Video game addiction is associated with early stage of inhibitory control problems: An event-related potential study using cued Go/NoGo task.

Video game addiction (VGA) is associated with cognitive problems, particularly deficits in inhibitory control. The present study aimed to investigate behavioural responses and event-related potential associated with specific response inhibition using the cued Go/NoGo task to examine the effects of VGA on brain activity related to response inhibition. Twenty-five individuals addicted to video games (action video games) and 25 matched healthy controls participated in the study. The results showed that the VGA group had significantly more commission error in the NoGo trials and faster reaction time in the Go trials compared with the control group. The event-related potential analyses revealed significant reductions in amplitudes of N2 cue and N2 NoGo in the VGA group. While there was no significant difference between the N2 amplitudes of the Go and NoGo trials in the VGA group, the control group had a larger N2 amplitude in the NoGo trials. These results indicate that VGA subjects have difficulties in the early stages of response inhibition, as well as some level of impairment in proactive cognitive control.

EEG-biomarker theta/beta ratio and attentional quotients in adults who stutter: An electrophysiological and behavioral study.

INTRODUCTION: There is increasing evidence that connects developmental stuttering to attention. However, findings have represented contradiction. Therefore, this study was conducted to investigate the possible relationship between stuttering and attention in resting and undertask conditions. METHODS: In a cross-sectional study, 26 right-handed AWS (adults who stutter) and 25 matched fluent speakers were enrolled. Demographic data were collected, and the Beck anxiety inventory (BAI) was filled out for all participants. Then, QEEG was conducted, followed by IVA2. CPT test for all subjects. Finally, data were analyzed using SPSS software version 16. RESULTS: AWS indicated significantly weaker auditory focus attention in the task (p = .02) than the control group, while a similar resting-state EEG marker of attention was found between groups (p > .05). Moreover, attention was not correlated between the two conditions (p > .05). CONCLUSION: The EEG marker of attention did not necessarily designate the attentional performance of AWS under the task. Furthermore, attentional skills could be considered in the assessment and therapeutic programs of at least some groups of AWS.

Proactive and reactive inhibitory control are differently affected by video game addiction: An event-related potential study.

INTRODUCTION: Video game addiction (VGA) is associated with physical and mental disorders, one of which is problem in executive function, particularly inhibitory control. The present study aimed to investigate reactive and proactive inhibitory controls by event-related potential (ERP). METHODS: Thirty video game (action video games)-addicted subjects and 30 matched healthy controls participated in the study, who were tested by the selective stop-signal task. RESULTS: The main results revealed that the VGA group had significantly more problems in preparatory processes and proactive stop trials, showing that VGA has a negative effect on proactive inhibition. CONCLUSION: Finding the problem in proactive inhibitory control might be helpful in developing new treatments and rehabilitation methods in these fields.

The role of basolateral amygdala orexin 1 receptors on the modulation of pain and psychosocial deficits in nitroglycerin-induced migraine model in adult male rats.

BACKGROUND: Migraine headaches have been associated with sensory hyperactivity and anomalies in social/emotional responses. The main objective of this study was to evaluate the potential involvement of orexin 1 receptors (Orx1R) within the basolateral amygdala (BLA) in the modulation of pain and psychosocial dysfunction in a nitroglycerin (NTG)-induced rat model of migraine. METHODS: Adult male Wistar rats were injected with NTG (5 mg/kg, intraperitoneal) every second day over nine days to induce migraine. The experiments were done in the following six groups (6 rats per group): untreated control, NTG, NTG plus vehicle, and NTG groups that were post-treated with intra-BLA microinjection of Orx1R antagonist SB-334867 (10, 20, and 40 nM). Thermal hyperalgesia was assessed using the hot plate and tail-flick tests. Moreover, the elevated plus maze (EPM) and open field (OF) tests were used to assess anxiety-like behaviors. The animals' sociability was evaluated using the three-chamber social task. The NTG-induced photophobia was assessed using a light-dark box. RESULTS: We observed no change in NTG-induced thermal hyperalgesia following administration of SB-334867 (10, 20, and 40 nM). However, SB-334867 (20 and 40 nM) aggravated the NTG-induced anxiogenic responses in both the EPM and OF tasks. The NTG-induced social impairment was overpowered by SB-334867 at all doses. Time spent in the dark chamber of light-dark box was significantly increased in rats treated with SB-334867 (20 and 40 nM/rat). CONCLUSIONS: The findings suggest a role for Orx1R within the BLA in control comorbid affective complaints with migraine in rats.

