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Time perception is known as a mental ability to discern time. Although relative nature of time leaves its numerous aspects undefined, several models have been developed to describe temporal information processing in the brain as well as several areas of the brain have shown to be involved. Time perception alteration has been reported in several neurological conditions; however, the effect of multiple sclerosis (MS) on time perception has yet to be explained. In this study, we aimed to investigate the domains of temporal processing involved in patients with MS and the probable factors affecting it, such as the location of brain demyelinating plaques and gender. Two groups of participants (MS

Deep brain electrical stimulation (DBS), as a potential therapy for drug resistive epileptic patients, has inhibitory action on epileptogenesis. In the present investigation, the role of dopamine DSeizures were induced in adult rats by stimulating the perforant path in a semi-rapid kindling method. Five minutes after the last kindling stimulation, daily DBS was applied to the perforant path at the pattern of low frequency stimulation (LFS; 1 Hz; pulse duration: 0.1 ms; intensity: 50-150 μA; 4 trains of 200 pulses at 5 min intervals). Sulpiride (10 μg/1 μl, i.c.v.), a selective dopamine DKindling stimulations increased cumulative daily behavioral seizure stages, daily afterdischarge duration (dADD), and population spike amplitude (PS) in dentate gyrus following perforant path stimulation, while applying LFS decreased the kindled seizures' parameters. In addition, kindling potentiated the early (at 10-50 ms inter-pulse interval) and late (at 150-1000 ms inter-pulse interval) paired-pulse inhibition and decreased the paired-pulse facilitation (at 70-100 ms inter-pulse interval). These effects were also inhibited by applying LFS. All inhibitory effects of LFS on kindling procedure were prevented by sulpiride administration.These data may suggest that LFS exerts its preventive effect on kindling development, at least partly, through the receptors on which sulpiride acts which are mainly dopamine D

Non-motor symptoms (NMS) have high prevalence in patients with Parkinson's disease (PD). These symptoms are mainly the result of increased oxidative stress and neuronal damage. In this study we investigated the possible neuroprotective effects of anethole as a potent antioxidant on rotenone-induced behavioral deficits, hippocampal neuronal death, and oxidative stress profile in rats.Male Wistar rats were administered with anethole (62.5, 125, and 250 mg/kg, i.g) concomitantly with rotenone (2 mg/kg, s.c) for 35 days. Shuttle box and novel object recognition tests were performed to determine cognitive functions, and tail flick test was used to measure pain sensitivity. The levels of BDNF, MDA, SOD, and GPx were assayed in the hippocampus. Hippocampal neuronal damage was evaluated using cresyl violet staining technique.Chronic administration of rotenone induced cognitive deficit and reduced thermal pain threshold. Rotenone also decreased SOD and GPx activities, increased MDA level, and reduced the expression of BDNF in the hippocampus. In addition, hippocampal neuronal loss was increased in rotenone treated rats. Treatment with high dose of anethole (250 mg/kg) improved cognitive function and increased pain threshold in all three doses (62.5, 125, and 250 mg/kg). Despite the unchanged SOD and GPx activities, hippocampal levels of MDA was significantly decreased after high-dose anethole treatment. Moreover, High dose of anethole increased the number of surviving neurons in the hippocampus, but couldn't increase the BDNF expression.Our findings indicated that anethole has antioxidant and neuroprotective effects against non-motor disorders induced by rotenone toxicity.

