Effects of Transcranial Direct Current Stimulation on Motor and Cognitive Dysfunction in an Experimental Traumatic Brain Injury Model.

AIM: To investigate the therapeutic and neuroprotective effects of transcranial direct current stimulation (tDCS) application on the traumatic brain injury (TBI)-induced glutamate and calcium excitotoxicity and loss of motor and cognitive functions. MATERIAL AND METHODS: Forty rats were equally divided in the sham, TBI, tDCS + TBI + tDCS, and TBI + tDCS groups. Mild TBI was induced by dropping a 450-g iron weight from a height of 1 m onto the skull of the rats. The tDCS + TBI + tDCS group was prophylactically administered 1 mA stimulation for 30 min for 7 days starting 5 days before inducing TBI. In the TBI + tDCS group, tDCS (1 mA for 30 min) was administered 2 h after TBI, on days 1 and 2. Cognitive and locomotor functions were assessed using the novel object recognition and open field tests. The calcium, glutamate, and N-methyl-D-aspartate receptor 1 (NMDAR1) levels in the hippocampus were measured using enzyme-linked immunosorbent assay. RESULTS: Although the motor and cognitive functions were substantially reduced in the TBI group when compared with the sham, they improved in the treatment groups (p < 0.05). The calcium, glutamate, and NMDAR1 levels were considerably higher in the TBI group than in the sham (p < 0.001). However, they were considerably lower in the tDCS + TBI + tDCS and TBI + tDCS groups than in the TBI groups (p < 0.05). In particular, the change in the tDCS + TBI + tDCS group was higher than that in the TBI + tDCS group. CONCLUSION: Application of tDCS before the development of TBI improved motor and cognitive dysfunction. It demonstrated a neuroprotective and therapeutic effect by reducing the excitotoxicity via the regulation of calcium and glutamate levels.

Investigation of the effects of Toxoplasma gondii on behavioral and molecular mechanism in bradyzoite stage.

Toxoplasma gondii is a single-celled parasite that causes a disease called toxoplasmosis. It can reach the central nervous system, but the mechanism of T. gondii disrupting the functioning of these brain regions occurs in bradyzoite stage of parasite, causing brain damage by forming tissue cysts in brain. In our study, the effects of T. gondii on locomotor activity, anxiety, learning and memory, and norepinephrine (NE), levodopa (L-DOPA), dopamine (DA) and 3,4-D-dihydroxyphenylacetic acid (DOPAC) catecholamines in amygdala, striatum, prefrontal cortex and hippocampus regions of the brain were investigated in bradyzoite stage. Twenty male Albino mice Mus musculus, 4-5 weeks old, weighing 20-25 g, were used. T. gondii inoculated to mice intraperitonealy with 48-50-hour passages of T. gondii RH Ankara strain. For intraperitoneal inoculation of mice 5x104 tachyzoites per mouse. No inoculation was made in control group (n: 20). Locomotor activity behavior in open field test (OFT), anxious behavior in elevated plus maze (EPM), and learning behavior in novel object recognition (NOR) tests were evaluated. NE, L-DOPA, DA and DOPAC were measured by HPLC in brain tissues of amygdala, striatum, prefrontal cortex and hippocampus. A decrease was observed in the locomotor activity, anxiety and learning values of the T. gondii group compared to the control group (p < 0.05). The heighten in NE and L-DOPA levels in amygdala tissue of T. gondii group compared to control group, an elevation in NE, L-DOPA, DA and DOPAC levels in striatum tissue, and an increase in levels of NE in prefrontal cortex tissue were detected in monoamine results. In hippocampus tissue, an increase was observed in DA levels, while a decrease was observed in NE, L-DOPA and DOPAC levels. In our study, it has been shown that T. gondii in bradyzoite stage reduces locomotor activity, causes learning and memory impairment, and has anxiogenic effects.

Effects of transcranial direct current stimulation on the glutamatergic pathway in the male rat hippocampus after experimental focal cerebral ischemia.

