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Koponen E Rantamäki T Voikar V Saarelainen T MacDonald E Castrén E 《Cellular and molecular neurobiology》2005,25(6):973-980
1. Neurotrophins and serotonin have both been implicated in the pathophysiology of depression and in the mechanisms of antidepressant treatments. 2. Brain-derived neurotrophic factor (BDNF) influences the growth and plasticity of serotonergic (5-HT) neurons via the activation of trkB receptor. 3. Transgenic mice overexpressing the full-length trkB receptor (TrkB.TK+) and showing increased trkB activity in brain, and their wild type (WT) littermates, were injected with the antidepressant fluoxetine or saline, and analyzed behaviorally in the forced swimming test paradigm and biochemically for the concentrations of brain monoamines and their metabolites. 4. The TrkB.TK+ mice displayed increased latency to immobility in the forced swim test, suggesting resistance to behavioral despair. 5. Fluoxetine increased the latency to immobility in wild-type mice to a similar level as seen in the trkB.TK+ mice after saline treatment, but had no further behavioral effect in the swimming behavior of the trkB.TK+ mice. 6. Only minor differences in the levels of brain monoamines and their metabolites were observed between the transgenic and wild-type mice. 7. These data, together with other recent observations, suggest that trkB activation may play a critical role in the behavioral responses to antidepressant drugs in mice. 相似文献
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Nicotine-Induced Changes in Neurotransmitter Levels in Brain Areas Associated with Cognitive Function 总被引:12,自引:0,他引:12
Singer S Rossi S Verzosa S Hashim A Lonow R Cooper T Sershen H Lajtha A 《Neurochemical research》2004,29(9):1779-1792
Nicotine, one of the most widespread drugs of abuse, has long been shown to impact areas of the brain involved in addiction and reward. Recent research, however, has begun to explore the positive effects that nicotine may have on learning and memory. The mechanisms by which nicotine interacts with areas of cognitive function are relatively unknown. Therefore, this paper is part of an ongoing study to evaluate regional effects of nicotine enhancement of cognitive function. Nicotine-induced changes in the levels of three neurotransmitters, dopamine (DA), serotonin (5-HT), norepinepherine (NE), their metabolites, homovanillic acid (HVA), dihydroxyphenylacetic acid (DOPAC), 5-hydroxyindoleacetic acid (5-HIAA), and their precursor, L-DOPA, were evaluated in the ventral and dorsal hippocampus (VH and DH), prefrontal and medial temporal cortex (PFC and MTC), and the ventral tegmental area (VTA) using in vivo microdialysis in awake, freely moving, male Sprague-Dawley rats. The animals were treated with acute nicotine (0.5 mg/kg, s.c.) halfway through the 300-min experimental period. The reuptake blockers, desipramine (100 microM) and fluoxetine (30 microM), were given to increase the levels of NE and 5-HT so that they could be detected. Overall, a nicotine-induced DA increase was found in some areas, and this increase was potentiated by desipramine and fluoxetine. The two DA metabolites, HVA and DOPAC, increased in all the areas throughout the experiments, both with and without the inhibitors, indicating a rapid metabolism of the released DA. The increase in these metabolites was greater than the increase in DA. 5-HT was increased in the DH, MTC, and VTA in the presence of fluoxetine; its metabolite, 5-HIAA, was increased in the presence and absence of fluoxetine. Except in the VTA, NE levels increased to a similar extent with desipramine and fluoxetine. Overall, nicotine appeared to increase the release and turnover of these three neurotransmitters, which was indicated by significant increases in their metabolites. Furthermore, DA, and especially HVA and DOPAC, increased for the 150 min following nicotine administration; 5-HT and NE changes were shorter in duration. As gas chromatography experiments showed that nicotine levels in the brain decreased by 75% after 150 min, this may indicate that DA is more susceptible to lower levels of nicotine than 5-HT or NE. In conclusion, acute nicotine administration caused alterations in the levels of DA, 5-HT, and NE, and in the metabolism of DA and 5-HT, in brain areas that are involved in cognitive processes. 相似文献
