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Migraine, a complex disorder, is characterized by recurrent headache episodes. The production of melatonin in the pineal gland, which is crucial for controlling circadian rhythms and sleep–wake cycles, is altered in various conditions, including neurological disorders such as migraine. Recent studies underscore the significance of serum melatonin levels in patients with chronic and episodic migraine, the focus of this study. This case‒control study, conducted from September 2017 to June 2020 in Tehran, Iran, selected potential participants aged 18–65 years from a headache clinic at Sina Hospital (affiliated with Tehran University of Medical Sciences). Both episodic migraine and chronic migraine were diagnosed following the diagnostic criteria in the International Classification of Headache Disorders' third edition. Melatonin levels were measured according to the instructions of the ELISA kits. There were significant differences in the frequency of headache days and the duration of abortive medication usage between the two groups (P value < 0.001). Besides, analysis revealed significantly lower serum melatonin levels in patients with episodic ((80.45–45.06) 72.83) and chronic migraine ((154.34–63.34) 70.38, P value < 0.001) than in healthy controls (281.25–160.86) 280). Although no considerable differences were found between episodic and chronic migraine patients, the current study demonstrated that serum melatonin levels were substantially greater in healthy controls than in patients with migraine. [ABSTRACT FROM AUTHOR]

Background: Regular moderate exercise and endogenous cannabinoid activity have independently been shown to alleviate seizure (SE) attacks. Objectives: This study aimed to investigate the effect of physical activity on the expression levels of cannabinoid CB1 and CB2 receptors in the brains Methods: Male Wistar rats were divided into five groups: Sham, SE, physical activity (PA), PA + SE, and PA before SE. Epileptic SEs were induced by administering pentylenetetrazol (PTZ; intraperitoneally, 35 mg/kg) every other day for four weeks in the SE, PA + SE, and PA before SE groups. Animals in the PA, PA + SE, and PA before SE groups participated in treadmill running (30 minutes per day, five days a week). The mean number of cortical and hippocampal (CA1, CA3) CB1 and CB2 receptors was assessed using immunohistochemistry. Results: The study data revealed a significant reduction of CB1 and CB2 receptors in the CA1, CA3, and cortex of the SE group compared to the sham group. A significant increase in CB1 receptors was observed in the PA and PA before SE groups compared to the SE group in both cortical and hippocampal areas. Physical activity significantly increased hippocampal and cortical CB2 receptor distribution in the PA, PA + SE, and PA before SE groups compared to the SE group. Conclusions: These findings suggest that exercise modulates the expression of hippocampal and cortical cannabinoid receptors in epileptic rats, highlighting the involvement of the endocannabinoid pathway in the anti-epileptic effects of exercise. [ABSTRACT FROM AUTHOR]

Background: Epilepsy is one of the most important diseases of the central nervous system, for which has no definitive treatment. Neurotrophic factors increase the survival of nerve cells and improve the treatment of neurological diseases. Identifying factors that affect the increase of neurotrophins in the brain is an important goal for brain health and function. Objectives: This study aimed to investigate the effectiveness of exercise on neurotrophic factors by influencing the expression of vanilloid receptor type 1 (TRPV1). Methods: Convulsions were induced by injecting pentylenetetrazol (PTZ; 35 mg/kg) five hours after exercise. Animals were divided into five groups: sham (Sham), seizure (PTZ), exercise (EX), exercise with seizure induction (EX+PTZ), and exercise before seizure induction (EX-PTZ). The exercise was 30 minutes of forced running on a treadmill, five days a week for four weeks. Results: The average percentage of NGF cells in the exercise groups (EX), exercise with seizure induction (EX+PTZ), and exercise before seizure induction (EX-PTZ), and GDNF in the exercise group with seizure induction (EX+PTZ) had a significant increase compared to the seizure group (PTZ). Also, TRPV1 activity in exercise groups (EX), exercise with seizure induction (EX+PTZ), and exercise before seizure induction (EX-PTZ) showed a significant increase compared to the seizure group (PTZ). Conclusions: Our findings suggested the possible antiepileptic and antiepileptogenesis effects of exercise through activation of neurotrophic factors and TRPV1 modulation. [ABSTRACT FROM AUTHOR]