This study aimed to assess the focal cerebral ischemia-induced changes in learning and memory together with glutamatergic pathway in rats and the effects of treatment of the animals with transcranial Direct Current Stimulation (tDCS). One hundred male rats were divided into five groups as sham, tDCS, Ischemia/Reperfusion (IR), IR + tDCS, and IR + E-tDCS groups. Learning, memory, and locomotor activity functions were evaluated by behavioral experiments in rats. Glutamate and glutamine levels, alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionate receptor (AMPAR1), N-Methyl-D-Aspartate receptors (NMDAR1 and NMDAR2A), vesicular glutamate transporter-1 (VGLUT-1), and excitatory amino acid transporters (EAAT1-3) mRNA expressions in hippocampus tissues were measured. Ischemic areas were analyzed by TTC staining. The increase was observed in IR + tDCS, and IR + E-tDCS groups compared to the IR group while a significant decrease was observed in IR group compared to the sham in the locomotor activity, learning, and memory tests. While glutamate and glutamine levels, AMPAR1, NMDAR1, NMDAR2A, VGLUT1, and EAAT1 mRNA expressions were significantly higher in IR group compared to the sham group, it was found to be significantly lower in IR + tDCS and IR + E-tDCS groups compared to the IR group. EAAT2 and EAAT3 mRNA expressions were significantly higher in IR + tDCS and IR + E-tDCS groups compared to the IR group. Ischemic areas were significantly decreased in IR + tDCS and IR + E-tDCS groups compared to the IR group. Current results suggest that tDCS application after ischemia improves learning and memory disorders and these effects of tDCS may be provided through transporters that regulate glutamate levels.

L-Carnitine improves mechanical responses of cardiomyocytes and restores Ca2+ homeostasis during aging.

L-Carnitine (ß-hydroxy-γ-trimethylaminobutyric acid, LC) is a crucial molecule for the mitochondrial oxidation of fatty acids. It facilitates the transport of long-chain fatty acids into the mitochondrial matrix. The reduction in LC levels during the aging process has been linked to numerous cardiovascular disorders, including contractility dysfunction, and disrupted intracellular Ca2+ homeostasis. The aim of this study was to examine the effects of long-term (7 months) LC administration on cardiomyocyte contraction and intracellular Ca2+ transients ([Ca2+]i) in aging rats. Male albino Wistar rats were randomly assigned to either the control or LC-treated groups. LC (50 mg/kg body weight/day) was dissolved in distilled water and orally administered for a period of 7 months. The control group received distilled water alone. Subsequently, ventricular single cardiomyocytes were isolated, and the contractility and Ca2+ transients were recorded in aging (18 months) rats. This study demonstrates, for the first time, a novel inotropic effect of long-term LC treatment on rat ventricular cardiomyocyte contraction. LC increased cardiomyocyte cell shortening and resting sarcomere length. Furthermore, LC supplementation led to a reduction in resting [Ca2+]i level and an increase in the amplitude of [Ca2+]i transients, indicative of enhanced contraction. Consistent with these results, decay time of Ca2+ transients also decreased significantly in the LC-treated group. The long-term administration of LC may help restore the Ca2+ homeostasis altered during aging and could be used as a cardioprotective medication in cases where myocyte contractility is diminished.

Transcranial direct current stimulation alleviates nociceptive behavior in male rats with neuropathic pain by regulating oxidative stress and reducing neuroinflammation.

Transcranial direct curent stimulation (tDCS) and trans-spinal direct current stimulation (tsDCS) are promising therapies for pain that can alter the excitability of neuronal activity in cerebral cortex. The aim of the study is to investigate the therapeutic effects of direct current stimulation (DCS) over the spinal cord and cerebral cortex on oxidative stress and neuroinflammation in rats with chronic constriction injury (CCI). Male Wistar rats were randomly divided into four experimental groups: Sham, CCI, CCI + tDCS and CCI + tsDCS. The neuropathic pain model was induced by using the CCI model. Rats with neuropathy were treated with cathodal tDCS and tsDCS stimulations consisting of 0.5 mA for 30 min a day for 7 days from day 8 onwards. Locomotor activity was measured by open-field test and nociceptive behavior was assessed by hot-plate, tail-flick and Randall-Selitto tests. Following the behavioral experiments, total oxidant capacity (TOC), total antioxidant capacity (TAC) and proinflammatory cytokine levels were evaluated in spinal cord and cerebral cortex tissues. The CCI model induced significant mechanical and thermal hyperalgesia. Nociceptive behaviors in rats with CCI were reversed by DCS treatment. Higher TOC and lower TAC levels were detected in the spinal cord and cerebral cortex tissues of the CCI rats compared to the control. tsDCS treatment amended oxidant/antioxidant status. Moreover, tsDCS modulated the central levels of Tumor necrosis factor-α (TNF-α), interleukin 1-beta (IL-1ß), IL-6 and IL-18. tsDCS stimulation showed better therapeutic effect on neuropathic pain by regulating oxidant/antioxidant levels and reducing neuroinflammation. DCS, especially at spinal level, may be a promising therapeutic strategy that can be used alone or in combination with other effective treatments for alleviating neuropathic pain.

