This manuscript reviews the extant literature on key issues related to mobile gambling and considers whether the potential risks of harm emerging from this platform are driven by pre-existing comorbidities or by psychological processes unique to mobile gambling. We propose an account based on associative learning that suggests this form of gambling is likely to show distinctive features compared with other gambling technologies. Smartphones are a rapidly growing platform on which individuals can gamble using specifically designed applications, adapted websites or text messaging. This review considers how mobile phone use interacts with psychological processes relevant to gambling, the games users are likely to play on smartphones, and the interactions afforded by smartphones. Our interpretation of the evidence is that the schedules of reinforcement found in gambling interact with the ways in which people tend to use smartphones that may expedite the acquisition of maladaptive learned behaviours such as problem gambling. This account is consistent with existing theories and frameworks of problem gambling and has relevance to other forms of mobile phone use.
Whilst the world sees the tremendous growth of mobile phone technology, radiofrequency electromagnetic radiation (RF-EMR) induced possible health effects have emerged as a topic of recent day debate. The current study is designed to test the hypothesis that chronic 900 MHz radiation exposure would potentially dysregulate the stress response system (HPA axis) in vivo, via, its non-thermal mechanisms, leading to alterations in the microarchitecture of the adrenal gland, vulnerable brain regions such as the hippocampus which may results in altered behaviours in rats. Male albino Wistar rats aged four weeks, weighing 50-60 g were subjected to 900 MHz radiation from a mobile phone for four weeks at a rate of one hour per day. On the 29th day, animals from the control, sham exposed and RF-EMR exposed groups were tested for contextual fear conditioning. They were later euthanized to study hippocampal and adrenal gland cytoarchitecture. Bright and dark compartment transitions in the avoidance box were considerably elevated in the RF-EMR exposed group and they exhibited a significant decrease in the latency to enter the dark compartment during the contextual fear conditioning test. Apoptosis was apparent in the CA3 region and perivascular space was significantly increased in the hippocampus of the radiation-exposed group. In addition to lymphocytic infiltrates, congested sinusoids, apoptotic-like changes were evident in the zona fasciculata of the adrenal gland. However, the cytoarchitecture of the adrenal medulla was comparable in all three groups. Chronic RF-EMR exposure caused changes in contextual fear conditioning, enlargement of hippocampal perivascular space, apparent CA3 apoptosis, and apoptotic-like changes in the zona fasciculata of the adrenal gland in rats.
Orexins (also called hypocretins) are implicated in reward and addiction, but little is known about their role(s) in the association between hippocampal synaptic plasticity and drug preference. Previously, we found that exogenous orexin via OX1 and OX2 receptors can impair low frequency stimulation-induced depotentiation, i.e. restoring potentiation of excitatory synaptic transmission (re-potentiation) in mouse hippocampal slices. Here, we found this re-potentiation in hippocampal slices from mice that had acquired conditioned place preference (CPP) to cocaine. Both 10 and 20 mg/kg of cocaine induced similar magnitudes of CPP in mice and re-potentiation in their hippocampal slices, but differed in their susceptibility to TCS1102, a dual (OX1 and OX2 ) orexin receptor antagonist. TCS1102 significantly attenuated CPP and hippocampal re-potentiation induced by cocaine at 10 mg/kg but not at 20 mg/kg. Nonetheless, SCH23390, an antagonist of dopamine D1-like receptors (D1-likeRs), inhibited the effects induced by both doses of cocaine. SKF38393, a D1-likeR-selective agonist, also induced hippocampal re-potentiation in vitro. Interestingly, this effect was attenuated by TCS1102. Conversely, SCH23390 prevented orexin A-induced hippocampal re-potentiation. These results suggest that endogenous orexins are released in mice during cocaine-CPP acquisition, which sustains potentiated hippocampal transmission via OX1 /OX2 receptors and may contribute to the addiction memory of cocaine. This effect of endogenous orexins, however, may be substituted by dopamine that may dominate hippocampal re-potentiation and CPP via D1-likeRs when the reinforcing effect of cocaine is high.