[Effects of amygdala cholinergic system on modulation of anxiety behaviors of rats by use of Elevated Plus Maze test]

Anxiety is a common psychological disorder in the society which can be accompanied by physiologic and behavior disorders. There is evidence that neurons and cholinergic receptors are involved in the neurobiology of anxiety. In the present study, we have investigated the effects of muscarinic and nicotinic receptors of cholinergic system in amygdala of rats on anxiety, by use of Elevated Plus Maze test. In this study the locations of amygdale in the rats were determined by stereotaxis method and leading cannulas were inserted into the same locations for drug injection into amygdala. The effects of muscarinic and nicotinic receptors of central amygdala for controlling anxiety in the rats were assessed by use of Elevated Plus Maz test. Bilateral intra amygdala injection of physostegmine [2 micro g/rat] decreased percentage of open arm time [OAT] and open arm entries [OAE] [p<0.05] which indicated an increase in the level of anxiety. However bilateral injection of the muscarinic receptor antagonist, pilocarpine [0.25, 0.5, and 1 micro g], did not show a significant change in anxiety-like behavior [p>0.05]. Bilateral administration of nicotine [1 and 2 micri g/rat] into central amygdala [intra-CeA] induced an anxiogenic effect, shown by decreases in the percentage of OAT and percentage of OAE [p<0.05]. Bilateral intra-CeA injection of mecamylamine [20, 30, 50 ng/rat], a selective nicotine acetylcholine receptor [nAChRs] antagonist led to a significant anxiolytic behavior in the rats [p<0.05]. The results of this study indicate the muscarinic and nicotinic receptors of amygdale have a role in controlling anxiety

[Interaction between JWH133-induced antinociception and two extreme doses of celecoxib]

JWH133 is known to have cannabinoid-2 [CB2] receptor agonist properties. Celecoxib, a selective cyclooxygenase-2 [COX-2] inhibitor, is also known to have antinociceptive properties. Endocannabinoids produce analgesia possibly through cyclooxygenase [COX] pathway. The aim of the present work was: to study the effect of celecoxib on JWH133 induced antinociception and to compare the effects of two different dose ranges of celecoxib [mg/kg and nano g/kg] on the JWH133 antiniciceptive effect. We have studied the possible interaction of administration of mg/kg [50-200 mg/kg] and Ultra-Low Dose [ULD] [25 and 50 ng/kg] of celecoxib on the antinociceptive effect of intraperitoneal [i.p.] injection of JWH133 using formalin test in mice. JWH133 [0.01, 0.1 and 1 mg/kg] induced antinociceptive effect just in phase I of the formalin test. Celecoxib [50-200 mg/kg] and its ULD [25 and 50 ng/kg] attenuated and potentiated, JWH133 induced antinociception, respectively. It is concluded that JWH-133 induced antinociception is modulated by celecoxib and mg/kg doses of celecoxib showed opposite effects compare to its ultra-low doses

[Analgesic effects of extremely low frequency electromagnetic fields in mice]

Environmental factors such as electromagnetic fields influence the pain sensation. To investigate the possible analgesic effect of extremely low frequency electromagnetic fields [ELF-EMFs] exposure and possible interaction between ELF-EMFs and opioid, alpha and beta adrenergic systems. This was an experimental study in which the effect of 60 Hz magnetic field [100mT] on the pain threshold of 80 male albino mice was investigated. Pain threshold was assessed by the tail immersion technique using water with a temperature of 52 C. The mean pain threshold was significantly increased in case group [5.85 +/- 0.69 sec] compared to control group [3.77 +/- 0.55 sec] following ELF-EMF exposure [p<0.0001]. Pretreatment of animals with naloxane [2 mg/kg] and phentolamine [10 mg/kg] significantly reduced the effect to [3.97 +/- 0.7 sec and 4.01 +/- 0.49 sec], respectively [p<0.0001]. There was no change in the value of mean pain threshold [5.77 +/- 0.68 sec] when propranolol [10 mg/kg] was administered [p<0.0001]. Based on our data, exposure to ELF-EMFs could induce analgesic behavior in mice and the associated effect is related to opioid and alpha-adrenergic systems