Wyniki wyszukiwania

1

Protective effects of nicotine against glutamate-induced neurotoxicity in PC12 cells

100%

Sun X., Liu Y., Hu G., Wang H.

Cellular and Molecular Biology Letters

|

2004

|

tom 09

|

nr 3

This study aimed to assess whether nicotine prevented glutamate neurotoxicity in PC12 cells, and to identify the molecular mechanisms of any effects. The results showed that glutamate neurotoxicity in PC12 cells could be prevented by treatment with nicotine at concentrations of 10 nmol.l-1-1 mmol.l-1. This effect was in turn found to be inhibited by the application of the nicotinic acetylcholine receptor (nAChR) antagonist mecamylamine. Nicotine significantly decreased the basal level of intracellular free Ca2+ and enhanced the buffering action on Ca2+ overload induced by high concentrations of glutamate (5 mmol.l-1). In addition, nicotine treatment up-regulated the mRNA and protein expression of apoptosis-related factors including bcl-2 mRNA and protein, but down-regulated the expression of bax mRNA and protein. It is concluded that the protective effects of nicotine against the neurotoxicity induced by glutamate are mediated by nAChRs, due to the increased buffering action on Ca2+ and the modulation of apoptotic processes.

2

Increased gene expression of selected vesicular and glial glutamate transporters in the frontal cortex in rats exposed to voluntary wheel running

86%

Graban J., Hlavacova N., Jezova D.

Journal of Physiology and Pharmacology

|

2017

|

tom 68

|

nr 5

3

Glutamate: glyoxylate aminotransferase from the seedlings of rye (Secale cereale L.)

86%

Paszkowski A., Niedzielska A.

Acta Biochimica Polonica

|

1989

|

tom 36

|

nr 1

4

The hydrosulfide groups of glutamate: glyoxylate and serine: glyoxylate aminotransferases from rye [Secale cereale L.] seedlings

86%

Paszkowski A.

Acta Physiologiae Plantarum

|

1995

|

tom 17

|

nr 1

5

Immunohistochemical investigations of excitotoxicity in experimental spinal cord trauma

86%

Adamek D., Kaluza J., Jasinski A.

Folia Histochemica et Cytobiologica

|

2001

|

tom 39

|

nr 2

6

Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik

Effects of glutamate and zinc ions on the contractility of vascular smooth muscle preparations

72%

Nguyen-Duong H.

Journal of Elementology

|

2010

|

tom 15

|

nr 3

559-572

It was shown in this study that isolated porcine coronary arteries (PCA) contracted by depolarization with high Ko or by histamine are dose-dependently relaxed by glutamic acid, aspartic acid, N-methyl-asparate (NMDA) and γ-aminobutyric acid (GABA). Zn2+ was also shown to relax dose-dependently PCA contractions induced by 50 mM KCl with an ED50 value of about 1.5 mM and to inhibit dose-dependently histamine-induced contractions, shifting ED50 values from 6μM to 40 μM, not affecting however corresponding cumulative concentration-response (CCR) curves established for acetylcholine-induced contractions. Furthermore, since Zn2+ ions are co-localized in many glutamatergic synapses of the central nervous system, it has been postulated in analogy to glutamate neurotoxicity that perturbations of the synaptic zinc concentrations might be a triggering factor in several cerebral diseases, such as ischemic strokes and sustained seizures. Unfortunately, little is known so far about effects of glutamate and zinc ions on the vascular tone. Although the nature of the glutamatergic receptors occurring in the blood vessels investigated in this study remains unclear, the results suggest that glutamate and Zn2+ ions interact with voltage-gated as well with ligand-operated Ca-channels. An interesting aspect might be the putative role of glutamate and zinc as long-term toxic agents in the early steps of the pathomechanisms leading to degenerative vascular lesions.

7

Involvement of oxytocin in the nucleus tractus solitarii on central cardiovascular control: interactions with glutamate

72%

Vela C., Diaz-Cabiale Z., Parrado C., Narvaez M., Covenas R., Narvaez J. A.

