Dopamine In Rat Brain Research Articles

Highly Sensitive and Biocompatible Microsensor for Selective Dynamic Monitoring of Dopamine in Rat Brain.

Highly selective and sensitive in vivo neurotransmitter dynamic monitoring of the central nervous system has long been a challenging endeavor. Here, an implantable and biocompatible microsensor with excellent performances was reported by electrodepositing poly(3,4-ethylenedioxythiophene)-electrochemically reduced graphene oxide (PEDOT-ERGO) nanocomposites and poly(tannic acid) (pTA) sequentially on the carbon fiber electrode (CFE) surface, and its feasibility in in vivo electrochemical sensing applications were demonstrated. Due to the synergistic electrocatalytic effect of PEDOT-ERGO nanocomposites with the negative-charged pTA on dopamine (DA) redox reaction, the microsensor exhibits high detection sensitivities of 1.1 and 0.37 nA μM-1 in the detection ranges of 0.02-0.5 and 0.5-20 μM with a low limit of detection of 9.2 nM. Also, the microsensor shows excellent selectivity, good sensing stability, repeatability, and reproducibility. In addition, the highly hydrophilic and negative-charged pTA inhibits the nonspecific adsorption of hydrophobic proteins, which endows the microsensor with good antifouling ability. Moreover, DA dynamics in rat brain were successfully monitored in real time, and the selective sensing ability of the microsensor in vivo was also demonstrated. The present study provides a new method for selective dynamics monitoring of DA in the brain, which would help to better understand the pathological and physiological functions of DA.

Tailoring Efficient Fluorogenic Tactic for Ultrasensitive Detection of Dopamine in Urine and Rat Brain through Real-Time and In Situ Formation of High-Performance Fluorophore.

Owing to the predominance of dopamine (DA) in controlling mental health, planning an innovative method for DA detection with simplicity and high efficacy is conducive to the assessment of neurological disorders. Herein, an efficient fluorogenic tactic has been elaborated for ultrasensitive detection of DA with remarkably enhanced turn-on response. Utilizing a twisted intramolecular charge-transfer (TICT)-suppressing strategy, a highly emissive azocine derivative 11-hydroxy-2,3,6,7,11,12,13,14-octahydro-1H,5H,10H-11,14a-methanoazocino[5',4':4,5]furo[2,3-f]pyrido[3,2,1-ij]quinolin-10-one (J-Aza) is generated via a one-step reaction between DA and 8-hydroxyjulolidine. It is marvelous that J-Aza not only possesses ideal fluorescence quantum yield (ΦF) as high as 0.956 but also exhibits bathochromic shifted fluorescence (green emissive) and stronger anti-photobleaching capacity superior to traditional azocine-derived 1,2,3,4-tetrahydro-5H-4,11a-methanobenzofuro[2,3-d]azocin-5-one (Aza) with moderate ΦF, blue fluorescence, and poor photostability. By confining the TICT process, the detection limit to DA can be reduced to 80 pM, which is competitive in contrast to previously reported fluorescence methods. Encouraged by the instant response (within 90 s), wide linear range (0.1-500 nM), great selectivity, and excellent sensitivity, this fluorogenic method has been used for the real-time measurement of DA contents in practical urine samples with satisfactory results. Furthermore, the cerebral DA level in the reserpine-induced depression rat model has also been evaluated by our designed method, demonstrating its potent analytical applicability in the biosensing field.

Neuroprotective potential of saroglitazar in 6-OHDA induced Parkinson's disease in rats.