The involvement of orexin 1 and cannabinoid 1 receptors within the ventrolateral periaqueductal gray matter in the modulation of migraine-induced anxiety and social behavior deficits of rats.

Orexin 1 receptors (Orx1R) and cannabinoid 1 receptors (CB1R) are implicated in migraine pathophysiology. This study evaluated the potential involvement of Orx1R and CB1R within the ventrolateral periaqueductal gray matter (vlPAG) in the modulation of anxiety-like behavior and social interaction of migraineurs rats. A rat model of migraine induced by recurrent administration of nitroglycerin (NTG) (5 mg/kg/i.p.). The groups of rats (n = 6) were then subjected to intra-vlPAG microinjection of orexin-A (25, 50 pM), and Orx1R antagonist SB334867 (20, 40 nM) or AM 251 (2, 4 µg) as a CB1R antagonist. Behavioral responses were evaluated in elevated plus maze (EPM), open field (OF) and three-chambered social test apparatus. NTG produced a marked anxiety like behaviors, in both EPM and OF tasks. It did also decrease social performance. NTG-related anxiety and social conflicts were attenuated by orexin-A (25, 50 pM). However, NTG effects were exacerbated by SB334867 (40 nM) and AM251 (2, 4 µg). The orexin-A-mediated suppression of NTG-induced anxiety and social conflicts were prevented by either SB334867 (20 nM) or AM251 (2 µg). The findings suggest roles for Orx1R and CB1R signaling within vlPAG in the modulation of migraine-induced anxiety-like behavior and social dysfunction in rats.

Phytohormone abscisic acid boosts pentobarbital-induced sleep through activation of GABA-A, PPARß and PPARγ receptor signaling.

BACKGROUND: Sleep disorders induce anxiety and forgetfulness and change habits. The chemical hypnotic drugs currently used have serious side effects and, therefore, people are drawn towards using natural compounds such as plant-based healing agents. Abscisic acid (ABA) is produced in a variety of mammalian tissues and it is involved in many neurophysiological functions. OBJECTIVE: To investigate the possible effect of ABA on pentobarbital-induced sleep and its possible signaling through GABA-A and PPAR (γ and ß) receptors, in male Wistar rats. METHODS: The possible effect of ABA (5 and 10 µg/rat, intracerebroventricularly) on sleep onset latency time and duration was evaluated in a V-maze model of sleep. Pentobarbital sodium (40 mg/kg, intraperitoneally) was injected to induce sleep 30 min after administration of ABA. PPARß (GSK0660, 80 nM/rat), PPARγ (GW9662, 3 nM/rat) or GABA-A receptor (bicuculline, 6 µg/rat) antagonists were given 15 min before ABA injection. Diazepam (2 mg/kg, intraperitoneally) was used as a positive control group. RESULTS: ABA at 5 µg significantly boosted the pentobarbital-induced subhypnotic effects and promoted induction of sleep onset in a manner comparable to diazepam treatment. Furthermore, pretreatment with bicuculline significantly abolished the ABA effects on sleep parameters, while the amplifying effects of ABA on the induction of sleep onset was not significantly affected by PPARß or PPARγ antagonists. The sleep prolonging effect of ABA was significantly prevented by both PPAR antagonists. CONCLUSIONS: The data showed that ABA boosts pentobarbital-induced sleep and that GABA-A, PPARß and PPARγ receptors are, at least in part, involved in ABA signaling.