Background: A variety of receptors may be involved in the pathogenesis of absence seizures. The c-Met receptors have a critical role in modulating the GABAergic interneurons and creating a balance between excitatory and inhibitory neurotransmission, sensorimotor gating, and normal synaptic plasticity. Objectives: This study aimed to assess the changes of the c-Met receptor during the appearance of absence attacks in the experimental model of absence epilepsy. Methods: A total of 48 animals were divided into four groups of two- and six-month-oldWAG/Rij and Wistar rats. EpilepticWAG/Rij rats showingSWPin electrocorticogram (ECoG) were included in the epileptic group. The two-month-oldWAG/Rij rats as well as twoand six-month-old Wistar rats not exhibiting SWP in ECoG were selected as the non-epileptic. Gene (RT-PCR) and protein expression (western blotting) of c-Met receptors as well as c-Met protein distribution (immunohistochemistry) in the somatosensory cortex and hippocampus were assessed during seizure development of the absence attacks. Results: According to the study findings, a lower c-Met gene and protein expression, as well as a lower protein distribution, were observed in the hippocampus (P < 0.001, P < 0.05, and P < 0.001, respectively) and cortex (P < 0.01, P < 0.001 and P < 0.001, respectively) of the two-month-old WAG/Rij rats compared to the same-age Wistar rats. Moreover, the data revealed a reduction of hippocampal and cortical c-Met protein expression (P < 0.001, for both) in six-month-old WAG/Rij rats compared to two-monthold ones. Six-month-oldWAG/Rij rats had a lower cortical c-Met gene (P < 0.05) and protein expression (P < 0.001) as well as lower hippocampal and cortical protein distribution (P < 0.05 and P < 0.001) than the same-age Wistar rats. Conclusions: In sum, the c-Met receptor was found to play a significant role in the development of absence epilepsy. This receptor, therefore, may have been considered as an effective goal for absence seizure inhibition. [ABSTRACT FROM AUTHOR]

Introduction: The footprint of Neuregulin 1 (NRG1) / ERbB4 in the pathophysiology of some neurological disorders and TRPV1 regulation has been indicated. The alterations in NRG1 and ErbB4 as well as the TRPV1 signaling pathway were investigated during the development of absence epilepsy in the genetic animal model of absence epilepsy. Methods: Male WAG/Rij and Wistar rats were divided into four experimental groups of two and six months of age. The protein levels of NRG1, ERbB4, and TRPV1 were measured in the somatosensory cortex and hippocampus. Results: The cortical protein levels of NRG1 and ErbB4 in the 6-month-old WAG/Rij rats were lower than in Wistar rats. Protein levels of TRPV1 were lower in two- and six-month-old WAG/Rij rats compared to age-matched Wistar rats. Hippocampal protein levels of NRG1 in 6-month-old WAG/Rij rats were lower than two-month-old WAG/Rij rats. Low levels of ErbB4 protein in two-month-old and high levels in six-month-old WAG/Rij rats were found compared to Wistar rats. Protein levels of TRPV1 were lower in the two-month-old and higher in the six-month-old WAG/Rij rats compared to age-matched Wistar rats. Furthermore, a high correlation between NRG1/ERbB4 and TRPV1 expressions in the cortex and hippocampus was indicated. The expression of NRG1/ERbB4 and TRPV1 followed a similar pattern during the life span of Wistar and WAG/Rij rats. Conclusion: Our findings indicated the potential role of the NRG1/ErbB4 pathway as well as TRPV1 in the pathogenesis of absence epilepsy. The regulatory effect of the ERbB4 receptor on the TRPV1 expression has been suggested following the similar pattern of expression. [ABSTRACT FROM AUTHOR]