Parkinson's disease (PD) is a neurodegenerative disorder that affects 2%-3% of the population worldwide. Clinical presentation of PD includes motor and non-motor symptoms. The interplay between pathogenic factors such as increased oxidative stress, neuroinflammation, mitochondrial dysfunction and apoptosis are responsible for neurodegeneration in PD. Intrastriatal administration of 6-hydroxy dopamine (6-OHDA) in rat brain provoked oxidative and nitrosative stress by decreasing endogenous antioxidants such as superoxide dismutase, catalase, glutathione, glutathione peroxidase and glutathione reductase. Consequently, interleukin-6, tumour necrosis-α, interferon-γ and cyclooxygenase-2 mediated neuroinflammation leads to mitochondrial dysfunction, involving inhibition of complex-II and IV activities, followed by apoptosis and degeneration of striatal dopaminergic neurons. Degeneration of dopaminergic neurons resulted in reduced dopamine turnover, consequently induced behavioural abnormalities in rats. Activation of peroxisome proliferator-activated receptors (PPARs) have protective role in PD by modulating response of antioxidant enzymes, neuroinflammation and apoptosis in various animal models of PD. Saroglitazar (SG) being dual PPAR-α/γ agonist activates both PPAR-α and PPAR-γ receptors and provide neuroprotection by reducing oxidative stress, neuroinflammation, mitochondrial dysfunction and apoptosis of dopaminergic cells in 6-OHDA induced PD in rats. Thereby, SG restored striatal histopathological damage and dopamine concentration in rat striatum, and behavioural alterations in rats. Thus, SG proved neuroprotective effects in rat model of PD. Potential benefits of SG in rat model of PD advocates to consider it for further preclinical and clinical evaluation.

Food restriction and hyperactivity induce changes in corticolimbic brain dopamine and serotonin levels in female rats

Compelling data support altered dopamine (DA) and serotonin (5-HT) signaling in anorexia nervosa (AN). However, their exact role in the etiopathogenesis of AN has yet to be elucidated. Here, we evaluated the corticolimbic brain levels of DA and 5-HT in the induction and recovery phases of the activity-based anorexia (ABA) model of AN. We exposed female rats to the ABA paradigm and measured the levels of DA, 5-HT, the metabolites 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), 5-hydroxyindoleacetic acid (5-HIAA), and the dopaminergic type 2 (D2) receptors density in feeding- and reward-implicated brain regions (i.e., cerebral cortex, Cx; prefrontal cortex, PFC; caudate putamen, CPu; nucleus accumbens, NAcc; amygdala, Amy; hypothalamus, Hyp; hippocampus, Hipp). DA levels were significantly increased in the Cx, PFC and NAcc, while 5-HT was significantly enhanced in the NAcc and Hipp of ABA rats. Following recovery, DA was still elevated in the NAcc, while 5-HT was increased in the Hyp of recovered ABA rats. DA and 5-HT turnover were impaired at both ABA induction and recovery. D2 receptors density was increased in the NAcc shell. These results provide further proof of the impairment of the dopaminergic and serotoninergic systems in the brain of ABA rats and support the knowledge of the involvement of these two important neurotransmitter systems in the development and progression of AN. Thus, providing new insights on the corticolimbic regions involved in the monoamine dysregulations in the ABA model of AN.

Neuro-protective potentials of N-acetylcysteine and zinc against di(2-ethylhexyl)-phthalate-induced neuro-histopathology and dys-regulations of Dopamine and Glutamate in rat brain

This study examined neuro-protective potentials of N-acetyl-cysteine (NAC) and Zinc on expression levels of Dopamine and Glutamate in the Cerebrum, Hypothalami and Pituitary Glands in Di(2-ethylhexyl)-phthalate (DEHP)-induced neurotoxicity in rats. Thirty-six adult male Wistar rats were randomly divided into 6 groups (n = 6). Group 1 was control. Groups 2-6 received oral administrations of 100 mg/kg NAC, 0.5 mg/kg Zinc, 750 mg/kg DEHP, DEHP + NAC doses and DEHP + Zinc doses respectively for 21 days. Brain histology (Heamatoxyline and Eosine technique), histochemical and enzyme-linked-immunosorbent assays of Dopamine and Glutamate in homogenates of Cerebrum, Hypothalami and Pituitary Glands were evaluated. Data were statistically analyzed using One-way-ANOVA with Tukey-post-hoc test at p ≤ 0.05. Histo-pathological evaluations of Cerebrum, Hypothalami and Pituitary Glands showed gross histo-alterations and neurodegenerative changes (Group 4), mild histo- and neuro-degenerative changes (Groups 5 and 6) and normal histology (Group 1). Histochemical analyses showed higher Dopamine levels in Hypothalami (Group 5) and Pituitary Glands (Groups 5 and 6), compared with Group 4. Furthermore, results showed lower Glutamate levels in Cerebrum, Hypothalami and Pituitary Glands of Groups 5 and 6, compared with Group 4. Overall, NAC and Zinc conferred neuro-protection and histo-protection against DEHP-induced neuro-toxicity, neuro-histopathology, decreased Dopamine levels and increased Glutamate levels.