Total sleep deprivation (TSD) causes several harmful changes in the brain, including memory impairment, increased stress and depression levels, as well as reduced antioxidant activity. Growth hormone (GH) has been shown to boost antioxidant levels while improving memory and depression. The present study was conducted to explain the possible effects of exogenous GH against behavioral and biochemical disorders caused by TSD and the possible mechanisms involved.To induce TSD, rats were housed in homemade special cages equipped with stainless steel wire conductors to induce general and inconsistent TSD. They received a mild repetitive electric shock to their paws every 10 min for 21 days. GH (1 ml/kg, sc) was administered to rats during induction of TSD for 21 days. Memory retrieval, anxiety, depression-like behaviors, pain behaviors, antioxidant activity, hippocampal level of BDNF, and simultaneously brain electrical activity were measured at scheduled times after TSD.The results showed that GH treatment improved memory (p 0.001) in the PAT test of rats exposed to TSD. These beneficial effects were associated with lowering the level of anxiety and depression-like behavior (p 0.001), rising the pain threshold (p 0.01), increasing the activity of antioxidants (p 0.01), hippocampal BDNF (p 0.001), and regular brain electrical activity.Our findings show that GH plays a key role in modulating memory, anxiety and depression behaviors, as well as reducing oxidative stress and improve hippocampal single-unit activity in the brain during TSD.

Background Medical education is a dynamic process, which needs to be improved to meet the new expectations of medical practitioners, health workers, and communities from different countries. An important part of medical students' education is to select an appropriate assessment method. In this regard, the objective structured practical examination (OSPE) can evaluate practical capabilities in a suitable step-wise, scientific, targeted and scheduled manner with direct consideration of student's performance during programmed test stations. The purpose of this study is to investigate the outcomes of the OSPE utilization versus traditional practical examination (TPE) for evaluating students in experimental physiology. Methods Totally, 120 medical students were chosen as the participants of this study: 1. TPE group (TPE used as a final exam; n=40); 2. TPE + OSPE group (TPE applied for half of topics and OSPE for another half; n=41); and 3. OSPE group (OSPE performed as a final exam; n=39). In order to evaluate the effect of OSPE, the average final grade of studied groups was compared. In addition, a 5-point Likert scale questionnaire, consisting of 10 questions was used to evaluate the students' attitudes toward using this method. Results The obtained results showed that the total grade in TPE group was significantly higher in comparison to TPE+OSPE and OSPE groups (respectively, P

Introduction: Many physiological, biochemical and toxicological reactions are occurred in liver. Therefore, healthy function of this organ is vital for the whole body. In spite of having potent endogenous antioxidant system, lots of reactions in liver make it more susceptible to stressors. It is established that improving the potency of liver antioxidants can increase its ability to resist against different kinds of oxidative stressors. Therefore, this study designed to determine whether p-coumaric alleviate ischemia-reperfusion-induced hepatic injury (IRI) in rats. Methods: Thirty-two rats were randomly assigned in sham, p-coumaric acid (PC), ischemia-reperfusion (IR) and p-coumaric acid pretreated IR (PC+IR) groups (n=8 in each group). Animals in sham group underwent laparotomy but not IR injury; rats in PC group did not experience any surgical procedures; IR and PC+IR groups underwent hepatic IR injury. P-coumaric acid at 100mg/kg were given for 7 consecutive days to PC and PC+IR groups. The last dose of p-coumaric acid was injected just before surgery on 7th days of experiment. The levels of malondialdehyde, TAC, ALT and AST were determined. A molecular evaluation to quantify the gene expression of SOD and GPx was done in liver homogenate. Results: P-coumaric mitigated the hepatic injuries induced by IR and improved TAC, ALT, AST, SOD and GPx. This pretreatment was also decreased MDA level. Conclusion: The current outcomes showed that PC via improving the endogenous level of antioxidants in liver tissues and inhibiting IR-induced inflammation maintain the liver structure and function of liver against IR.