[6]-Shogaol and [6]-Gingerol active ingredients may improve neuropathic pain by suppressing cytokine levels in an experimental model.

Background/aim: Neuropathic pain (NP) is a type of chronic pain usually caused by damage to the somatosensory system. Bioactive antioxidant compounds, such as curcumin and ginger, are widely preferred in the treatment of NP. However, the ingredient-based mechanism that underlies their pain-relieving activity remains unknown. The aim of this study was to investigate the therapeutic effects of trans-[6]-Shogaol and [6]-Gingerol active ingredients of the Zingiber officinale Roscoe extract on the spinal cord and cortex in the neuroinflammatory pathway in rats with experimental sciatic nerve injury. Materials and methods: Forty-six volatile phenolic components were identified in ginger samples using gas chromatography-mass spectrometry analysis. Thirty 3-month-old male 250-300 g Wistar Albino rats were divided into three groups as (i) sham, (ii) chronic constriction injury (CCI), and (iii) CCI+ginger. NP was induced using the CCI model. A ginger extract treatment enriched with trans-[6]-shogaol and [6]-gingerol active ingredients was administered by gavage at 200 mg/kg/day for 7 days. On the 14th day of the experiment, locomotor activity was evaluated in open field and hyperalgesia in tail flick tests. Results: In behavioural experiments, a significant decrease was observed in the CCI group compared to the sham group, while a significant increase was observed in the CCI+ginger group compared to the CCI group (p < 0.05). In the spinal cord and cortex tissues, there was a significant increase in the TNF-α, IL-1ß, and IL-18 neuroinflammation results of the CCI group compared to the sham group, while there was a significant decrease in the CCI+ginger group compared to the CCI group. Conclusion: In this study, ginger treatment was shown to have a therapeutic effect on neuroinflammation against sciatic nerve damage.

The effect of increase in blood glucose level on hearing loss

Abstract Objective: Previous studies have shown that hearing function is also vulnerable to the effects of diabetes mellitus which can be shown by brainstem auditory evoked potential and distortion product otoacoustic emission recordings. This study aimed to investigate the changes of brainstem auditory evoked potential and distortion product otoacoustic emission in hyperglycemia and whether there is a relationship between reactive oxygen substances production and hearing deterioration in the rat model. Methods: 25 streptozotocin induced diabetic rats were divided into three groups: control, high blood glucose, and diabetes mellitus. Brainstem auditory evoked potential and distortion product otoacoustic emission were recorded, and thiobarbituric acid reactive substances levels were measured in the brainstem tissue. Results: At 8 kHz, the latencies of I, II, III, IV, and V brainstem auditory evoked potential waves in high blood glucose and diabetes mellitus groups were elongated, at 16 kHz, only these wave latencies of the diabetes mellitus group were prolonged compared with the control group. A significant decrease was also found in distortion product otoacoustic emission amplitudes at 4, 6, 8, and 10 kHz in the high blood glucose and diabetes mellitus groups compared to the control group. There was a significant increase in thiobarbituric acid reactive substances values due to the increase in blood glucose levels in the high blood glucose and diabetes mellitus groups compared to the control group. Conclusion: These results suggested that high blood glucose levels may cause hearing impairment not only in the diabetic state but also in the period of hyperglycemia before the onset of manifest diabetes mellitus and reactive oxygen substances may play an important role in the pathophysiology of diabetes mellitus. We suggest that regulating high glucose levels even before the onset of manifest diabetes mellitus may prevent hazardous effects on hearing function. Level of evidence: Level 3.