Introduction: Intermittent fasting diet (IFD) has been known as a supplementary therapy for epilepsy. The main mechanisms involved in the anti-epileptic effect of IFD have not been well understood. This study has investigated the effect of IFD on hippocampal glutamic acid decarboxylase enzyme (GAD65) expression as a critical enzyme to fast modulation of GABA level. Method: Male adult rats were divided into 4 groups of sham, seizure, fasting & seizure, and pre-seizure fasting. Seizures were induced by pentylenetetrazol (PTZ) injection every other day for 4 weeks. The protocol of IFD was alternate-day feeding (24 hours of access to food every 48). In the pre-seizure fasting group, rats were put on the alternate-day feeding schedule for weeks 1-8 and PTZ was injected every other day in weeks 5-8. Hippocampal level and distribution of GAD65 have evaluated using western blotting and immunofluorescence analysis respectively. Result: Study findings revealed a significant reduction of seizure behavior scores in the pre-seizure fasting group on days 10, 16, 20, and 22. In the CA3 area, expression of GAD65 decreased in the seizure group compared to the sham group. In the CA1 area, expression of GAD65 increased significantly in both fasting groups compared to the seizure group. Moreover, the hippocampal protein level of GAD65 increased significantly in both fasting groups compared to the seizure group. Conclusion: The IFD before seizure induction has more potential to modulate the development of seizure behaviors, compared to IFD simultaneously with seizure. [ABSTRACT FROM AUTHOR]

INTRODUCTION: Autism spectrum disorder (ASD) is a neurodevelopmental disorder. The major etiological mechanism lies in glutamatergic/GABAergic imbalance. The aim of this study was to evaluate the plasma levels of glutamic acid decarboxylase 65 ( GAD65) protein in mildly and severely autistic patients, and also to compare plasma GAD65 concentration in mild and severe autism. METHOD: In total, 62 autistic patients (aged 6-9 years) and 17 age-matched neurotypically healthy controls were included in the study. The diagnosis, as well as the level of autism, was assessed by applying the Gilliam Autism Rating Scale. Plasma GAD65 protein level was determined using an enzyme-linked immunosorbent assay (ELISA) kit for GAD65. RESULTS: Our findings showed no remarkable alteration in plasma GAD65 concentration in patients with mild autism as compared to healthy subjects, while patients with severe autism showed an increased plasma level of GAD65 as compared to healthy controls and mildly autistic patients. CONCLUSION: Our findings suggest the level of plasma GAD65 to be considered a potential diagnostic biomarker for the severity of autism (Fig. 2, Ref. 40). Text in PDF www.elis.sk [ABSTRACT FROM AUTHOR]

Objectives: This study aimed to investigate the role of serum levels of transient receptor potential cation channel subfamily V member 1 (TRPV1), vasoacive intestinal peptide (VIP), and pituitary adenylate cyclase-activating polypeptide (PACAP) in the development and also the transformation of migraine in patients suffering from migraine. Methods: Eighty-nine participants with a mean age of 39 years were divided into 23 episodic migraine (EM), 36 chronic migraine (CM), and 30 healthy control groups. Demographic, anthropometric, and headache characteristic information, and also blood samples, was collected. Serum levels of TRPV1, VIP, and PACAP were measured using the enzyme-linked immunosorbent assay (ELISA) technique. Results: Based on our findings, the serum level of TRPV1 was significantly higher in CM compared to the control group (p < 0.05), whereas serum levels of VIP (p < 0.01) and PACAP (p < 0.05) in the EM group were significantly more than the control group. There was no significant difference between EM and CM groups. Conclusions: An elevation in the serum levels of TRVP1 among chronic migraineurs and increments in the levels of VIP and PACAP were observed among EM patients compared to healthy subjects. However, our data failed to demonstrate the probable role of these biomarkers in migraine progression, and more studies are needed to clarify the molecular mechanisms involved in migraine progression. [ABSTRACT FROM AUTHOR]