Dynamics of Dopamine and Other Monoamines Content in Rat Brain after Single Low-Dose Carbon Nuclei Irradiation

Space radiation, presented primarily by high-charge and -energy particles (HZEs), has a substantial impact on the central nervous system (CNS) of astronauts. This impact, surprisingly, has not only negative but also positive effects on CNS functions. Despite the fact that the mechanisms of this effect have not yet been elucidated, several studies indicate a key role for monoaminergic networks underlying these effects. Here, we investigated the effects of acute irradiation with 450 MeV/n carbon (12C) nuclei at a dose of 0.14 Gy on Wistar rats; a state of anxiety was accessed using a light–dark box, spatial memory in a Morris water maze, and the dynamics of monoamine metabolism in several brain morphological structures using HPLC. No behavioral changes were observed. Irradiation led to the immediate suppression of dopamine turnover in the prefrontal cortex, hypothalamus, and striatum, while a decrease in the level of norepinephrine was detected in the amygdala. However, these effects were transient. The deferred effect of dopamine turnover increase was found in the hippocampus. These data underscore the ability of even low-dose 12C irradiation to affect monoaminergic networks. However, this impact is transient and is not accompanied by behavioral alterations.

NMDA Receptor‐ Mediated Release of Norepinephrine and Dopamine in Rat Brain: Effects of Ageing

A greater understanding of the neural changes occurring in the aging brain can facilitate the identification of possible molecular target(s) for pharmacological intervention to offset age-related cognitive deficits. Selective age-related vulnerabilities of glutamate neurotransmission have been found, as well as studies indicating age-related changes in the interaction between glutamate and other neurotransmitters (e.g. norepinephrine, dopamine). Previously, we have demonstrated that in brains from aged Fischer 344 rats, a model of neurocognitive aging, there is a marked deficit in glutamate-stimulated norepinephrine (NE) release measured in vitro in the hippocampus and cerebral cortex, and that this deficit is rescued by the addition of d-amphetamine sulfate (Dezfuli et al., 2019). Thus, amphetamine potentiates glutamate-stimulated NE release (and possibly release of other neurotransmitters). The purpose of the present study was to expand on our previous findings by (a) determining if glutamate-stimulated NE release is mediated by NMDA receptors and (b) investigating if there is a comparable deficit in glutamate-stimulated dopamine (DA) release in the aged Fischer 344 rat brain and whether it can also be rescued by amphetamine. To this end, experiments were performed in both young (2-3 months old) and aged Fischer 344 rats (18-22-month-old). The cerebral cortex was used for measuring glutamate-stimulated NE release, and the olfactory tubercle and striatum were used for measuring glutamate-stimulated DA release. Our results show that glutamate-stimulated NE release in the rat cortex is mediated exclusively by NMDA receptors. Results from the dopamine studies are ongoing and will be reported.

Monoaminergic Neurotransmission on the Antidepressant Effect of Leaf and Root Extracts of Rauwolfia vomitoria on the Locomotion and Immobility of Sprague‐Dawley Rats