Effects of biotin deficiency on short term memory: The role of glutamate, glutamic acid, dopamine and protein kinase A.

Insufficient dietary biotin intake, biotinidase deficiency, drug-biotin interactions can cause biotin deficiency which may result in central nervous system dysfunctions. We hypothesized that biotin deficiency could disrupt learning and memory functions by altering glutamate, glutamine, dopamine levels and protein kinase A (PKA) activity in the hippocampus. Sixteen female and 4 male Wistar rats were mated and females were separated into 4 groups. Three pups were selected from each mother and a total of 48 pups were divided into the following experimental groups. NN group, normal diet in the prenatal and postnatal period. NB group, normal diet in the prenatal and a biotin-deficient diet in the postnatal period. BN group: biotin-deficient diet in the prenatal and a normal diet in the postnatal period, BB group: biotin-deficient diet in both the prenatal and postnatal period. Open Field, Y-Maze, Object Location, and Novel Object Recognition Tests were performed in all groups and rats were sacrificed. Glutamine, glutamate, dopamine levels and PKA activity were analyzed in the hippocampi. In the open field test, distance and velocity values of NB, BN and BB groups were decreased with respect to the NN group. Learning and memory functions of NB, BN and BB groups were found to be impaired in behavioral tests. Dopamine levels and PKA activity were also decreased in all rat pups fed with a biotin deficient diet. In conclusion, we demonstrated that biotin deficiency deteriorates short-term memory and locomotor activity. This impairment may relate to decreased dopamine levels and PKA activity in the hippocampus.

The Role of Acetylcholine on the Effects of Different Doses of Sulfite in Learning and Memory.

In this study, the effects of different doses of sulfite on learning, memory, and long term potentiation as well as the relationship of these effects with acetylcholine pathways, Arc and synapsin 1 levels were investigated. Sixty male Wistar albino rats were randomly divided into three groups as control, S100, and S260. Sodiummetabisulfite (S100;100 mg/kg/day, S260;260 mg/kg/day) was given by oral administration. Behavioral changes were evaluated. After long term potentiation recordings from the perforant pathway-dentate gyrus synapses, animals were sacrificed. Acetylcholinesterase activity, choline acetyltransferase activity, acetylcholine level as well as Arc and Synapsin 1 expressions were analyzed on the hippocampi. The total distance and average velocity values in the open field and Morris water maze tests increased in the sulfite groups, while the discrimination index in the novel object recognition test decreased compared to controls. Acetylcholine levels and choline acetyltransferase activity were also increased in the sulfite groups, while acetylcholinesterase activity was decreased compared to controls. Sulfite intake attenuated long term potentiation in the hippocampus. It has been observed that the excitatory postsynaptic potential slope and population spike amplitude of the field potentials obtained in sulfite groups decreased. This impairment was accompanied by a decrease in Arc and synapsin 1 expressions. In conclusion, it has been shown that sulfite intake in adults impairs learning and memory, possibly mediated by the cholinergic pathway. It is considered that the decrement in Arc and synapsin expressions may play a role in the mechanism underlying the impairment in long term potentiation caused by toxicity.

The effect of increase in blood glucose level on hearing loss.

OBJECTIVE: Previous studies have shown that hearing function is also vulnerable to the effects of diabetes mellitus which can be shown by brainstem auditory evoked potential and distortion product otoacoustic emission recordings. This study aimed to investigate the changes of brainstem auditory evoked potential and distortion product otoacoustic emission in hyperglycemia and whether there is a relationship between reactive oxygen substances production and hearing deterioration in the rat model. METHODS: 25 streptozotocin induced diabetic rats were divided into three groups: control, high blood glucose, and diabetes mellitus. Brainstem auditory evoked potential and distortion product otoacoustic emission were recorded, and thiobarbituric acid reactive substances levels were measured in the brainstem tissue. RESULTS: At 8 kHz, the latencies of I, II, III, IV, and V brainstem auditory evoked potential waves in high blood glucose and diabetes mellitus groups were elongated, at 16 kHz, only these wave latencies of the diabetes mellitus group were prolonged compared with the control group. A significant decrease was also found in distortion product otoacoustic emission amplitudes at 4, 6, 8, and 10 kHz in the high blood glucose and diabetes mellitus groups compared to the control group. There was a significant increase in thiobarbituric acid reactive substances values due to the increase in blood glucose levels in the high blood glucose and diabetes mellitus groups compared to the control group. CONCLUSION: These results suggested that high blood glucose levels may cause hearing impairment not only in the diabetic state but also in the period of hyperglycemia before the onset of manifest diabetes mellitus and reactive oxygen substances may play an important role in the pathophysiology of diabetes mellitus. We suggest that regulating high glucose levels even before the onset of manifest diabetes mellitus may prevent hazardous effects on hearing function. LEVEL OF EVIDENCE: Level 3.