Abstract Background Essential oil of Pimpinella anisum L. Apiaceae (anise oil) has been widely used in traditional Persian medicine to treat a variety of diseases, including some neurological disorders. This study was aimed to test the possible anti-seizure and anti-hypoxia effects of anise oil. Methods The effects of different concentrations of anise oil were tested on seizure attacks induced by pentylenetetrazol (PTZ) injection and neuronal hypoxia induced by oxygen withdrawal as well as on production of dark neurons and induction of long-term potentiation (LTP) in in vivo and in vitro experimental models of rat brain. Results Anise oil significantly prolonged the latency of seizure attacks and reduced the amplitude and duration of epileptiform burst discharges induced by injection of intraperitoneal PTZ. In addition, anise oil significantly inhibited production of dark neurons in different regions of the brain in epileptic rats. Anise oil also significantly enhanced the duration of the appearance of anoxic terminal negativity induced by oxygen withdrawal and inhibited induction of LTP in hippocampal slices. Conclusions Our data indicate the anticonvulsant and neuroprotective effects of anise oil, likely via inhibition of synaptic plasticity. Further evaluation of anise oil to use in the treatment of neurological disorders is suggested.

Introduction: Absence epilepsy is a brief non-convulsive seizure associated with sudden abruptness in consciousness. Because of the unpredictable occurrence of absence seizures and the ethical issues of human investigation on the pathogenesis and drug assessment, researchers tend to study animal models. This paper aims to review the advantages and disadvantages of several animal models of nonconvulsive induced seizure. Methods: The articles that were published since 1990 were assessed. The publications that used genetic animals were analyzed, too. Besides, we reviewed possible application methods of each model, clinical types of seizures induced, purposed mechanism of epileptogenesis, their validity, and relevance to the absence epileptic patients. Results: The number of studies that used genetic models of absence epilepsy from years of 2000 was noticeably more than pharmacological models. Genetic animal models have a close correlation of electroencephalogram features and epileptic behaviors to the human condition. Conclusion: The validity of genetic models of absence epilepsy would motivate the researchers to focus on genetic modes in their studies. As there are some differences in the pathophysiology of absence epilepsy between animal models and humans, the development of new animal models is necessary to understand better the epileptogenic process and, or discover novel therapies for this disorder. [ABSTRACT FROM AUTHOR]

AMPA receptors, consisting of glutamate receptor type1 (GluR1) subunit are involved in the pathophysiology of some neurological disorders. In this study, the role of the GluR1 subunit in the development, as well as features of absence seizures were assessed. Both Wistar and WAG/Rij (a genetic animal model of absence epilepsy) rats with 2 and 6-month ages were included in the study. The expression of GluR1 was measured in the somatosensory cortex. Moreover, the effects of pharmacological activation and inhibition of AMPA receptors on the characteristic of absence epileptic activities were evaluated by microinjection of agonist or antagonist of AMPA receptors on the somatosensory cortex in the epileptic WAG/Rij rats. Distribution of the GluR1 subunit of AMPA receptors in the both IV (p < 0.001) and VI (p < 0.01) layers of the somatosensory cortex in the epileptic WAG/Rij rats was higher than non-epileptic animals. In addition, the microinjection of AMPA receptors agonist on the somatosensory cortex of the WAG/Rij rats increased both amplitude (p < 0.01) and duration (p < 0.001) of spike-wave discharges (SWDs), while injection of antagonist reduced amplitude (p < 0.001) and duration (p < 0.01) of SWDs in the somatosensory cortex of epileptic rats. The high expression of GluR1 in the somatosensory cortex of epileptic rats suggests the role of AMPA receptors consisting of the GluR1 subunit in the development of absence seizures. The modulatory effects AMPA receptors on the feature of SWDs suggest the potential of AMPA receptors antagonists as a therapeutic target for absence epilepsy. [ABSTRACT FROM AUTHOR]

