The molecular cloud, embedding AFGL 2591, has a “head-and-tail” structure with a total mass of ∼ 1800 M⊙, about half of the mass (∼ 900 M⊙) in the head (size ∼ 1.2 pc in diameter), and another half in the envelope (∼ 3.5 pc in the east-west direction). We found a new cloud in the direction toward north-east from AFGL 2591 (projected distance ∼ 2.4 pc), which is probably associated with the AFGL 2591 cloud. The 12CO spectrum clearly shows a blue-shifted high-velocity wing at around the velocity −20 ∼ −10 km s−1, but it is not clear whether this high-velocity component has a bipolar nature in our observations. The observed CN spectra also show blue-shifted wing component but the existence of the red-shifted component is not clear, either. In some CN and HCN spectra, the highvelocity components appear as a different velocity component, not a broad line-wing component. The dense cores, traced by CN and HCN, exist in the ‘head’ of the AFGL 2591 cloud with an elongated morphology roughly in the north-south direction with a size of about 0.5 pc. The abundance ratio between CN and HCN is found to be about 2 − 3 within the observed region, which may suggest a possibility that this core is being affected by the embedded YSOs or by possible shocks from outside.

The present study investigated the role of peripheral group I, II, and III metabotropic glutamate receptors (mGluRs) in mustard oil (MO)-induced nociceptive response in the masseter muscles of lightly anesthetized rats. Experiments were carried out on male Sprague-Dawley rats weighing 300-350 gm. After initial anesthesia with sodium pentobarbital (40 mg/kg, i.p.), one femoral vein was cannulated and connected to an infusion pump for intravenous infusion of sodium pentobarbital. The rate of infusion was adjusted to provide a constant level of anesthesia. MO (30 μL) was injected into the mid-region of the left masseter muscle via a 30-gauge needle over 10 seconds. After 30 mL injection of 5, 10, 15, or 20% MO into the masseter muscle, total number of hindpaw-shaking behavior was monitored. Intramuscular administration of MO significantly produced hindpawshaking behavior in a dose-dependent manner, as compared with the vehicle (mineral oil)-treated group. Intramuscular pretreatment with 10 or 100 ng DHPG, a group I mGluRs agonist, enhanced MO-induced hindpaw-shaking behavior, while APDC (20 or 200 μg), a group II mGluRs agonist, or L-AP4 (2 μg), a group III mGluRs agonist, significantly reduced MO-induced nociceptive behavior. The antinociception, produced by group II or III mGluRs agonists, was abolished by pretreatment with LY341495, a group II mGluRs antagonist, or CPPG, a group III mGluRs antagonist, res-pectively. Based on these observations, peripheral mGluRs differentially modulated MO-induced nociceptive behavior response in the craniofacial muscle pain and peripheral group II and III mGluRs agonists could be used in treatment of craniofacial muscle nociception.