Introduction: Coronavirus disease 2019 (COVID-19), started in December 2019, affects many organs and systems of the body, such as the central nervous system. Case Presentation: We describe a case of a 66-year-old female patient with positive results for COVID-19 using real-time PCR (RT-PCR) testing from her cerebrospinal fluid (CSF) and the coronavirus antibodies (Ig G and Ig M) using serology test. Her clinical presentation showed the misbalance and acute weakness of upper and lower limbs with preference of proximal parts of the limbs, pinprick, and the absence of deep tendon reflexes. Taken together, these symptoms, neurological tests and the result of CSF analysis (high protein) were in favor of Guillain-Barre syndrome (GBS). In addition, because the neurological symptoms worsted four days after hospitalization, plasmapheresis was started over the course of 8 days (on every alternate day) with a volume of 2000 mL. Although the results of electromyogram (EMG) - nerve conduction velocity (NCV) following plasmapheresis showed the motor and sensory neuropathy, which was generally accompanied by demyelination, but it leads to the recovery of upper and lower limbs from 2/5 to 4/5 and improvement of neck flexor muscles from 3/5 to 5/5. Conclusions: GBS should be considered as a neurological outcome of COVID-19. In addition, regarding the beneficial effects of plasmapheresis on GBS (following coronavirus infection), it can be suggested as a part of the treatment protocol in these patients.

Hypoxia-induced neonatal seizure mainly leads to deleterious effects on brain function, especially cognitive impairments and increased susceptibility to epilepsy later in life. Early inflammation plays an important role in the pathology of these consequences. Therefore, we explored the long-term outcomes of Fingolimod treatment as an anti-inflammatory and neuroprotective agent in a rat model of HINS. Seizures were induced in rats (postnatal day 10) by 5% O2 exposure for 15 min. Sixty minutes after the onset of hypoxia, pups received FTY720 (0.3 mg.kg-1) or normal saline for 12 consecutive days (lactation period), and they were used at P60-P63 for behavioral tests, ELISA and Pentylenetetrazole kindling model. The results of open field, novel object recognition and elevated plus maze tasks showed that Fingolimod prevents hippocampal memory dysfunction and anxiety-like behavior in both male and female hypoxic groups, which was accompanied with decreased TNF-α level in hippocampus. In addition, FTY720 postponed epileptogenesis just in female hypoxic + FTY group and decreased severity of seizures in both genders. Our results suggest that, FTY720 treatment in immature rats, which were previously subjected to HINS, prevented the long-lasting deficits, like cognitive impairments, decreased the severity of seizures and related inflammation. In addition, FTY720 did not show significant interaction with gender in most of the experiments, except the average day to reach fully kindled state. Taken together, FTY720 has therapeutic potential for long lasting effects of HINS in both male and female animals at puberty.

Background The precise effect of low frequency stimulation (LFS) as a newly postulated, anticonvulsant therapeutic approach on seizure-induced changes in synaptic transmission has not been completely determined. Hypothesis In this study, the LFS effect on impaired, synaptic plasticity in kindled rats was investigated. Methods Hippocampal kindled rats received LFS (4 trials consisting of one train of 200 monophasic square waves, 0.1 ms pulse duration, 1 Hz) on four occasions. LTP induction was evaluated using whole-cell recordings of evoked excitatory and inhibitory post-synaptic potentials (EPSPs and IPSPs respectively) in CA1 neurons in hippocampal slices. In addition, the hippocampal excitatory and inhibitory post-synaptic currents (EPSCs and IPSCs), and the gene expression of NR2A, GluR2 and γ2 were evaluated. Results LTP induction was attenuated in excitatory and inhibitory synapses in hippocampal slices of kindled rats. When LFS was applied in kindled animals, LTP was induced in EPSPs and IPSPs. Moreover, LFS increased and decreased the threshold intensities of EPSCs and IPSCs respectively. In kindled animals, NR2A gene expression increased, while γ2 gene expression decreased. GluR2 gene expression did not significantly change. Applying LFS in kindled animals mitigated these changes: No significant differences were observed in NR2A, γ2 and GluR2 gene expression in the kindled+LFS and control groups. Conclusion The application of LFS in kindled animals restored LTP induction in both EPSPs and IPSPs, and returned the threshold intensity for induction of EPSCs, IPSCs and gene expression to similar levels as controls.