Rauwolfia vomitoria is one of the medicinal plants which is used traditionally to manage hypertension, diabetes and mental disorder. This study is to investigate antidepressant-like effect of the leaf and root aqueous and ethanol extracts of R. vomitoria in the rat model using neurobehavioural indices; open field test and forced swimming test. The effect of the plant extracts on monoamine neurotransmiters’ system was also investigated. The neurobehavioural response of rats by open field test and forced swim test showed that there was a reduction in the explorative tendencies of the rats administered the aqueous and ethanol root extracts (0, 100, 200, 300, 400, 500mg/kg) compared to the control, while forced swim test reduced the immobility time of rats across all treatment groups, except 500mg/kg group. Neurotransmitter levels (serotonin, dopamine and norepinephrine) in plasma and brain of rats administered the different concentrations of root extracts exhibited significant (p <0.05) increase.The reduction in monoamine oxidase activity by the standard drugs and R. vomitoria extracts confirm that the mechanism of action R. vomitoria root extracts could be through inhibition of monoamine oxidase activity. Therefore, the mode of action may be due in part to the increase in monoamine levels or by suppression of the reuptake of the monoamine neurotransmiters. This study established that R. vomitoria root extract has antidepressant-like effect in rats.

Role of Monoaminergic Neurotransmission on the Antidepressant Effect of Leaf and Root Extracts of Rauwolfia vomitoria on the Locomotion and Immobility of Sprague-Dawley Rats

Rauwolfia vomitoria is one of the medicinal plants which is used traditionally to manage hypertension, diabetes and mental disorder. The scientific evidence to suggest its medicinal use especially in mental health treatment is lacking. This study aimed to investigate the antidepressant-like effect of the leaf and root extracts of R. vomitoria in the rat model using neurobehavioural indices; open field test and forced swimming test. Subsequently, the effect of the extracts on monoamine neurotransmitters system was investigated. The neurobehavioral response of rats by open field test and forced swim test showed that there was a reduction in the explorative tendencies of the rats administered the aqueous and ethanol root extracts (125, 250, 500 mg/kg) compared to the control while forced swim test reduced the immobility time of rats across all treatment groups except 500 mg/kg group. Neurotransmitter levels (serotonin, dopamine and norepinephrine) in plasma and brain of rats administered the different concentration of root extracts exhibited significant (p&lt;0.05) increase. Thus, the mode of action may be due in part to the increase in monoamine levels or by suppression of the reuptake of the monoamine neurotransmitters. This study established that R. vomitoria root extract has antidepressant-like effect in rats.

Short-Term Effect of MgSO4 on the Expression of NRG-ErbB, Dopamine, GABA, and Glutamate Systems in the Fetal Rat Brain.

MgSO4 has been used for the past two decades as neuroprotective treatment in a variety of preterm conditions. Despite the putative advantages of MgSO4 as a neuroprotective agent in the preterm brain, the short- and long-term molecular function of MgSO4 as a neuroprotective agent has not been fully elucidated. Neuregulin (NRG1)-ErbB4 signaling plays a critical role in embryonic brain development, in the biology of dopaminergic, GABAergic, and glutamatergic systems. We hypothesize that this pathway may be associated with the neuroprotective role of MgSO4. The current study aims to investigate the ability of MgSO4 to modulate the normal developing expression pattern of selected genes related to the NRG1-ErbB, dopaminergic, GABAergic, and glutamatergic systems. We demonstrate that overall short-term treatment of dam rats with MgSO4 affects the expression of fetal brain NRG1, NRG3, ErbB4, GAD67, tyrosine hydroxylase (TH), dopamine D2 and D1 receptors, GluN1, and GluN2B. More specifically, the administration of MgSO4 alters the expression of NRG-ErbB, GAD67, TH, and D2R at early gestation day 16 (GD16) regardless of the activation of the maternal immune system by lipopolysaccharide (LPS). Our data suggest that MgSO4 treatment may affect the expression of major neuronal systems and pathways mostly at an early gestation day. These changes might be an initial clue (foundation stone) in the molecular mechanism that underlies the beneficial effect of MgSO4 as a neuroprotective agent for the developmental brain.

