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1. When the movement of the nictitating membrane is recorded in the usual way, pulled out under load in cat, dog, or rabbit, end-plate-depolarizing drugs such as succinylcholine, decamethonium, nicotine, and 2268F, cause a retraction.

2. This movement is due to activation of orbital striated muscle, as evidenced by the resistance of the movement to ganglion block or excision of the superior cervical ganglion and to administration of phentolamine or atropine, and by its great sensitivity to dimethyltubocurarine.

3. End-plate-depolarizing drugs produce contractions of the superior and inferior oblique and of the recti muscles strong enough to account for the movements of the nictitating membrane, provided the known fascial connexions of the orbit allow transmission of a fraction of the extraocular muscle movement to the membrane.

4. In post mortem specimens with the front of the orbit undisturbed, retraction of the central end of any of the ocular muscles produces movement of the nictitating membrane; the movement was greatest with the superior oblique and medial rectus. In vivo, detaching the superior oblique from its insertion into the globe sometimes abolished or reduced the response to end-plate-depolarizing drugs.

5. With the membrane unloaded and retracted into the medial canthus, in the lightly anaesthetized or unanaesthetized dog or cat, these drugs cause a protrusion of the membrane, which can be sufficient to cover the cornea. This response also resists ganglion-block and is highly sensitive to dimethyltubocurarine.

6. It is suggested that in the normal conscious animal the nictitating membrane is held retracted by a relatively small amount of sympathetic activity, and that its protrusion is an active mechanism under voluntary control mediated by the striated muscles of the orbit.

7. The importance of these mechanisms in the interpretation of experiments in which the nictitating membrane is used are discussed.