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Ken-ichiro Katsura† Jaroslava FolbergrovᆠGunilla Gidö Bo K. Siesjö 《Journal of neurochemistry》1994,62(4):1511-1515
Abstract: The present study was undertaken to explore how transient ischemia in rats alters cerebral metabolic capacity and how postischemic metabolism and blood flow are coupled during intense activation. After 6 h of recovery following transient forebrain ischemia 15 min in duration, bicuculline seizures were induced, and brains were frozen in situ after 0.5 or 5 min of seizure discharge. At these times, levels of labile tissue metabolites were measured, whereas the cerebral metabolic rate for oxygen (CMRO2 ) and cerebral blood flow (CBF) were measured after 5 min of seizure activity. After 6 h of recovery, and before seizures, animals had a 40–50% reduction in CMRO2 , and CBF. However, because CMRO2 rose threefold and CBF fivefold during seizures, CMRO2 and CBF during seizures were similar in control and postischemic rats. Changes in labile metabolites due to the preceding ischemia encompassed an increased phosphocreatine/ creatine ratio, as well as raised glucose and glycogen concentrations. Seizures gave rise to minimal metabolic perturbation, essentially comprising reduced glucose and glycogen contents and raised lactate concentrations. It is concluded that although transient ischemia leads to metabolic depression and a fall in CBF, the metabolic capacity of the tissue is retained, and drug-induced seizures lead to a coupled rise in metabolic rate and blood flow. 相似文献
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Alexa Orand Arpana Gupta Wendy Shih Angela P. Presson Christian Hammer Beate Niesler Nuwanthi Heendeniya Emeran A. Mayer Lin Chang 《PloS one》2015,10(8)
Background
Genetic and environmental factors contribute to the pathophysiology of irritable bowel syndrome (IBS). In particular, early adverse life events (EALs) and the catecholaminergic system have been implicated.Aims
To investigate whether catecholaminergic SNPs with or without interacting with EALs are associated with: 1) a diagnosis of IBS, 2) IBS symptoms and 3) morphological alterations in brain regions associated with somatosensory, viscerosensory, and interoceptive processes.Methods
In 277 IBS and 382 healthy control subjects (HCs), 11 SNPs in genes of the catecholaminergic signaling pathway were genotyped. A subset (121 IBS, 209 HCs) underwent structural brain imaging (magnetic resonance imaging [MRI]). Logistic and linear regressions evaluated each SNP separately and their interactions with EALs in predicting IBS and GI symptom severity, respectively. General linear models determined grey matter (GM) alterations from the SNPs and EALs that were predictive of IBS.Results
1) Diagnosis: There were no statistically significant associations between the SNPs and IBS status with or without the interaction with EAL after adjusting for multiple comparisons. 2) Symptoms: GI symptom severity was associated with ADRA1D rs1556832 (P = 0.010). 3) Brain morphometry: In IBS, the homozygous genotype of the major ADRA1D allele was associated with GM increases in somatosensory regions (FDR q = 0.022), left precentral gyrus (q = 0.045), and right hippocampus (q = 0.009). In individuals with increasing sexual abuse scores, the ADRAβ2 SNP was associated with GM changes in the left posterior insula (q = 0.004) and left putamen volume (q = 0.029).Conclusion
In IBS, catecholaminergic SNPs are associated with symptom severity and morphological changes in brain regions concerned with sensory processing and modulation and affect regulation. Thus, certain adrenergic receptor genes may facilitate or worsen IBS symptoms. 相似文献7.
1. The purpose of the present study was to determine the effect of zinc on the status of various neurotransmitters as well
as behavioral patterns of lithium-treated rats. The study was designed with a view to find out whether zinc affords protection
to brain against lithium toxicity.
2. Animals were segregated into four different groups. Animals in group I were fed with standard laboratory feed and water
ad libitum and served as normal controls. Animals in group II and IV were given lithium in the form of lithium carbonate in their diet
at a dose level of 1.1 g/Kg diet. Animals in group III and IV were given zinc treatment in the form of zinc sulfate at a dose
level of 227 mg/L mixed in drinking water of animals.