Modulation and role of brain neurotransmitters in pilocarpine-induced seizures in the rat

Epilepsy, a group of serious disorders of the central nervous system characterized by a predisposition to recurrent unprovoked seizures due to abnormal excessive synchronous neural activity. Animal models of pilocarpine-induced seizures have been employed to demonstrate that ongoing epileptic activity in the brain can affect both excitatory and inhibitory synapses and thus neuronal plasticity. Neurotransmitters play a vital role in the functioning of brain. Our study aimed to investigate the changes in brain neurotransmitters in Wistar rat models of pilocarpine-induced seizures. Total 75 animals of pilocarpine-induced seizures models for epilepsy were studied. Behavioral, electroencephalographic and morphological changes induced by systemic administration of pilocarpine hydrochloride were studied in 3–90-day-old rats. Pilocarpine, 100, 200 and 380 mg/kg, presented a characteristic array of behavioral patterns in developing rats. Determination of brain norepinephrine, Gamma-aminobutyric acid (GABA), dopamine and serotonin was carried out using high performance liquid chromatography (HPLC) system, Agilent technologies 1100 series. The mean values of brain norepinephrine, dopamine and serotonin levels in pilocarpine-induced seizures rat brain were significantly increased compared to control group, which consequently, may reduce seizure susceptibility and epilepsy comorbidities. There was a significant decrease in Gamma-aminobutyric acid (GABA) values in treatment group compared to control. Neurotransmitters play a vital role in brain functioning and also have important function in epilepsy status.

Effect of novel phenothiazine derivatives on brain dopamine in Wistar rats

BackgroundNeurotransmitters are involved in several functions in the brain and the body of living things. Changes in the level of neurotransmitters in the brain are associated with several illnesses. Some of the drugs are controlling the neurotransmitter by adjusting the level in the brain and are exclusively used in the treatment of psychological disorders. The purpose of the study was to find out the effect of novel synthesised phenothiazine derivatives (GC1, GC2 and GC8) either alone (7.5 mg/kg or 15 mg/kg, oral) or in combination with amphetamine on the experimental animals.ResultsDopamine level in rat brain was estimated by a spectroscopic method using the UV-visible double beam spectrophotometer at 735 nm. The results revealed that these derivatives blocked the brain dopamine level significantly. The compound GC8 (15 mg/kg) significantly reduced the level of dopamine (0.151 ± 0.04, 0.284 ± 0.03) as similar to that of a standard drug. Furthermore, compounds GC2 (15 mg/kg) and GC1 (15 mg/kg) exhibited a varying level of dopamine inhibition level and have been found at 0.203 ± 0.06 μg/ml, 0.302 ± 0.04 μg/ml, 0.234 ± 0.02 μg/ml and 0.318 ± 0.07 μg/ml, respectively, after the administration of these derivatives either alone or in combination with amphetamine.ConclusionsThe study revealed that the compound 2-amino-6-(3-hydroxy-4-methyl phenyl) pyrimidine-4-yl) (7-chloro-10-(3- (N, N-dimethylamino) propyl)-10H-phenothiazine-3-yl) methanone (GC8, 15 mg/kg) extensively reduced the dopamine level. The order of dopamine-inhibiting effect of the selected compound was found to be GC8 > GC2 > GC1. The increased body weight and relative brain-body weight were also observed in the tested animals due to more intake of food and fluid retention.Graphical abstract

Insulin plus zinc induces a favorable biochemical response effects on oxidative damage and dopamine levels in rat brain.

The aim was to determine the effect of zinc (Zn) and insulin on oxidative stress and levels of dopamine in brain of rats. Wistar rats were treated either with zinc alone or combined with insulin during 10 days. After the last dose blood glucose was measured. Their brains were extracted to measure H2O2, Ca+2, Mg+2 ATPase, glutathione (GSH), lipid peroxidation (Tbars) and Dopamine. Zn does not possess anti-glycemic effect like Insulin however, it is noticeable that the combination of Insulin plus Zn induces a major glucose reduction (p < 0.0001) than Insulin alone. In cerebellum/medulla oblongata, the groups treated with Insulin and Zn show a significantly increase in dopamine (p < 0.005). Insulin plus Zn reduced GSH level in cortex. Insulin plus Zn reduced level of H2O2 in Striatum and in cerebellum/medulla oblongata. Lipid peroxidation was significantly reduced by the administration of Insulin as in the combination of Insulin and Zn in all regions (p < 0.0001). In cerebellum medulla oblongata, ATPase activity showed an increase only in the group treated with Insulin + Zn. CONCLUSION: These results suggest that the use of insulin plus Zn produce favorable changes on oxidative stress and this as consequence on the levels of dopamine.

