Veterinary Research Forum

Abstract Thymoquinone (TQ), the bioactive compound found in black seed, possesses beneficial properties. In the present study, the effects of oral administration of TQ were investigated on acute corneal and orofacial pains in rats. To clarify the central mechanism of action, muscarinic cholinergic, cannabinergic 1 (CB1) and 5-hydroxytryptamine receptor antagonists were delivered into the 4^th ventricle of the brain after oral administration of TQ. Acute corneal and orofacial pains were induced by dropping of hypertonic saline (50.00 µL; 5.00 M) on the corneal surface and subcutaneous injection of capsaicin (1.50 µg; 20.00 µL) in the vibrissal pad, respectively. The eye wiping number and face rubbing duration were recorded as corneal and orofacial pains behavioral responses, respectively. Locomotor activity was measured using an open-field test. The TQ (5.00 mg kg^-1) had no effects, while it reduced pain responses at 10.00, 20.00, and 40.00 mg kg^-1. Intracerebro-ventricular injections of naloxone (an antagonist of opioid receptors), (N-(Piperidin-1-yl)-5-(4-iodophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide (an antagonist of CB1 receptors), atropine (an antagonist of muscarinic cholinergic receptors), and ondansetron (an antagonist of 5-hydroxytryptamine 3 receptors) at a similar dose of 10.00 µg kg^-1 inhibited corneal and orofacial pains suppression caused by 40.00 mg kg^-1 TQ. The tested drugs did not affect locomotor activity. It is concluded that TQ caused analgesia in the acute corneal and orofacial pains. Central opioid, cholinergic muscarinic, CB1, and 5-hydroxytryptamine 3 receptors might be involved in the anti-nociceptive effects of TQ.

Abstract In this study, the effects of subcutaneous (SC) injection of pilocarpine (a cholinomimetic agent) and atropine (a muscarinic receptors antagonist) were investigated on a tonic model of orofacial pain in rats. The contribution of the endogenous analgesic opioid system was assessed using naloxone (an opioid receptors antagonist). Tonic orofacial pain was induced by SC injection of a diluted formalin solution (1%, 50 μL) in the right upper lip, and the time spent face rubbing was measured in five min blocks for 1 h. Formalin induced a biphasic (first phase: 0-5 min and second phase: 15-35 min) pain response. Pilocarpine significantly (P < 0.05) suppressed both phases of orofacial pain. Atropine did not have any effect and naloxone non-significantly increased the intensity of pain when used alone. In the pre-injection examinations, atropine prevented, but naloxone did not reverse the antinociceptive effect of pilocarpine. The results indicated that SC injection of formalin in the orofacial region induced a marked biphasic pain. Pilocarpine via muscarinic cholinergic receptors produced antinociceptive effect in the orofacial formalin-induced pain. The endogenous opioid analgesic system may not have a role in pilocarpine-induced antinociception.

Abstract The present study investigated the effects of microinjections of acetylcholine (a cholinergic agonist), physostigmine (a cholinesterase inhibitor), atropine (an antagonist of muscarinic cholinergic receptors) and hexamethonium (an antagonist of nicotinic cholinergic receptors) into the parafascicular nucleus of thalamus on the acute corneal nociception in rats. Acute corneal nociception was induced by putting a drop of 5 M NaCl solution onto the corneal surface of the eye and the number of eye wipes was counted during the first 30s. Both acetylcholine and physostigmine at the same doses of 0.5, 1 and 2 μg significantly (P < 0.05) reduced the number of eye wipes. The intensity of corneal nociception was not changed when atropine and hexamethonium were used alone. Atropine (4 μg), but not hexamethonium (4 μg) significantly (P < 0.05) prevented acetylcholine (2 μg)- and physostigmine (2 μg)-induced antinociceptive effects. The results indicated that at the level of the parafascicular nucleus of thalamus, the muscarinic cholinergic receptors might be involved in the antinociceptive effects of acetylcholine and physostigmine.