The critical role of Notch signaling has been shown in the pathogenesis of some neurological disorders including schizophrenia, epilepsy and Alzheimer's disease. This study was aimed to evaluate the role of Notch 1 receptor in epileptogenesis as well as seizure characteristics. The animals were divided into three groups of sham, early stage and end stage. In sham group: Normal saline was injected intraperitoneally (ip) in the same as protocol of pentylenetetrazol (PTZ) injection. PTZ was injected (ip) every 48 hr over a period of 1 week in the group of early stage and over a period of 4 weeks in the end stage. The gene expression as well as distribution of Notch 1 receptor was assessed in the parietal cortex and hippocampus. In addition, the effect of agonist or antagonist of Notch 1 receptor was assessed on the epileptic discharges induced by PTZ injection. The gene expression of Notch 1 decreased in the hippocampus significantly in the end‐stage group compared with sham, and early groups. Furthermore, distribution of Notch 1 receptor increased in the somatosensory cortex and decreased in the CA1 hippocampal area in the end‐stage group. Intraventricular microinjection of Notch 1 agonist significantly increased the amplitude as well as frequency of spikes and decreased the latency of first epileptic discharges. Our findings illustrate the critical role of Notch signalling as a potential pathway in the epileptogenesis during development of chronic seizures. [ABSTRACT FROM AUTHOR]

• Soluting effect occurring in alcoholic systems composed of two polymers. • Ethanolic, propanolic, or butanolic solutions of two polymers were studied. • Iso-solvent activity lines of the systems were obtained by the isopiestic method. • The polymers PVP, PEG, PPG, and PEGDME were considered. • The mixtures of PVP with PEG, PPG and PEGDME show the soluting-in effect. • The mixtures of two polymers of PEG, PPG and PEGDME show the semi-ideal behavior. Aiming at scrutinizing the soluting effect occurring in alcoholic systems composed of two polymers (polymer 1 + polymer 2 + alcohol systems), the systematic isopiestic measurements of the vapor-liquid equilibrium behavior were carried out on some ternary ethanolic, propanolic, and butanolic solutions of two polymers at 298.1 K. In order to cover a wide range of hydrophilic and lipophilic behaviors, the polymers: polyethylene glycol 400 (PEG400), polyethylene glycol dimethyl ether 250 (PEGDME250), polyethylene glycol dimethyl ether 500 (PEGDME500), polypropylene glycol 400 (PPG400), polypropylene glycol 1000 (PPG1000) and polyvinylpyrrolidone 10,000 (PVP10000) were selected. Deviations of isosolvent activity lines from the linear isopiestic relation (LIR) were considered as a benchmark to identify the soluting effects of polymer 1 on polymer 2 in these systems. It was found that all the investigated solutions containing PVP show the soluting-in effect (positive deviation from the linear isopiestic relation), and the other solutions including PEG-PPG, PEG-PEGDME, PPG-PEGDME, PEG-PEG, PPG-PPG and PEGDME-PEGDME show the semi-ideal (linear isopiestic relation) behavior. The effect of alcohol type, polymer type, and polymer molar mass on the solvent activity of binary alcohol-polymer solutions as well as on the deviations of ternary systems from the semi-ideal behavior was studied. Finally, the obtained solvent activity data were used to calculate the vapor pressure of solutions as a function of concentration, and the segment-based local composition Wilson model was used to correlate the experimental solvent activity data. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is the most popular type of dementia in elderly and is described by a progressive loss of cognitive capacity and severe neurodegeneration which typically begins with memory deficits. The major biomarkers of AD include total tau, phosphorylated-tau and 42 amino acid isoform of amyloid beta that reflect neurodegeneration and indicate the pathophysiological processes in AD. Biomarkers have been analyzed in different kinds of body fluid. Cereberospinal fluid (CSF) biomarkers are particularly valuable to discriminate early AD from other diseases associated with memory impairment. However, access to CSF is invasive and researchers try to find valuable biomarkers in other body fluids. In this article, we reviewed different kinds of biomarkers and their validity to diagnose and effectiveness in AD therapy. [ABSTRACT FROM AUTHOR]