Phytohormone abscisic acid boosts pentobarbital-induced sleep through activation of GABA-A, PPARß and PPARγ receptor signaling / O fito-hormônio ácido abscísico estimula o sono induzido por fenobarbital por meio de ativação da sinalização de receptores GABA-A, PPARß e PPARγ

ABSTRACT Background: Sleep disorders induce anxiety and forgetfulness and change habits. The chemical hypnotic drugs currently used have serious side effects and, therefore, people are drawn towards using natural compounds such as plant-based healing agents. Abscisic acid (ABA) is produced in a variety of mammalian tissues and it is involved in many neurophysiological functions. Objective: To investigate the possible effect of ABA on pentobarbital-induced sleep and its possible signaling through GABA-A and PPAR (γ and β) receptors, in male Wistar rats. Methods: The possible effect of ABA (5 and 10 µg/rat, intracerebroventricularly) on sleep onset latency time and duration was evaluated in a V-maze model of sleep. Pentobarbital sodium (40 mg/kg, intraperitoneally) was injected to induce sleep 30 min after administration of ABA. PPARβ (GSK0660, 80 nM/rat), PPARγ (GW9662, 3 nM/rat) or GABA-A receptor (bicuculline, 6 µg/rat) antagonists were given 15 min before ABA injection. Diazepam (2 mg/kg, intraperitoneally) was used as a positive control group. Results: ABA at 5 µg significantly boosted the pentobarbital-induced subhypnotic effects and promoted induction of sleep onset in a manner comparable to diazepam treatment. Furthermore, pretreatment with bicuculline significantly abolished the ABA effects on sleep parameters, while the amplifying effects of ABA on the induction of sleep onset was not significantly affected by PPARβ or PPARγ antagonists. The sleep prolonging effect of ABA was significantly prevented by both PPAR antagonists. Conclusions: The data showed that ABA boosts pentobarbital-induced sleep and that GABA-A, PPARβ and PPARγ receptors are, at least in part, involved in ABA signaling.

RESUMO Introdução: Os distúrbios do sono induzem a ansiedade e esquecimento e mudam hábitos. Os medicamentos hipnóticos químicos utilizados atualmente têm efeitos colaterais graves e, portanto, as pessoas são atraídas para o uso de compostos naturais, como agentes de cura à base de plantas. O ácido abscísico (ABA) é produzido em uma variedade de tecidos de mamíferos e está envolvido em muitas funções neurofisiológicas. Objetivo: Investigar o possível efeito do ABA no sono induzido por pentobarbital e sua possível sinalização por meio dos receptores GABA-A e PPAR (γ e β), em ratos Wistar machos. Métodos: O possível efeito do ABA (5 e 10 µg/rato, intracerebroventricularmente) no tempo de latência e duração do início do sono foi avaliado em um modelo de labirinto em V de sono. Pentobarbital sódico (40 mg/kg, intraperitonealmente) foi injetado para induzir o sono 30 minutos após a administração de ABA. PPARβ (GSK0660, 80 nM/rato), PPARγ (GW9662, 3 nM/rato) ou antagonistas do receptor GABA-A (bicuculina, 6 µg/rato) foram administrados 15 minutos antes da injeção de ABA. Diazepam (2 mg/kg, intraperitonealmente) foi utilizado como grupo de controle positivo. Resultados: ABA a 5 µg aumentou significativamente os efeitos sub-hipnóticos induzidos por pentobarbital e promoveu a indução do início do sono de forma comparável ao tratamento com diazepam. Além disso, o pré-tratamento com bicuculina aboliu significativamente os efeitos do ABA nos parâmetros do sono, ao passo que os efeitos amplificadores do ABA na indução do início do sono não foram significativamente afetados pelos antagonistas do PPARβ ou PPARγ. O efeito de prolongamento do sono do ABA foi significativamente prevenido por ambos os antagonistas do PPAR. Conclusões: Os dados mostraram que o ABA estimula o sono induzido por pentobarbital e que os receptores GABA-A, PPARβ e PPARγ estão, pelo menos em parte, envolvidos na sinalização ABA.

Symmetrical electrophysiological brain responses to unilateral and bilateral auditory stimuli suggest disrupted spatial processing in schizophrenia.

