An extension of the " squirming test" is described which makes the method specific for nonnarcotic analgesics. The intraperitoneal injection of acetic acid causes squirming and an increase in capillary permeability that is measured by direct estimation of plasma-bound dye (Pontamine Sky Blue) which has leaked into the peritoneal cavity. Nonnarcotic analgesics inhibit squirming and leakage of dye. Values for the oral ED50s for both effects are given for a number of typical compounds. Narcotic analgesics, in doses that produce analgesia, inhibit squirming but do not significantly affect leakage of dye. Drugs that stimulate the central nervous system and also inhibit squirming have no significant effect on leakage of dye over the range of doses which inhibit squirming. Corticosteroids do not significantly inhibit either squirming or leakage of dye.

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The effect of cannabinoids on motion-induced emesis is unknown. The present study investigated the action of phytocannabinoids against motion-induced emesis in Suncus murinus . Suncus murinus were injected intraperitoneally with either cannabidiol (CBD) (0.5, 1, 2, 5, 10, 20 and 40 mg/kg), ∆ 9 -tetrahydrocannabinol ( ∆ 9 -THC; 0.5, 3, 5 and 10 mg/kg) or vehicle 45 min. before exposure to a 10-min. horizontal motion stimulus (amplitude 40 mm, frequency 1 Hz). In further investigations, the CB 1 receptor antagonist, N-(piperidin-1-yl)-5-(4-iodophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1 Hpyrazole-3-carboxamide (AM 251; 5 mg/kg), was injected 15 min. prior to an injection of ∆ 9 -THC (3 mg/kg). The motion stimulus was applied 45 min. later. The number of emetic episodes and latency of onset to the first emetic episode were recorded. Pre-treatment with the above doses of CBD did not modify the emetic response to the motion stimulus as compared to the vehicle-treated controls. Application of the higher doses of ∆ 9 -THC induced emesis in its own right, which was inhibited by AM 251. Furthermore, pre-treatment with ∆ 9 -THC dose-dependently attenuated motion-induced emesis, an effect that was inhibited by AM 251. AM 251 neither induced an emetic response nor modified motion-induced emesis. The present study indicates that ∆ 9 -THC, acting via the CB 1 receptors, is anti-emetic to motion, and that CBD has no effect on motion-induced emesis in Suncus murinus .The signs and symptoms of motion sickness including vomiting, nausea, pallor and general malaise are seen, to some degree, in most people on sufficient exposure to a motion stimulus [1]. As such, motion sickness is a significant problem not only in civilian transport, but also in military training and travel, and also in space travel. The most widely accepted hypothesis regarding the initiation of motion sickness is the sensory conflict or sensory mismatch theory [2].It is proposed that sensory conflict occurs when vestibular, visual and non-vestibular information from somatosensory receptors concerning motion and balance of the body do not relate to each other or to what is anticipated from previous exposure; this leads to motion sickness. The neuronal pathways and the degree of their involvement in the mediation of motion sickness are not fully known. Experiments involving deaf-mutes [3] were the first to show that a functional vestibular system is critical for the development of motion sickness. This was confirmed when labyrinthine-defective individuals [4,5] and labyrinthectomized dogs [6] were shown to possess a total immunity to seasickness. Following discrete removal of the area postrema (the chemosensitive trigger zone for emesis), it was demonstrated that although this structure is involved in the development of motion-induced emesis, it is not an essential component [7]. The vestibulocerebellum conveys information from the vestibular system regarding the position of the head and is involved in the generation of reflex eye movements and changes in ...

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