Childhood absence epilepsy (CAE) is an epilepsy syndrome with seizures occurring in the early childhood, highlighting that seizures susceptibility in CAE is dependent on brain development. The Notch 1 signalling pathway is important in brain development, yet the role of the Notch1 signalling pathway in CAE remains elusive. We here explored Notch1 and its modulator notchless homologue 1 (NLE1) expression in WAG/Rij and control rats using immunohistochemistry. Functional Notch 1 effects were assessed in WAG/Rij rats in vivo. WAG/Rij rats lack the developmental increase in cortical Notch1 and NLE 1 mRNA expression seen in controls, and Notch 1 and NLE1 mRNA and protein expression were lower in somatosensory cortices of WAG/Rij rats when compared to controls. This coincided with an overall decreased cortical GFAP expression in the early development in WAG/Rij rats. These effects were region-specific as they were not observed in thalamic tissues. Neuron-to-glia ratio as a marker of the impact of Notch signalling on differentiation was higher in layer 4 of somatosensory cortex of WAG/Rij rats. Acute application of Notch 1 agonist Jagged 1 suppressed, whereas DAPT, a Notch antagonist, facilitated spike and wave discharges (SWDs) in WAG/Rij rats. These findings point to Notch1 as an important signalling pathway in CAE which likely shapes architectural organization of the somatosensory cortex, a region critically involved in developmental epileptogenesis in CAE. More immediate effects of Notch 1 signalling are seen on in vivo SWDs in CAE, pointing to the Notch 1 pathway as a possible treatment target in CAE. [ABSTRACT FROM AUTHOR]

Objectives: The potential use of garlic for prevention and treatment of different types of headaches has been suggested by several medieval literatures. Cortical spreading depression (CSD), a propagating wave of neuroglial depolarization, was established as a target for anti-migraine drugs. This study was designed to investigate the effect of garlic extract on CSD in adult rats. Methods: CSD was induced by KCl microinjection in the somatosensory cortex. The effects of five different concentrations of garlic oil (1–500 μl/l) were tested on different characteristic features of CSD in necocortical slices. Inin vivoexperiments, the effects of garlic oil on electrophysiological and morphological changes induced by CSD were investigated. Results: Garlic oil in a dose-dependent manner decreased the amplitude of CSD but not its duration and velocity in neocortical brain slices. Garlic oil at concentration of 500 μl/l reversibly reduced the amplitude of the field excitatory post-synaptic potentials and inhibited induction of long-term potentiation in the third layer of neocortical slices. Inin vivostudies, systemic application of garlic oil (1 ml/l) for three consecutive days reduced the amplitude and repetition rate of CSD. Garlic oil also prevented of CSD-induced reactive astrocytosis in the neocortex. Discussion: Garlic oil suppresses CSD, likely via inhibition of synaptic plasticity, and prevents its harmful effects on astrocyte. Further studies are required to identify the exact active ingredient(s) of garlic oil that inhibit CSD and may have the potential to use in treatment of CSD-related disorders. [ABSTRACT FROM PUBLISHER]

Introduction: Transforming Growth Factor-Beta 1 (TGF-β1) is a pleiotropic cytokine with potent anti-inflammatory property, which has been considered as an essential risk factor in the inflammatory process of Ischemic Stroke (IS), by involving in the pathophysiological progression of hypertension, atherosclerosis, and lipid metabolisms. -509C/T TGF-β1 gene polymorphism has been found to be associated with the risk of IS. The aim of this meta-analysis was to provide a relatively comprehensive account of the relation between -509C/T gene polymorphisms of TGF-β1 and susceptibility to IS. Methods: Male Wistar rats were divided into sham (receiving phosphate buffered saline within dorsal hippocampus), pilocarpine (epileptic model of TLE), single injection BDNF (epileptic rats which received single high dose of BDBF within dorsal hippocampus), and multiple injections BDNF (epileptic rats which received BDNF in days 10, 11, 12, and 13 after induction of TLE) groups. Their electrocorticogram was recorded and amplitude, frequency, and duration of spikes were evaluated. Results: Amplitude and frequency of epileptiform burst discharges were significantly decreased in animals treated with BDNF compared to pilocarpine group. Conclusion: Our findings suggested that BDNF may modulate the epileptic activity in the animal model of TLE. In addition, it may have therapeutic effect for epilepsy. More studies are necessary to clarify the exact mechanisms of BDNF effects. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder. It is characterized by formation of amyloid plaques and neurofibrillary tangles in the brain, degeneration of the cholinergic neurons and neural cell death. This study was aimed to investigate the effect of a triazine derivative, C16H12Cl2N3S, on learning in an Alzheimer's rat model. Animals were divided into seven groups; each group contained seven animals. Control group: animals received no surgery and treatment; saline group: animals received normal saline after recovery; sham group: animals received 10% DMSO after recovery; STZ group (Alzheimer's model): animals received streptozotocin (STZ) in four and six days after recovery; T5, T10 and T15 groups: animals were treated with triazine derivative, C16H12Cl2N3S, at doses of 5, 10 and 15 μM, respectively. All drugs were injected intracerebroventricular. The spatial learning and histological assessment were performed in all groups. Animals in STZ group had more deficits in spatial learning than the control group in Morris water maze. C16H12Cl2N3S improved spatial learning significantly compared to STZ group. The CA1 pyramidal layer thicknesses in STZ group were reduced significantly compared to control group. C16H12Cl2N3S increased the CA1 pyramidal layer thickness in T15 group compared to STZ group. Current findings suggest C16H12Cl2N3S may have a protective effect on learning deficit and hippocampal structure in AD. [ABSTRACT FROM AUTHOR]