Vortioxetine ameliorates motor and cognitive impairments in the rotenone-induced Parkinson's disease via targeting TLR-2 mediated neuroinflammation.

Parkinson's disease (PD) is characterized by motor and non-motor symptoms associated with dopaminergic and non-dopaminergic injury. Vortioxetine is a multimodal serotonergic antidepressant with potential procognitive effects. This study aimed to explore the effects of vortioxetine on motor functions, spatial learning and memory, and depression-like behavior in the rotenone-induced rat model of PD. Male Sprague-Dawley rats were daily administered with the rotenone (2 mg kg-1, s.c.) and/or vortioxetine (10 mg kg-1, s.c.) for 28 days. Motor functions (rotarod, catalepsy, open-field), depression-like behaviors (sucrose preference test), anxiety (elevated plus maze), and spatial learning and memory abilities (novel object recognition and Morris water maze) were evaluated in behavioral tests. Then immunohistochemical, neurochemical, and biochemical analysis on specific brain areas were performed. Vortioxetine treatment markedly reduced rotenone-induced neurodegeneration, improved motor and cognitive dysfunction, decreased depression-like behaviors without affecting anxiety-like parameters. Vortioxetine also restored the impaired inflammatory response and affected neurotransmitter levels in brain tissues. Interestingly, vortioxetine was thought to trigger a sort of dysfunction in basal ganglia as evidenced by increased Toll-like receptor-2 (TLR-2) and decreased TH immunoreactivity only in substantia nigra tissue of PD rats compared to the control group. The present study indicates that vortioxetine has beneficial effects on motor dysfunction as well as cognitive impairment associated with neurodegeneration in the rotenone-induced PD model. Possible mechanisms underlying these beneficial effects cover TLR-2 inhibition and neurochemical restoration of vortioxetine.

The influence of syringic acid treatment on total dopamine levels of the hippocampus and on cognitive behavioral skills.

BACKGROUND: Natural polyphenols have been investigated and are claimed to be mediators of the relationship between dopamine (DA) and memory. Therefore, we aimed to measure and evaluate the effect of syringic acid (SA) on DA expression by behavioral tests related to short-term and recognition memory in Wistar rats. METHODS: Rats were randomly assigned to control (0.5 cc corn oil, n = 10), SA (25 mg/kg/day, o.g, n = 10), Deltamethrin (DTM) (1.28 mg/kg/day o.g, n = 10) and DTM (1.28 mg/kg/day o.g, n = 10) + SA (25 mg/kg/day) groups. The Y-maze and Novel Object Recognition (NOR) tests were performed to assess cognitive and behavioral functions in the rats. Dopamine levels in the hippocampus were measured by mass spectrometry. RESULTS: Syringic acid significantly increased DA (5.45 ± 1.06 ng/ml, p = 0.0026, p < 0.05) compared with the other groups. SA increased the percent alternation (34.85 ± 0.72%, p < 0.05), time spent in the novel arm (2.88 ± 0.18 min, p < 0.05), and frequency of novel arm entries (44.91 ± 2.28%, p < 0.05), of the rats after the Y-maze test. The SA elevated the discrimination index (70.42 ± 3.59%, p < 0.001), and exploration time (30.44 ± 1.8 sec, p < 0.05) in the NOR test, and increased the short term and recognition memory in behavioral tests. CONCLUSION: Our findings support the hypothesis that SA-induced DA levels of the hippocampus may facilitate recognition and short-term memory in Wistar rats through the activation of dopaminergic receptors or pathways during the learning process, and that this can be seen in the cognitive behavior of SA-treated rats.