Research has found auditory spatial processing deficits in patients with schizophrenia (SCZ), but no study has examined SCZ patients' auditory spatial processing at both pre-attentional and attentional stages. To address this gap, we investigated schizophrenics' brain responses to sounds originating from different locations (right, left, and bilateral sources). The event-related potentials (ERPs) of 25 chronic schizophrenic patients and 25 healthy subjects were compared. Mismatch negativity (MMN) in response to frequency and duration deviants was assessed. Two P3 components (P3a and P3b) were elicited via a frequency discrimination task, and MMN and P3 were recorded through separate monaural and dichotic stimulation paradigms. Our results corroborated the previously published finding that MMN, P3a, and P3b amplitudes are reduced in SCZ patients, but they showed no significant effect of stimulus location on either MMN or P3. These results indicated similarity between the SCZ patients and healthy individuals as regards patterns of ERP responses to stimuli that come from different directions. No evidence of auditory hemispatial bias in the SCZ patients was found, supporting the existence of non-lateralized spatial processing deficits in such patients and suggesting compensatory changes in the hemispheric laterality of patients' brains.

Intra-periaqueductal gray matter administration of orexin-A exaggerates pulpitis-induced anxiogenic responses and c-fos expression mainly through the interaction with orexin 1 and cannabinoid 1 receptors in rats.

Different types of trigeminal pains are frequently associated with psychophysiological concerns. Orexin-A and orexin 1 receptor (OX1R) are involved in modulation of both trigeminal pain and anxiety responses. Ventrolateral periaqueductal gray matter (vlPAG), a controlling site for nociception and emotion, receives orexinergic inputs. Here, the role of vlPAG OX1Rs and their interaction with cannabinoid 1 (CB1) receptor was evaluated in anxiety-like behavior following capsaicin-induced dental pulp pain. Rats were cannulated in the vlPAG and orexin-A was injected at the doses of 0.17, 0.35 and 0.51 µg/rat prior to the induction of pain. The elevated plus maze (EPM) and open field (OF) tests were used for assessing the anxiety responses. In addition, the induction of c-fos, in the vlPAG, was investigated using immunofluorescence microscopy. Capsaicin-treated rats displayed significantly higher anxiogenic behavior on EPM and OF tests. Pretreatment with orexin-A (0.51 µg/rat) attenuated capsaicin-mediated nociception, while exaggerated anxiogenic responses (p < 0.05). In addition, orexin-A effects were diminished by the administration of OX1R (SB-334867, 12 µg/rat) and cannabinoid 1 (AM251, 4 µg/rat) receptor antagonists. Intradental capsaicin induced a significant increase in c-fos expression in the vlPAG that was exaggerated by orexin-A (0.51 µg/rat). Blockage of OX1R and CB1 receptors attenuated the effect of orexin-A on c-fos expression in capsaicin-treated rats. In conclusion, the data suggest that manipulation of OX1R and CB1 receptors in the vlPAG alters capsaicin-evoked anxiety like behaviors and c-fos induction in rats.

Numerical distance effect in patients with schizophrenia.

There is growing evidence showing that mental representation of numbers is impaired in patients with schizophrenia. Yet, no study has examined the distance effect in the patients. We assessed the distance effect using two number size comparison tasks, with different number references (5 and 7) in 23 patients and 28 healthy individuals. Response times and error rates significantly increased when the distances between the centered references and the targets decreased in both groups. However, patients responded significantly slower and had more error rates compared to controls. Our finding indicates distance effect in patients is similar to the controls, indicating an automatic numerical processing is preserved in patients with schizophrenia.

An evidence for lack of pseudoneglect in patients with schizophrenia: an ERP study.

Studies have reported an altered expression of pseudoneglect in patients with schizophrenia, but no study has examined pseudoneglect in schizophrenia at the neural level. We investigated pseudoneglect using the visual P3 event-related potential and the mental number bisection (MNB) task in 21 patients and 25 controls. Using an oddball task, participants were asked to discriminate an infrequent ('one' or 'nine') from a frequent written number ('five'). The P3 ERP components were delayed to the targets on the right of the MNL ('nine') compared to the targets on the left ('one') in controls. The effect of number magnitude on the P3 latency was not observed in the patients. In MNB task, the patients did not show the normal leftward bias observed in healthy individuals. Our findings indicate a lack of pseudoneglect and the presence of an anomalous brain asymmetry in schizophrenia.