Journal of Physiology and Pharmacology

|

2010

|

tom 61

|

nr 1

59-65

Oxytocin (OT) is a peptide involved in several physiological functions in the central nervous system including central cardiovascular regulation. To clarify the role of endogenous OT in cardiovascular control, one group of anesthetized rats received unilateral microinjections of the OT receptor antagonist [d(CH2)5,Tyr(Me)2,Orn8]-vasotocin (OTA) in the nucleus tractus solitarii (NTS) and a second group was injected with specific OT antiserum (Anti-OT). Moreover, the modulation of the cardiovascular effect of L-glutamate (GLU) by OT was also evaluated by cardiovascular analysis using effective and threshold doses of GLU. Mean arterial pressure (MAP) and heart rate (HR) were measured from a femoral catheter. OTA significantly (p<0.01) decreased the vasopressor and tachycardiac long-lasting response elicited by an effective dose of OT. Microinjections of Anti-OT antibody did not modify the values of MAP and HR compared with the control group. With regard to the OT/GLU coinjections, a subthreshold dose of OT significantly (p<0.001) counteracted the vasodepressor and bradycardiac responses induced by GLU. The coinjection of subthreshold doses of OT and GLU did not produce a change in MAP or in HR. These findings seem to exclude an endogenous tonic action of OT on central regulation of MAP and HR, although they confirm the significant role of OT on central cardiovascular control within the NTS. In fact, the modulation of GLU responses by OT supports the importance of OT on the central cardiovascular adjustments likely acting on the baroreceptor reflex sensitivity.

8

Electrophysiology and pharmacology of the optic input to the rat intergeniculate leaflet in vitro

72%

Blasiak A., Blasiak T., Lewandowski M. H.

Journal of Physiology and Pharmacology

|

2009

|

tom 60

|

nr 1

171-180

The mammalian intergeniculate leaflet (IGL) of the thalamus is a neuronal element of the circadian timing system, which receives direct photic input from the retina. The purpose of this study was to analyze responses of rat IGL neurons in vitro to optic tract stimulation and to identify neurotransmitters released from the terminals of retinal ganglion cells in this structure. Following optic tract stimulation, most of the responding IGL cells were excited and only a minority of them were inhibited. Neurons showing the excitatory response were tested in the presence of AP-5, a selective antagonist of NMDA receptors. In most cases the responses were only partially inhibited by the presence of AP-5. Complete disappearance of excitatory responses was achieved by adding CNQX, an AMPA/kainate receptor-selective antagonist, to the standard incubation fluid. Inhibitory responses were blocked or considerably attenuated in the presence of bicuculline, a GABAA receptor antagonist, in the ACSF. This study demonstrated that glutamate is the main neurotransmitter mediating optic tract input to the IGL, acting mainly via non-NMDA ionotropic receptors. It was also shown that NMDA and GABAA receptors are involved in passing photic input to the IGL, albeit to a much lesser extent.

9

Effect of VMAT2 inhibition on glutamate and adenosine in rat frontal cortex

72%

Kaminska K., Golembiowska K.