Neuropeptide-S affects cognitive impairment and depression-like behavior on MPTP induced experimental mouse model of Parkinson's disease

Background/aim: The present study proposes to investigate the effect of neuropeptide­S (NPS) on cognitive functions and depression-like behavior of MPTP-induced experimental model of Parkinson's disease (PD). Materials and methods: Three-month-old C57BL/6 mice were randomly divided into three groups as; Control, Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and MPTP + NPS 0.1 nmol (received intraperitoneal injection of MPTP and intracerebroventricular injection of NPS, 0.1 nmol for seven days). The radial arm maze and pole tests were carried out, and the levels of tyrosine hydroxylase (TH) were determined using western blotting. A mass spectrometer was used to measure the levels of dopamine, glutamic acid, and glutamine. Results: The T-turn and time to descend enhanced in MPTP group, while these parameters were decreased by NPS treatment. In the MPTP group, the number of working memory errors (WME) and reference memory errors (RME) increased, whereas NPS administration decreased both parameters. Sucrose preference decreased in the MPTP group while increasing in the NPS group. MPTP injection significantly reduced dopamine, glutamic acid, and glutamine levels. NPS treatment restored the MPTP-induced reduction in glutamine and glutamic acid levels. Conclusion: NPS may be involved in the future treatment of cognitive impairments and depression-like behaviors in PD.

The effect of chronic neuropeptide-S treatment on non-motor parameters in experimental model of Parkinson's disease.

AIM: Besides motor impairment, non-motor symptoms including cognitive decline, anxiety, and depression are observed in Parkinson's Disease (PD). The aim of this study was to investigate whether chronic administration of central neuropeptide-S (NPS) improves non-motor symptoms in 6-hydroxydopamine (6-OHDA)-induced parkinsonian rats. MATERIAL AND METHODS: Experimental PD was utilized by unilateral stereotaxic injection of the 6-OHDA into the medial forebrain bundle (MFB), while the sham-operated animals underwent the same surgical procedures. NPS (1 nmol) or vehicle was daily administered through an intracerebroventricular (icv) cannula for 7 days. Radial arm maze (RAM) test was used to evaluate the working memory; whereas, elevated plus maze (EPM) test and sucrose preference test were used to monitor the anxiety and depression status, respectively. The levels of dopamine, glutamic acid, and glutamine was determined in harvested striatal and hippocampal tissue samples. The immunoreactivities for tyrosine hydroxylase (TH) was determined using immunohistochemistry. RESULTS: In the RAM test, the 6-OHDA-induced increases in the reference and working memory errors were reduced by the central NPS administration. The decreased sucrose preference in the parkinsonian rats was increased by centrally administered NPS. The levels of dopamine levels in striatum and hippocampus were decreased in the parkinsonian rats, however, they were not altered by the centrally administered NPS. Additionally, NPS treatment significantly attenuated the 6-OHDA-induced loss of TH neuronal number. CONCLUSION: Consequently, NPS appears to be a therapeutic candidate for the treatment of non-motor complications of PD.

Possible effects of different doses of 2.1 GHz electromagnetic radiation on learning, and hippocampal levels of cholinergic biomarkers in Wistar rats.

The present study evaluated whether short-term exposure to different doses of 2.1 GHz radiofrequency electromagnetic radiation (RF-EMR) has different effects on rats' behaviour and hippocampal levels of central cholinergic biomarkers. Animals were divided into three equal groups namely; group 1 was sham-exposed group, group 2-3 were exposed to 45 V/m and 65 V/m doses of 2.1 GHz frequency for 1 week respectively. Numerical dosimetry simulations were carried out. Object location and Y-maze were used as behavioural tasks. The protein and mRNA expression levels of AChE, ChAT, and VAChT, in the hippocampus were tested using Western Blotting and Real-Time PCR. The impairment performance of rats subjected to 65 V/m dose of 2.1 GHz RF-EMR in both object location and Y-maze tasks was observed. The hippocampal levels of AChE, ChAT, and VAChT, were significantly lower in rats exposed to 65 V/m dose of 2.1 GHz RF-EMR than others. The stronger effect of "65 V/m" dose on both rat's hippocampal-dependent behavioural performances and hippocampal levels of cholinergic biomarkers may be due to the stronger effect of "65 V/m" dose where rats' snouts were located at the nearest distance from the monopole antenna. Furthermore, the simulated SAR values were high for 65 V/m electric-field strengths. For the first time, we report the potential dose-dependent effects of short-term exposure to 2.1 GHz radiation on rat's behavioural performances as well as hippocampal levels of cholinergic biomarkers. Further studies are needed to understand the mechanisms by which RF-EMR influences the function of the central cholinergic system in the brain.