Effect of Cardioxane and Selenium on Lipoperoxidation and Levels of Dopamine in Rat Brain and Heart

Background: Cardioxane has been probed in patients with advanced malignancies to protect the heart. Selenium, an essential micronutrient exerts varieties of functions such as antioxidant. The aim of this study was to test if cardioxane (CDX) and selenium (Se) have additive antioxidant protective effect on brain and heart, and their relation with dopamine levels. Methods: Thirty-six male Wistar rats divided in groups of 6 animals each, were treated as follows: G1, saline solution 0.9% (control); G2, 100 mg/kg of CDX; G3, 60 μg/kg of Se; G4, 20 mg/kg of 3-nitropropionic acid (3NP); G5, 3NP + CDX and G6, 3NP + Se. 3NP was used as an oxidative stress inducer. Drugs were administered intraperitoneally for 5 days. The animals were sacrificed on the last day of treatment and the brain and heart were extracted and used to measure lipid peroxidation, dopamine, glutathione (GSH), ATPase, calcium, and H2O2. Results: In G2 and G5, dopamine decreased in cortex and striatum while GSH increased in heart, cortex and cerebellum/medulla oblongata. ATPase activity increased in heart and cortex of groups 2, 3, 5 and 6. Lipoperoxidation and H2O2 increased in cortex of animals treated with 3NP. Conclusion: These results suggest that CDX increases antioxidant capacity in the brain and heart while selenium promotes alteration in dopamine metabolism in view of the capacity of 3NP to generate free radicals.

Relationship between Dopamine and Serotonin on the Effect of Ginkgo biloba Extract in the Treatment of Obsessive Compulsive Disorder in Rodents

In this study, the effect of EGb-761, the standardized extract of Ginkgo biloba at dose levels of 50, 100 and 200 mg/kg was investigated on experimental models of obsessive compulsive disorder such as quinpirole-induced compulsive checking in rats and marble burying behaviour in mice. Water maze test was used to evaluate the effect on spatial memory and the underlying mechanisms were predicted based on rat brain dopamine and serotonin levels. EGb-761 at 100 and 200 mg/kg showed significant improvement against quinpirole-induced compulsions. A protective effect on memory task was observed in EGb-761-treated rats. This could be attributed to the increase in serotonin and decrease in the dopamine levels. The protective effect of EGb-761 in the treatment of obsessive compulsive disorder is apparent through the performance in the open field and marble burying behaviour.

Effect of a binge-like dosing regimen of methamphetamine on dopamine levels and tyrosine hydroxylase expressing neurons in the rat brain

Methamphetamine, an amphetamine derivative, is a powerful psychomotor stimulant and commonly used drug of abuse. This study examined the effect of binge-like methamphetamine (MA) dosing (4 × 4 mg/kg, s.c., 2 h apart) on regional dopamine and dopaminergic metabolite levels in rat brain at a range of early time points after final dose (2–48 h). Body temperature was elevated when measured 2 h after the last dose. MA increased dopamine levels in the frontal cortex 2 and 24 h after the last dose. The dopamine level was also increased in the amygdala at 24 h. No change was observed in the striatum at any time point, but levels of the dopamine metabolite DOPAC were markedly reduced at 24 and 48 h. Tyrosine hydroxylase expression is induced downstream of dopamine activity, and it is the rate limiting enzyme in dopamine synthesis. The effect of MA binge-like dosing on the volume of tyrosine hydroxylase containing cell bodies and the area fraction of tyrosine hydroxylase containing fibres was also assessed. MA increased the area fraction of tyrosine hydroxylase fibres in the frontal cortex and reduced the volume of tyrosine hydroxylase containing cell bodies 2 h after last dose in the ventral tegmental area and the substantia nigra. An increase in cell body volume in the substantia nigra was observed 48 h after treatment. These findings collectively highlight the importance of the dopaminergic system in methamphetamine induced effects, identify the frontal cortex, amygdala and striatum as key regions that undergo early changes in response to binge-like methamphetamine dosing and provide evidence of time-dependent effects on the cell bodies and fibres of tyrosine hydroxylase expressing neurons.