Acta Neurobiologiae Experimentalis

|

2013

|

tom 73

|

nr 1

Our earlier studies showed that inhibition of VMAT2 caused depletion of dopamine in rat striatum accompanied with outflow of glutamate and production of hydroxyl radical. Inhibition of VMAT2 is observed in an early phase of Parkinson’s Disease (PD) as evidenced by PET studies in PD patients and in non-human primates. Recently it is observed that many neurons also release a classical transmitter other than the one with which they are usually associated. It is shown that neurons releasing monoamines can also release the excitatory transmitter glutamate. All neurons contain glutamate for its role in protein synthesis and metabolism, but they also express VGLUTs required for excitotoxic glutamate release. Moreover, it is also shown that several catecholamine cells such as VTA dopamine neurons are able corelease glutamate. Disturbed function of both, VMAT 2 and VGLUT may start catecholamine neurons degeneration that occurs at the early pre-clinical stage of PD. Accumulation of cytosolic dopamine may be neurotoxic for neurons through the generation of free radicals. Similarly, glutamate released from neurons or glial cells via GLT-1 transporter or cystine-glutamate exchanger or purinergic P2X7 receptor may stimulate glutamate receptors on various cells, induce increase in intracellular calcium which leads to excitotoxicity and generation of free radicals. ATP is required for packing of dopamine or glutamate in neuronal and glial vesicles and disturbed vesicular function results in ATP metabolism to adenosine in the presence of 5’-nucleotidase. In our study we tried to understand the early changes in dopamine synapses and glial cell responses which may provide insights on PD pathology. We injected animals with reserpine to inhibit vesicular transport and measured veratridine-evoked (100 µM) dopamine, glutamate and adenosine release using microdialysis in frontal cortex of freely moving rats. Extracellular dopamine, adenosine and glutamate were assayed by HPLC with electrochemical, fluorescenece and VIS detection. Reserpine at a single dose of 2.5 mg/kg increased veratridine-evoked glutamate release to 200% and adenosine release to 5 000% of baseline 20 h after administration. Reserpine at a dose of 0.25 mg/kg given repeatedly for 14 days increased evoked-glutamate release to maximum 210% and adenosine to 1 400% of baseline. At the same time veratridine-induced DA release was also markedly increased as compared to control animals. Veratridine-evoked glutamate and adenosine release were increased by 150 and 600% of baseline, respectively in intact rats. Obtained results indicate that under conditions of damaged vesicular transport there is significant overflow of glutamate and adenosine as well as increase in dopamine release in the rat frontal cortex. Marked increase in extracellular adenosine release may lead to activation of adenosine A2A receptors located in glutamate terminals or glial cells causing damage through induction of oxidative stress by glutamate or dopamine. Corelease of neurotransmitters and neuromodulators from neuronal or glial cells with disturbed vesicular transport may underline cortical pathology observed in PD.

10

Chronic stress changes prepulse inhibition after amphetamine challenge: the role of the dopaminergic system

72%

Lehner M. H., Karas-Ruszczyk K., Zakrzewska A., Gryz M., Wislowska-Stanek A., Kolosowska K., Chmielewska N., Skorzewska A., Turzynska D., Sobolewska A., Mierzejewski P., Plaznik A.

Journal of Physiology and Pharmacology

|

2018

|

tom 69

|

nr 3

11

Histochemical and biochemical studies on the glutamate transmitter metabolism

72%

Wolf G.

Folia Histochemica et Cytobiologica

|

1984

|

tom 22

|

nr 3-4

12

Excitatory neurosteroids attenuate apoptotic and excitotoxic cell death in primary cortical neurons

72%

Leskiewicz M., Jantas D., Budziszewska B., Lason W.

Journal of Physiology and Pharmacology

|

2008

|

tom 59

|

nr 3

457-475

Some neurosteroids show neuroprotective action in in vitro and in vivo studies, but their interaction with apoptotic/necrotic processes has been only partially unraveled. The aim of the present study was to examine the effect of dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEAS), pregnenolone (PGL) and allopregnanolone (Allo) on staurosporine-, glutamate-, and NMDA-induced damage in primary cortical neuronal culture. DHEA, DHEAS and PGL (0.1 and 1 µM) inhibited the staurosporine-evoked LDH release and decreased the number of apoptotic cells as shown by Hoechst`s staining, whereas Allo was without effect. The neurosteroids affected neither the staurosporine-evoked changes in caspase-3 activity nor the decrease in mitochondrial membrane potential. It was also shown that protective effects of DHEA, DHEAS and PGL against staurosporine-induced LDH release were attenuated by extracellular signal-regulated kinase (ERK) - mitogen-activated protein kinase (MAPK) inhibitor – PD 98059 (5 µM) but not by phosphatidylinositol-3-kinase (PI3-K) inhibitors such as LY 294002 (1 µM) or wortmannin (10 nM). The involvement of ERK2-MAPK in protective effects of neurosteroids was confirmed by Western blot study. Further study demonstrated that glutamate-induced cell damage was attenuated by DHEA, DHEAS, and PGL, but not by Allo. None of the steroids influenced NMDA-induced LDH release. The results of the present in vitro studies suggest that excitatory neurosteroids DHEA, DHEAS and PGL at physiological concentrations participate in the inhibition of cortical neuronal degeneration elicited by staurosporine and glutamate, whereas the most potent positive modulator of GABAA receptor - Allo - has no effect. Moreover, neurosteroids appear to attenuate the staurosporine-induced cell damage in a caspase-3 independent way and their neuroprotective mechanism of action involves the increase in ERK-MAPK phosphorylation.

