Tapioca Melanoma of the Iris: A Case Report.

PURPOSE: To report an extremely rare case of tapioca melanoma of the iris in an Iranian patient. CASE REPORT: A 50-year-old male patient presented with ocular pain and redness in the right eye for two weeks. The visual acuity was 7/10 and the intraocular pressure (IOP) was 30 mmHg. A lobulated amelanotic vascularized and nodular (tapioca-like) iris mass with a 180 o extent was seen in the right eye. Incisional biopsy of the mass revealed atypical mixed type (epithelioid and spindle cell) melanoma. Brachytherapy with the ruthenium-106 plaque resulted in complete regression of the tumor. CONCLUSION: Tapioca melanoma of the iris should be considered in the differential diagnosis of patients presenting with nodular vascularized amelanotic iris mass and elevated IOP. Brachytherapy with ruthenium-106 seems to be an effective treatment for tapioca melanoma of the iris.

Functional interaction between the orexin-1 and CB1 receptors within the nucleus accumbens in the conditioned place preference induced by the lateral hypothalamus stimulation.

Several studies have shown that chemical stimulation of the lateral hypothalamus (LH) by carbachol induces the conditioned place preference (CPP) in rats. LH is the main source of the orexinergic neurons and sends projections to some areas of the brain such as the nucleus accumbens (NAc). We tried to determine the role of intra-accumbal orexin-1 (OX1) receptors in development (acquisition) and expression of reward-related behaviors induced by LH stimulation and involvement of CB1 cannabinoid receptors in this area. Adult male Wistar rats were unilaterally implanted by two separate cannulae into the LH and NAc. The CPP paradigm was done; conditioning scores and locomotor activities were recorded. The results showed that intra-accumbal administration of SB334867 as a selective OX1 receptor antagonist (1, 3, 10 and 30nM/0.5µl DMSO) 5min before intra-LH carbachol (250nM/0.5µl saline) during 3-day conditioning phase, could dose-dependently inhibit the development of LH-induced CPP. In expression experiments, intra-NAc administration of SB334867 on the test day could decrease the expression of LH stimulation-induced CPP. Furthermore, concurrent intra-accumbal administration of effective/ineffective doses of SB334867 and AM251 (45 and 15µM) as a CB1 receptor antagonist, before carbachol during the conditioning phase, could attenuate the development of LH stimulation-induced CPP. It seems that the orexinergic projection from the LH to the NAc is involved in the LH stimulation-induced CPP and OX1 receptor in the NAc has a substantial role in this phenomenon. Our findings also suggest the existence a functional interaction between OX1 and CB1 receptors within the NAc in place preference.

Interaction between the dopaminergic and opioidergic systems in dorsal hippocampus in modulation of formalin-induced orofacial pain in rats.

The hippocampus is a region of the brain that serves several functions. The dopaminergic system acts through D1- and D2-like receptors to interfere in pain modulation and the opioid receptors play major roles in analgesic processes and there are obvious overlaps between these two systems. The present study investigated the interaction between the opioidergic and dopaminergic systems in the dorsal hippocampus (CA1) region for formalin-induced orofacial pain. Two guide cannulae were stereotaxically implanted in the CA1 region and morphine (0.5, 1, 2 and 4 µg/0.5 µl saline) and naloxone (0.3, 1 and 3 µg/0.5 µl saline) were used as the opioid receptor agonist and antagonist, respectively. SKF-38393 (1 µg/0.5 µl saline) was used as a D1-like receptor agonist, quinpirole (2 µg/0.5 µl saline) as a D2-like receptor agonist, SCH-23390 (0.5 µg/0.5 µl saline) as a D1-like receptor antagonist and sulpiride (3 µg/0.5 µl DMSO) as a D2-like receptor antagonist. To induce orofacial pain, 50 µl of 1% formalin was subcutaneously injected into the left side of the upper lip. Our results showed that different doses of morphine significantly reduced orofacial pain in both phases induced by formalin. Naloxone (1 and 3 µg) reversed morphine induced analgesia in CA1. SKF-38393 and quinpirole with naloxone (1 µg) significantly decreased formalin-induced orofacial pain in both phases. SCH-23390 had no effect on the antinociceptive response of morphine in both phases of orofacial pain. Sulpiride reversed the antinociceptive effects of morphine only in the first phase, but this result was not significant. Our findings suggest that there is cross-talk between the opioidergic and dopaminergic systems. Opioidergic neurons also exerted antinociceptive effects by modulation of the dopaminergic system in the CA1 region of the brain.