3. The effects of all the treatments were studied for a duration of 1, 2, and 4 months with regard to the parameters, which
included estimation of serotonin and dopamine concentrations as well as the activity of acetylcholinesterase in cerebral cortex
of rat brain. Further, passive avoidance, active avoidance, and behavior despair tests were conducted to assess the short-term
memory, cognitive behavior, and psychomotor dysfunction of the animals, respectively.
4. Initially, a decrease in the acetylcholinesterase activity was reported in cerebral cortex followed by an increase in the
enzyme activity after 2 and 4 months of lithium treatment. Serotonin concentration significantly decreased after 2 and 4 months
of lithium treatment, whereas dopamine concentration increased significantly after 4 months of lithium treatment. Zinc administration
to the lithium-treated group significantly improved the acetylcholinesterase activity as well as the concentration of dopamine
and serotonin. Further, lithium-treated rats showed an increase in depression time as compared to normal controls both after
1 and 4 months of treatment. Short-term memory significantly improved in lithium-treated rats in all treatment groups. However,
no change in the cognitive behavior of the animals was reported after lithium treatment. Zinc co-administration with lithium
significantly improved the short-term memory and cognitive functions of the animals. From the above results it can be concluded
that zinc proved beneficial in altering the status of neurotransmitters as well as the behavior patters of the animals treated
with both short and long-term lithium therapy. 相似文献
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Human activities in protected areas can affect wildlife populations in a similar manner to predation risk, causing increases in movement and vigilance, shifts in habitat use and changes in group size. Nevertheless, recent evidence indicates that in certain situations ungulate species may actually utilize areas associated with higher levels of human presence as a potential refuge from disturbance-sensitive predators. We now use four-years of behavioral activity budget data collected from pronghorn (Antilocapra americana) and elk (Cervus elephus) in Grand Teton National Park, USA to test whether predictable patterns of human presence can provide a shelter from predatory risk. Daily behavioral scans were conducted along two parallel sections of road that differed in traffic volume - with the main Teton Park Road experiencing vehicle use that was approximately thirty-fold greater than the River Road. At the busier Teton Park Road, both species of ungulate engaged in higher levels of feeding (27% increase in the proportion of pronghorn feeding and 21% increase for elk), lower levels of alert behavior (18% decrease for pronghorn and 9% decrease for elk) and formed smaller groups. These responses are commonly associated with reduced predatory threat. Pronghorn also exhibited a 30% increase in the proportion of individuals moving at the River Road as would be expected under greater exposure to predation risk. Our findings concur with the ‘predator shelter hypothesis’, suggesting that ungulates in GTNP use human presence as a potential refuge from predation risk, adjusting their behavior accordingly. Human activity has the potential to alter predator-prey interactions and drive trophic-mediated effects that could ultimately impact ecosystem function and biodiversity. 相似文献
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Ian W. MacPhee 《BMJ (Clinical research ed.)》1953,1(4818):1023-1028
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The influence of a single injection of delta-sleep-inducing peptide (DSIP; 30 g/kg body weight) on neurochemical parameters of rats' brain was studied under the conditions of chronic administration of dopamine analogs inducing DA-system hyperactivity – 50 mg/kg body weight of L-DOPA for 30 days or 2,5 mg/kg body weight of amphetamine for 21 days. The parameters of serotonergic system (MAO A activity, 5-HT, and 5-HIAA contents) and of dopaminergic system (MAO B activity, DA, NA, and HVA contents) were investigated in the cortex and caudate nucleus of control, DA or amphetamine, and DSIP receiving rats. Changes caused by the two DA-system activating drugs had both similarities and differences, and the corrective action of DSIP also had certain peculiarities depending on the pharmacological preparation used for the induction of DA-system hyperactivity and on the investigated brain structure. It is supposed that DSIP action might be based on the activation of serotonergic system that ensures the adaptive behavior of the animals. 相似文献