Low frequency stimulation (LFS) has been proposed as a new approach in the treatment of epilepsy. The anticonvulsant mechanism of LFS may be through its effect on GABAA receptors, which are the main target of phenobarbital anticonvulsant action. We supposed that co-application of LFS and phenobarbital may increase the efficacy of phenobarbital. Therefore, the interaction of LFS and phenobarbital on GABAergic inhibitory post-synaptic currents (IPSCs) in kindled and control rats was investigated. Animals were kindled by electrical stimulation of basolateral amygdala in a semi rapid manner (12 stimulations/day). The effect of phenobarbital, LFS and phenobarbital+LFS was investigated on GABAA-mediated evoked and miniature IPSCs in the hippocampal brain slices in control and fully kindled animals. Phenobarbital and LFS had positive interaction on GABAergic currents. In vitro co-application of an ineffective pattern of LFS (100 pulses at afterdischarge threshold intensity) and a sub-threshold dose of phenobarbital (100μM) which had no significant effect on GABAergic currents alone, increased the amplitude and area under curve of GABAergic currents in CA1 pyramidal neurons of hippocampal slices significantly. Interestingly, the sub-threshold dose of phenobarbital potentiated the GABAergic currents when applied on the hippocampal slices of kindled animals which received LFS in vivo. Post-synaptic mechanisms may be involved in observed interactions. Obtained results implied a positive interaction between LFS and phenobarbital through GABAA currents. It may be suggested that a combined therapy of phenobarbital and LFS may be a useful manner for reinforcing the anticonvulsant action of phenobarbital.

Epileptic seizures are characterized with cognitive disorders. In this study we investigated the effect of electrical low frequency stimulation (LFS), as a potential anticonvulsant agent, on kindled seizure-induced cognitive impairments. Animals were kindled through electrical stimulation of hippocampal CA1 area in a semi-rapid manner (12 stimulations/day). One group of animals received LFS 4 times at 0.5, 6.5, 24 and 30h following the last kindling stimulation. Applied LFS was consisted of 4 packages at 5min intervals. Each package contained 200 monophasic square wave pulses of 0.1ms duration at 1Hz. The Y-maze test was performed in all animals to measure the spontaneous alternation behavior. Kindled animals showed significant impairment in spontaneous alternation behavior compared to the control group. Application of LFS improved the observed impairment in spontaneous alternation behavior in kindled animals, so that there was no significant difference between kindled+LFS and control group. The observed improving effect of LFS was accompanied with a significant increase in calcineurin gene expression within the hippocampal area. Therefore, it may be postulated that application of LFS in kindled animals, which resulted in increment of calcineurin gene expression, can improve the seizure-induced impairment in spontaneous alternation behavior in Y-maze test.

Insulin is a potent vasoactive hormone which induces vasodilatation at physiological concentrations. Aerobic exercise is known to improve insulin vasodilatory activity in humans and experimental animals. Since both insulin and physical training is known to activate K(ATP) and K(Ca2+) channels and increase nitric oxide (NO) synthesis, we hypothesized that insulin and exercise might use a common mechanism in mediating their vascular effect. The present study was carried out to investigate the role of NO, K(ATP) and K(Ca2+) channels in enhancement of insulin-induced cutaneous vasorelaxation by exercise in rats. Male Wistar rats were submitted to exercise training for 8weeks on a treadmill. Cutaneous microvascular response to insulin was recorded from soles skin using a laser Doppler flowmeter. Systemic arterial blood pressure and heart rate were measured using a tail-cuff during assessment of cutaneous blood flow. Subcutaneous injection of insulin induced a dose-dependent increase in skin blood flow in control rats which was significantly higher in exercised animals. Local inhibition of NO synthesis (l-NAME, 10(-4)M) was associated with a marked inhibitory effect on insulin-induced vasodilatation and this inhibition was significantly greater in exercised rats. Likewise, a selective K(Ca2+) channel blocker (iberiotoxin, 10(-9)M) inhibited insulin-induced vasodilatation and this inhibition was significantly exaggerated in exercised animals. Local K(ATP) blockade (glybenclamide, 10(-5)M) showed an identical response in sedentary and exercised animals. Insulin induced a marked vasodilatation in cutaneous microcirculation following aerobic exercise in rats. Both NO and K(Ca2+) channels might be involved in the genesis of this effect.