Involvement of dopamine receptors within the dorsal hippocampus in suppression of the formalin-induced orofacial pain.

It is widely established that the dopaminergic system has profound effects on pain modulation in different regions of the brain including the hippocampus, the salient area for brain functions. The orofacial region is one of the most densely innervated (by the trigeminal nerves) areas of the body susceptible to acute and chronic pains. In this study, we tried to examine the effects of dopamine receptors located in the dorsal hippocampus (CA1) region upon the modulation of orofacial pain induced by the formalin test. To induce orofacial pain in male Wistar rats, 50µl of 1% formalin was subcutaneously injected into the upper lip. In control and experimental groups, two guide cannulae were stereotaxically implanted in the CA1, and SKF-38393 (0.25, 0.5, 1 and 2µg/0.5µl saline) as a D1-like receptor agonist, SCH-23390 (1µg/0.5µl saline) as a D1-like receptor antagonist, Quinpirole (0.5, 1, 2 and 4µg/0.5µl saline) as a D2-like receptor agonist and Sulpiride(3µg/0.5µl DMSO) as a D2-like receptor antagonist or vehicles were microinjected. For induction of orofacial pain, 50µl of 1% formalin was subcutaneously injected into the left side of the upper lip. Results indicated that SKF-38393 at the dose of 1 and 2µg significantly reduced pain during the first and second phases of observed pain while SCH-23390 reversed such analgesic effect. Moreover, there is a significant difference between groups in which animals received 2 and 4µg quinpirole or vehicle in the first phase (early phase) of pain. The three high doses of this compound (1, 2 and 4µg) appeared to have an analgesic effect during the second (late) phase. Furthermore, Sulpiride could potentially reverse the observed analgesic effects already induced by an agonist. Current findings suggest that the dorsal hippocampal dopamine receptors exert an analgesic effect during the orofacial pain test.

Involvement of CB1 receptors in the ventral tegmental area in the potentiation of morphine rewarding properties in acquisition but not expression in the conditioned place preference model.

The ventral tegmental area (VTA) is a critical part of the brain reward system and has been engaged in mediating rewarding actions. CB1 receptors are one of the receptors that mediate the actions of cannabinoids and endocannabinoids in the central nervous system. Our aim was to determine the potentiating effects of CB1 receptors within the VTA in the acquisition and expression of morphine conditioned place preference (CPP). Stereotaxic surgery was performed bilaterally on each rat to administrate WIN55,212-2 (1, 2 and 4 mmol/0.3 µl DMSO) as CB1 receptor agonist and AM251 (15, 45 and 90 mmol/0.3 µl DMSO) as CB1 receptor antagonist. A three-compartment apparatus was used for the CPP test. The results showed that two doses of WIN55,212-2 (2 and 4 mmol) potentiates the rewarding effects of ineffective dose of morphine (2 mg/kg). We did not see any significant difference between any other doses of WIN55,212-2 and vehicle in the group which received the effective dose of morphine (5mg/kg). Additionally, conditioning scores decreased significantly with the highest administrated dose of AM251 (90 mmol) compared to the vehicle group. We did not observe any significant differences in the experiments for CPP expression by WIN55,212-2 or AM251. It seems that the cannabinoid and opioid systems are in interaction with each other and affect dopaminergic and/or non-dopaminergic neurons in the VTA. Blockade of CB1 receptors may increase GABA release, resulting in the reduction of dopamine output followed by a decrease in the acquisition of morphine-induced CPP in rats.