13

Effects of xylazine on glutamate and GABA contents in the hippocampus and thalamencephal in the rat

72%

Yin B. S., Wang H. B., Gong D. Q., Li G. J., Gao L.

Bulletin of the Veterinary Institute in Puławy

|

2011

|

tom 55

|

nr 3

The purpose of the study was to define if anaesthetic action of xylazine could conceivably result from the potentiation of inhibitory neurotransmitters or the inhibition of excitatory neurotransmitter systems in the brain. Rats were injected with xylazine at a dose of 50 mg/kg b.w., and then the hippocampus and thalamencephal were removed at 0.1, 0.25, 0.5, 1, 1.5, 2, 4, and 6 h after the injection. Glutamate (Glu) and γ-aminobutyric-acid (GABA) were measured in the brain tissue by reversed-phase high-performance liquid chromatography. The results revealed that the hippocampus Glu level decreased significantly 0.1 h after the injection of xylazine, the thalamencephal GABA increased significantly 0.1 h after the injection, while the changes in hippocampus GABA and thalamencephal Glu were not significant. However, all of these changes returned to the normal level after 2 and 4 h, respectively. The results indicated the relative effects of xylazine on Glu and GABA levels in the hippocampus and thalamencephal.

14

NMDA glutamate receptor antagonism and the ventilatory response to hypoxia in the anesthetized rat

72%

Tarakanov I., Dymecka A., Pokorski M.

Journal of Physiology and Pharmacology. Supplement

|

2004

|

tom 55

|

nr 3

139-147

This study seeks to discern the influence of the NMDA glutamate-mediated pathway in the early stimulatory and late depressant phases of the hypoxic ventilatory response. We addressed this issue by recording ventilation before and after intravenous administration of the NMDA receptor antagonist MK-801 during acute, steady-state hypoxic challenges in the anesthetized, spontaneously breathing rats. Minute ventilation and its volume and frequency components were calculated and compared at the peak and nadir of the hypoxic response. We found that NMDA receptor antagonism appreciably affected both ventilatory phases of hypoxia. The early stimulation of ventilation was attenuated and the late depression was accentuated. The latter consisted of abolishment of the characteristic sustenance of hypoxic ventilation above the baseline level in the depressant phase, so that ventilation declined down to the baseline after NMDA receptor blockade. The inability to uphold ventilation in the depressant phase suggests that the NMDA glutamate-mediated pathway is operative in shaping the late hypoxic ventilatory response. The role of the glutamatergic pathway may thus be extended beyond the hitherto recognized early ventilatory stimulation of hypoxia.

15

Glia and glutamate: new key players in the pathology of major depression

72%

Rajkowska G.

Acta Neurobiologiae Experimentalis

|

2009

|

tom 69

|

nr 3

Postmortem studies in depression reveal age-dependent cell pathology in prefrontal cortex. Prominent reductions in glia and specifi cally, in astrocytes, are observed in younger depressed, whereas neuronal pathology is found in elderly with depression. As astrocytes regulate extracellular concentrations of glutamate (via glial glutamate transporters), an early defi cit in astrocytes could lead to increases in extracellular glutamate and toxic damage to neurons as depression progresses. This is supported by postmortem studies of reduced expression of mRNA and protein for the glial glutamate transporter in younger depressed and by reductions in glutamatergic neurons in elderly depressed. Moreover, alterations in glutamate metabolism are reported in neuroimaging studies of depressed patients. Interestingly, agents increasing expression of glial glutamate transporters and/or altering glutamate neurotransmission show antidepressant activity. Our hypothesis that glial pathology is an initial stage of cellular and neurochemical changes in depression was confi rmed by observations of glial/glutamate defi cits in chronically stressed rodents. Pharmacologically-induced loss of astroglia, but not neurons in the rat prefrontal cortex will induce depressive-like behaviors. Moreover, treatment with riluzole (a modulator of glutamate release) reverses stress-induced depressive-like behaviors and blocks glia impairments providing a link between dysfunction of glia and glutamate in depression.

