molecule or protein. This entry does not map to a druggable molecular target but rather describes a coordinated series of neural elements, making it *not a conventional therapeutic target* as normally defined in pharmacology or drug development contexts.
Cholinergic agonism at muscarinic acetylcholine receptors in the lacrimal gland (increases tear secretion)\nNeurostimulation via trigeminal afferents activating central and peripheral pathways\nAnticholinergic blockade reduces tear secretion (therapeutic concern, not desired effect)
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