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Background: Borderline personality disorder (BPD) has been considered a psychiatric disorder, the effective pharmacological treatments for which have not been well established. Objectives: This study aimed to assess the efficacy of memantine (10 mg/day) in reducing BPD severity and cognitive impairment. Methods: The BPD patients diagnosed by psychologists were included and divided into the placebo (n = 19) and memantine (n = 20) groups. Included participants were randomized, double-blinded, and stabilized on the medication and psychotherapy for at least four weeks. The patients in the memantine group received oral memantine (10 mg/day) for four weeks. The severity of BPD was assessed by a self-reported questionnaire named Borderline Evaluation of Severity Over Time (BEST). Moreover, the Wisconsin test was carried out to assess executive function. Results: The mean score of the BEST test significantly decreased in week eight post-treatment in the memantine group. In addition, a significant decrease in this score was indicated in the memantine group compared to the placebo group in week eight. The mean total score of the BEST test was not significantly different before and after the placebo administration. There was no significant difference in the Wisconsin subscales, including the number of wrong answers and categories achieved after memantine or placebo administration. Perseverative errors rose after the administration of memantine. Adverse side effects did not occur in any of the participants. Conclusions: Our findings suggested the potential therapeutic effects of memantine for BPD. Furthermore, we found that a low dose of meantime might be preferable to prevent the side effects. [ABSTRACT FROM AUTHOR]

Background: Neurostimulation is one of the new therapeutic approaches in patients with drug-resistant epilepsy, and despite its high efficiency, its mechanism of action is still unclear. On the one hand, electrical stimulation in the human brain is immoral; on the other hand, the creation of the epilepsy model in laboratory animals affects the entire brain network. As a result, one of the ways to achieve the neurostimulation mechanism is to use epileptiform activity models In vitro. In vitro models, by accessing the local network from the whole brain, we can understand the mechanisms of action of neurostimulation., Methods: A literature search using scientific databases including PubMed, Google Scholar, and Scopus, using "Neurostimulation" and "epileptiform activity" combined with "high-frequency stimulation", " low-frequency stimulation ", and "brain slices" as keywords were conducted, related concepts to the topic gathered and are used in this paper., Results: Electrical stimulation causes neuronal depolarization and the release of GABAA, which inhibits neuronal firing. Also, electrical stimulation inhibits the nervous tissue downstream of the stimulation site by preventing the passage of nervous activity from the upstream to the downstream of the axon., Conclusion: Neurostimulation techniques consisting of LFS and HFS have a potential role in treating epileptiform activity, with some studies having positive results. Further investigations with larger sample sizes and standardized outcome measures can be conducted to validate the results of previous studies., Competing Interests: The authors declare that they have no competing interests., (© 2023 Iran University of Medical Sciences.)

Introduction: Spreading depression (SD) is a propagating wave of depolarization followed by depression of the neuroglial activities and can modulate extracellular dopamine concentrations in the neocortex. It has been shown that the dopaminergic system plays a role in migraine. SD has been suggested as a critical phenomenon in the pathophysiology of migraine. The aim of this study was to investigate the effect of dopamine D2 receptors on the characteristic features of SD in rat neocortical tissues., Methods: The effect of dopamine D2 receptor agonist quinpirole and D2 receptor antagonist sulpiride was tested on different characteristic features (amplitude, duration and velocity) of KCl-induced SD in somatosensory neocortical slices of adult rats. The effect of above-mentioned substances on production of long-term potentiation (LTP) in the neocortex was also evaluated., Results: The present data revealed a dose-dependent suppression of the amplitude and duration of SD in the presence of the dopamine D2 receptor antagonist sulpiride in the neocortex. D2 dopamine receptor agonist quinpirole dose-dependently enhanced the amplitude and duration of the neocortical SD. Furthermore, application of D2 receptor antagonist significantly suppressed induction of LTP., Discussion: These results indicate that D2 receptors modulate the initiation of SD in the neocortex. This finding refers to the potential role of D2 receptor antagonist in treatment of migraine pain.