16

Possible consequences of disruption of neuromuscular contacts in early development for motoneurone survival

72%

Greensmith L., Sieradzan K., Vrbova G.

Acta Neurobiologiae Experimentalis

|

1993

|

tom 53

|

nr 1

17

Metabolism of amino acids in germinating yellow lupine seeds. I. The decomposition of 14 C-aspartate and 14 C-glutamate during the imbibition

72%

Ratajczak W., Lehmann T., Polcyn W., Ratajczak L.

Acta Physiologiae Plantarum

|

1996

|

tom 18

|

nr 1

18

Gene expression of NMDA receptor subunits in rat adrenals under basal and stress conditions

72%

Schwendt M., Jezova D.

Journal of Physiology and Pharmacology

|

2001

|

tom 52

|

nr 4,2

In addition to the central nervous system, glutamate receptors have been recently identified in a number of peripheral tissues, including adrenals. Pharmacological evidence indicates that adrenal glutamate receptors may be involved in stress response, particularly in catecholamine release. However, possible stress-induced changes at the level of local receptors themselves have not been evaluated yet. This study was aimed to investigate gene expression of N-methyl-D-aspartate (NMDA) receptor subunits (NR1, NR2A, NR2B) in rat adrenal gland under basal and stress conditions, using RT-PCR. NR1 mRNA was found to be present in the adrenal gland, while mRNAs coding for NR2-type subunits failed to be detected in adrenal tissue. The distribution of NR1 mRNA in rat adrenals showed higher concentrations in the adrenal medulla (228%) compared to those in the cortex. Single stress stimulus (immobilization) induced a significant increase of NR1 gene expression in both medullar (by 25%) and cortical (by 66%) regions of the adrenal gland at 24 h, while no changes were observed at 3 h after the stress exposure. It is possible that delayed rise in adrenal NR1 gene expression following stress exposure represents one of the factors by which stress exerts long-term effects on adrenal function at the molecular level.

19

Inhibition of p38 kinase mimics survival signal-linked protection against apoptosis in rat cerebellar granule neurons

72%

Nath R., McGinnis K., Dutta S., Shivers B., Wang K. K. W.

Cellular and Molecular Biology Letters

|

2001

|

tom 06

|

nr 2

20

Glutamate excitotoxicity in transient global cerebral ischemia

72%

Paschen W.

Acta Neurobiologiae Experimentalis

|

1996

|

tom 56

|

nr 1

Ograniczanie wyników

Protective effects of nicotine against glutamate-induced neurotoxicity in PC12 cells

Increased gene expression of selected vesicular and glial glutamate transporters in the frontal cortex in rats exposed to voluntary wheel running

Glutamate: glyoxylate aminotransferase from the seedlings of rye (Secale cereale L.)

The hydrosulfide groups of glutamate: glyoxylate and serine: glyoxylate aminotransferases from rye [Secale cereale L.] seedlings

Immunohistochemical investigations of excitotoxicity in experimental spinal cord trauma

Effects of glutamate and zinc ions on the contractility of vascular smooth muscle preparations

Involvement of oxytocin in the nucleus tractus solitarii on central cardiovascular control: interactions with glutamate

Electrophysiology and pharmacology of the optic input to the rat intergeniculate leaflet in vitro

Effect of VMAT2 inhibition on glutamate and adenosine in rat frontal cortex

Chronic stress changes prepulse inhibition after amphetamine challenge: the role of the dopaminergic system

Histochemical and biochemical studies on the glutamate transmitter metabolism

Excitatory neurosteroids attenuate apoptotic and excitotoxic cell death in primary cortical neurons

Effects of xylazine on glutamate and GABA contents in the hippocampus and thalamencephal in the rat

NMDA glutamate receptor antagonism and the ventilatory response to hypoxia in the anesthetized rat

Glia and glutamate: new key players in the pathology of major depression