Effect of chronic L-carnitine supplementation on carnitine levels, oxidative stress and apoptotic markers in peripheral organs of adult Wistar rats.

This study investigated the effects of L-carnitine supplementation on carnitine levels, oxidative stress and apoptotic markers in the stomach, kidney, liver and testis tissues in adult rats. Rats were randomized to control and L-carnitine supplemented (LCAR) groups. Control group received distilled water for 7 months by intragastric gavage and the LCAR group was given 50 mg/kg/day L-carnitine via intragastric intubation for the same period. L-carnitine concentrations and caspase-3 activity were measured by fluorometric methods while cleaved caspase-3 was determined by Western blot analysis. Bcl-2 associated X protein (Bax) and B-cell lymphoma/leukemia-2 (Bcl-2) were quantified by enzyme immunoassay and Western blot analysis. Oxygen/nitrogen species (ROS/RNS) and total antioxidant capacity (TAC) were analyzed by colorimetric assay. Tissue L-carnitine concentrations were significantly increased in the LCAR group compared to controls. Anti-apoptotic Bcl-2 levels were significantly increased while pro-apoptotic Bax was significantly decreased in LCAR group rats compared to controls. Tissue caspase-3 was significantly alleviated in the LCAR group compared to controls. L-carnitine supplementation increased TAC and decreased ROS/RNS generation in the kidney, liver, stomach and testis tissues compared to controls. Obtained data suggests that L-carnitine supplementation can potentially be used to lessen both oxidative and apoptotic progression in peripheral organs.

Protective effects of syringic acid on neurobehavioral deficits and hippocampal tissue damages induced by sub-chronic deltamethrin exposure.

Recent developments in the field of insecticide exposure have led to a renewed interest in alternative antioxidant therapy. The present study was to investigate the neuroprotective role of syringic acid (SA, 25 mg/kg/day) on the neurotoxicity and oxidative damage induced by deltamethrin (DTM, 1.28 mg/kg/day during two months) in CA1/3 pyramidal neurons. Animals were divided into 4 groups (n = 16/group) (250-270 g) for control, DTM, SA and DTM + SA. DTM and SA were administered by oral gavage daily. Rats that were given sub-chronic DTM had revealed a significant increase in caspase-3 levels, impaired recognition memory, reduced antioxidant activity and enhanced free radicals in the hippocampus. The results showed that SA ameliorated neurobehavioral alterations, reduced reactive oxygen/nitrogen species, pyknosis in the CA1/3 and increased antioxidant enzyme activity. In conclusion, SA (25 mg/kg/day) had potential neuroprotective and therapeutic impacts against sub-chronic DTM exposure via its antioxidant and antiapoptotic efficacy. Therefore, it can be used as a neuroprotective natural plant-derived agent against DTM-induced neurotoxicity.

Ab initio study on the rare-earth iron-pnictides RFeAsO (R = Pr, Nd, Sm, Gd) in the low-temperature Cmma phase.

We present density functional theory calculations on the iron-based pnictides RFeAsO (R = Pr, Nd, Sm, Gd). The calculations have been carried out using plane waves and the projector augmented wave (PAW) pseudopotential approach. Structural, magnetic and electronic properties are studied within the generalized gradient approximation (GGA) and also within GGA + U in order to investigate the influence of electron correlation effects. The low-temperature Cmma structure is fully optimized by the GGA considering both non-magnetic and magnetic cells. We have found that the spin-polarized structure improves the agreement with experiments on equilibrium lattice parameters, particularly the c lattice parameter and the Fe-As bond-lengths. The electronic band structure, total density of states, and spin-dependent orbital-resolved density of states are also analyzed and discussed in the frameworks of GGA and GGA + U. For all materials, by including an on-site Coulomb correction, the rare-earth 4f states move away from the Fermi level and the Fermi level features of the systems are found to be mostly defined by the 3d electron-electron correlations in Fe.