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 KClinduced 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. [ABSTRACT FROM AUTHOR]

ABSTRACT Modulation of glutamatergic NMDA receptors affects the synchronization of spike discharges in in WAG/Rij rats, a valid genetic animal model of absence epilepsy. In this study, we describe the alteration of NR2B subunit of NMDA receptors expression in WAG/Rij rats in different somatosensory cortical layers and in hippocampal CA1 area. Experimental groups were divided into four groups of six rats of both WAG/Rij and Wistar strains with 2 and 6 months of age. The distribution of NR2B receptors was assessed by immunohistochemical staining in WAG/Rij and compared with age-matched Wistar rats. The expression of NR2B subunit was significantly decreased in different somatosensory cortical layers in 2- and 6-month-old WAG/Rij rats. In addition, the distribution of NR2B in hippocampal CA1 area was lower in 6-month-old WAG/Rij compared with age-matched Wistar rats. The reduction of NR2B receptors in different brain areas points to disturbance of glutamate receptors expression in cortical and subcortical areas in WAG/Rij rats. An altered subunit assembly of NMDA receptors may underlie cortical hyperexcitability in absence epilepsy. Synapse 67:839-846, 2013. © 2013 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Objectives: Periodic fasting (PF) was suggested to display antiepileptic and neuroprotective effects, which is in stark contrast to severe fasting or starvation. However, these beneficial effects seem to depend on the type and duration of the used feeding protocol. There are discrepancies concerning both antiepileptic and neuroprotective effects of a PF-diet during repetitive seizures in different epilepsy models. This study was designed to evaluate the effects of different PF protocols on behavioural and histopathological consequences of epilepsy in adult rats. Methods: Recurrent generalized seizures were caused by repetitive injection of pentylenetetrazol (PTZ) for a period of 4 weeks every other day. While control animals had free access to food and water, animals on a PF-diet were on intermittent fasting for 24 hours every 48 hours for 4 weeks before (T1), after (T2), or both before and after (T3) the injection of PTZ. Behavioural studies were carried out after PTZ injections and histological investigations were performed after the experiments were completed. Results: Seizure assessment showed that the severity of seizures was significantly decreased in groups T1 and T3 when compared with control rats. Dark neuron densities in hippocampal CA1 and CA3 areas were decreased in PF groups, but never in the temporal cortex. The PF-diet also decreased the number of terminal deoxynucleotidyl transferase-mediated dUTP nick end-labelling-positive neurons in the hippocampus in both areas and all PF-diet protocols. Discussion: These results support the idea that a PF-diet has anticonvulsive and neuroprotective effects on epileptic rats but underlines that different PF-diet protocols can have varying effects. Anticonvulsive effects were strongest when the PF-diet started before the onset of excitotoxic injuries, the number of dark neurons was decreased and apoptosis was prevented by all PF-diet protocols investigated in this work. Further evaluation of PF-diet protocols for possible clinical anticonvulsant and neuroprotective effects is suggested. [ABSTRACT FROM AUTHOR]

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]