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Since the time of Plato, philosophers and educational policy-makers have assumed that the study of mathematics improves one''s general ‘thinking skills’. Today, this argument, known as the ‘Theory of Formal Discipline’ is used in policy debates to prioritize mathematics in school curricula. But there is no strong research evidence which justifies it. We tested the Theory of Formal Discipline by tracking the development of conditional reasoning behavior in students studying post-compulsory mathematics compared to post-compulsory English literature. In line with the Theory of Formal Discipline, the mathematics students did develop their conditional reasoning to a greater extent than the literature students, despite them having received no explicit tuition in conditional logic. However, this development appeared to be towards the so-called defective conditional understanding, rather than the logically normative material conditional understanding. We conclude by arguing that Plato may have been correct to claim that studying advanced mathematics is associated with the development of logical reasoning skills, but that the nature of this development may be more complex than previously thought. 相似文献
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Mauro E. Nunes Talise E. Müller Marcos M. Braga Barbara D. Fontana Vanessa A. Quadros Aline Marins Cíntia Rodrigues Charlene Menezes Denis B. Rosemberg Vania Lucia Loro 《Molecular neurobiology》2017,54(6):3925-3934
Paraquat (PQ) administration consists in a chemical model that mimics phenotypes observed in Parkinson’s disease (PD), due to its ability to induce changes in dopaminergic system and oxidative stress. The aim of this study was to evaluate the actions of PQ in behavioral functions of adult zebrafish and its influence on oxidative stress biomarkers in brain samples. PQ (20 mg/kg) was administered intraperitoneally with six injections for 16 days (one injection every 3 days). PQ-treated group showed a significant decrease in the time spent in the bottom section and a shorter latency to enter the top area in the novel tank test. Moreover, PQ-exposed fish showed a significant decrease in the number and duration of risk assessment episodes in the light–dark test, as well as an increase in the agonistic behavior in the mirror-induced aggression (MIA) test. PQ induced brain damage by decreasing mitochondrial viability. Concerning the antioxidant defense system, PQ increased catalase (CAT) and glutathione peroxidase (GPx) activities, as well as the non-protein sulfhydryl content (NPSH), but did not change ROS formation and decreased lipid peroxidation. We demonstrate, for the first time, that PQ induces an increase in aggressive behavior, alters non-motor patterns associated to defensive behaviors, and changes redox parameters in zebrafish brain. Overall, our findings may serve as useful tools to investigate the interaction between behavioral and neurochemical impairments triggered by PQ administration in zebrafish. 相似文献
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pH Changes Associated with Iron-Stress Response 总被引:3,自引:0,他引:3
When Fe-inefficient T3238fer and Fe-efficient T3238FER tomatoes were supplied iron, and nitrogen as nitrate, they increased the pH of the nutrient culture. When they were supplied nitrogen as ammonium, they decreased the pH. When Fe supply was limited, Fe-stress response developed in T3238FER that opposed the usual nitrate response and decreased, rather than increased, the pH. A “reductant” which reduced Fe3+ to Fe2+ was released from the roots of these plants and lowered the pH; and there was a tremendous increase in the uptake of Fe. T3238fer did not produce “reductant” in response to Fe-stress; the pH increased, and the plants developed Fe-deficiency when nitrogen was supplied as nitrate. Nitrogen nutrition and iron-stress response are important factors associated with iron chlorosis in plants. Release of hydrogen ions from roots of Fe-stressed plants is caused by more than response to imbalanced uptake of cations and anions. 相似文献
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Medeiros Rita de Cássia Noronha Moraes Juliana Oliveira Rodrigues Samara Dias Cardoso Pereira Leidiano Martins Aguiar Helen Quézia da Silva de Cordova Clarissa Amorim Silva Yim Júnior Alberto de Cordova Fabiano Mendes 《Neurochemical research》2020,45(4):940-955
Neurochemical Research - Thiamine deficiency (TD) produces severe neurodegenerative lesions. Studies have suggested that primary neurodegenerative events are associated with both oxidative stress... 相似文献
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