Development, validation and comparison of surrogate matrix and surrogate analyte approaches with UHPLC-MS/MS to simultaneously quantify dopamine, serotonin and γ-aminobutyric acid in four rat brain regions.

As biomarkers, endogenous neurotransmitters play critical roles in the process of neuropsychiatric diseases, and neurotransmitter levels in different brain regions can contribute to neurological disease diagnosis and treatment. Due to the lack of a blank matrix for endogenous neurotransmitters, surrogate-matrix and surrogate-analyte approaches have been used for the determination of neurotransmitters to solve this problem. In this study, we capitalised on the high accuracy, precision, and throughput of UHPLC-MS/MS and developed new methods based on the two approaches. Both approaches satisfied FDA and EMA validation criterias after an appropriate parallelism assessment, and they were used to further quantify the three endogenous neurotransmitters, including dopamine (DA), serotonin (5-HT) and γ-aminobutyric acid (GABA) in rat brain four regions (cortex, striatum, hypothalamus and hippocampus) which represent the catecholamines, indolamines, and amino acids, respectively. Comparison of the results in the same rats (n=10) showed there was no significant difference in DA, 5-HT, or GABA levels between the two approaches (P > 0.05). The concentrations of DA and GABA were highest in striatum and hypothalamus, respectively, and the levels of 5-HT were paralleled in striatum and hippocampus almost 2-fold higher than other regions. This is the first study to compare these two approaches in the determination of endogenous neurotransmitter content in the rat brain, and the surrogate-matrix approach proved to be simple, rapid, and reliable, considering cost, matrix similarity, and practicality.

Intranasal instillation of iron oxide nanoparticles induces inflammation and perturbation of trace elements and neurotransmitters, but not behavioral impairment in rats.

Over the last decades, engineered nanomaterials have been widely used in various applications due to their interesting properties. Among them, iron oxide nanoparticles (IONPs) are used as theranostic agents for cancer, and also as contrast agents in magnetic resonance imaging. With the increasing production and use of these IONPs, there is an evident raise of IONP exposure and subsequently a higher risk of adverse outcome for humans and the environment. In this work, we aimed to investigate the effects of sub-acute IONP exposure on Wistar rat, particularly (i) on the emotional and learning/memory behavior, (ii) on the hematological and biochemical parameters, (iii) on the neurotransmitter content, and (vi) on the trace element homeostasis. Rats were treated during seven consecutive days by intranasal instillations at a dose of 10mg/kg body weight. The mean body weight increased significantly in IONP-exposed rats. Moreover, several hematological parameters were normal in treated rats except the platelet count which was increased. The biochemical study revealed that phosphatase alkaline level decreased in IONP-exposed rats, but no changes were observed for the other hepatic enzymes (ALT and AST) levels. The trace element homeostasis was slightly modulated by IONP exposure. Sub-acute intranasal exposure to IONPs increased dopamine and norepinephrine levels in rat brain; however, it did not affect the emotional behavior, the anxiety index, and the learning/memory capacities of rats.

Endosulfan and its toxicity on GABA, 5-HT and Dopamine in albino rat brain

Endosulfan and its toxicity on GABA, 5-HT and Dopamine in albino rat brain

MWCNTs/MoS2 Decorated Cobalt Oxide Polyhedrons Composite Film Modified Electrode for Electrochemical Determination of Dopamine in Rat Brain and Human Blood Serum Samples

MWCNTs/MoS2 Decorated Cobalt Oxide Polyhedrons Composite Film Modified Electrode for Electrochemical Determination of Dopamine in Rat Brain and Human Blood Serum Samples