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1

Evoked cardiac response components in cognitive processing: differential effects of amyotrophic lateral sclerosis

100%
Kaiser J., Wronka E., Barry R. J., Szczudlik A.
Acta Neurobiologiae Experimentalis
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1999
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tom 59
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nr 4
2
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Different receptor subtypes are involved in the serotonin-induced modulation of epileptiform activity in rat frontal cortex in vitro

100%
Bobula B., Zahorodna A., Bijak M.
Journal of Physiology and Pharmacology
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2001
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tom 52
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nr 2
3

Frontal cortex, laterality, and memory: encoding versus retrieval

100%
Kavcic V., Zhong J., Yoshiura T., Doty R. W.
Acta Neurobiologiae Experimentalis
|
2003
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tom 63
|
nr 4
4

The development of sustained attention in children might be related to the maturation of frontal cortical functions

84%
Paus T.
Acta Neurobiologiae Experimentalis
|
1989
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tom 49
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nr 1
5

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

84%
Kaminska K., Golembiowska K.
Acta Neurobiologiae Experimentalis
|
2013
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tom 73
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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.
6

Metabolic enhancer piracetam attenuates rotenone induced oxidative stress: a study in different rat brain regions

84%
Verma D. K., Joshi N., Raju K. S., Wahajuddin M., Singh R. K., Singh S.
Acta Neurobiologiae Experimentalis
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2015
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tom 75
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nr 4
Piracetam is clinically being used nootropic drug but the details of its neuroprotective mechanism are not well studied. The present study was conducted to assess the effects of piracetam on rotenone induced oxidative stress by using both ex vivo and in vivo test systems. Rats were treated with piracetam (600 mg/kg b.w. oral) for seven constitutive days prior to rotenone administration (intracerebroventricular, 12µg) in rat brain. Rotenone induced oxidative stress was assessed after 1 h and 24 h of rotenone administration. Ex vivo estimations were performed by using two experimental designs. In one experimental design the rat brain homogenate was treated with rotenone (1 mM, 2 mM and 4 mM) and rotenone+piracetam (10 mM) for 1 h. While in second experimental design the rats were pretreated with piracetam for seven consecutive days. On eighth day the rats were sacrificed, brain homogenate was prepared and treated with rotenone (1 mM, 2 mM and 4 mM) for 1h. After treatment the glutathione (GSH) and malondialdehyde (MDA) levels were estimated in brain homogenate. In vivo study showed that pretreatment of piracetam offered significant protection against rotenone induced decreased GSH and increased MDA level though the protection was region specific. But the co-treatment of piracetam with rotenone did not offer significant protection against rotenone induced oxidative stress in ex vivo study. Whereas ex vivo experiments in rat brain homogenate of piracetam pretreated rats, showed the significant protection against rotenone induced oxidative stress. Findings indicated that pretreatment of piracetam significantly attenuated the rotenone induced oxidative stress though the protection was region specific. Piracetam treatment to rats led to its absorption and accumulation in different brain regions as assessed by liquid chromatography mass spectrometry/mass spectrometry. In conclusion, study indicates the piracetam is able to enhance the antioxidant capacity in brain cells in region specific manner. The study is also revealing the rationale for its clinical use in cognitive impairment and other neurological diseases.
7
Content available remote

Imipramine and citalopram reverse corticosterone-induced alterations in the effects of the activation of 5-HT1A and 5-HT2 receptors in rat frontal cortex

84%
Zahorodna A., Hess G.
Journal of Physiology and Pharmacology
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2006
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tom 57
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nr 3
Using extracellular recording we studied changes in the reactivity of rat frontal cortical slices to the 5-HT1A, 5-HT2 and 5-HT4 receptor agonists, (±)-2-dipropyloamino-8-hydroxy-1,2,3,4-tetrahydronaphtalene hydrobromide (8-OH-DPAT), (±)-2,5-dimethoxy-4-iodoamphetamine hydrochloride (DOI) and zacopride, respectively, induced by an earlier treatment of animals with corticosterone lasting 1 or 3 weeks. Spontaneous bursting activity was recorded in ex vivo slices incubated in a medium devoid of Mg2+ ions and containing picrotoxin (30 µM). Repetitive, but not single, corticosterone administration resulted in an attenuation of the effect of the activation of 5-HT1A receptors and in an enhancement of the effect related to 5-HT2 receptors. The effect of 5-HT4 receptor activation remained unchanged. In separate two sets of experiments rats were treated with corticosterone for 3 weeks and additionally with imipramine or citalopram, beginning on the eighth day of corticosterone administration. In the corticosterone plus imipramine as well as corticosterone plus citalopram groups the effects of 8-OH-DPAT and DOI were not different from control indicating that corticosterone-induced functional modifications in the reactivity of 5-HT1A and 5-HT2 receptors were reversed by antidepressant treatments.
8
Content available remote

The influence of repeated administration of clozapine and haloperidol on the effects of the activation of 5-HT1A, 5-HT2 and 5-HT4 receptors in rat frontal cortex

84%
Zahorodna A., Bobula B., Grzegorzewska M., Tokarski K., Hess G.
Journal of Physiology and Pharmacology
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2004
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tom 55
|
nr 2
The effects of a repeated treatment with antipsychotic drugs, clozapine and haloperidol, on the modulation of network activity ex vivo by 5-HT receptors were examined in rat frontal cortical slices using extracellular recording. Rats were treated for 21 days with clozapine (30 mg/kg p.o.), or haloperidol (1 mg/kg p.o.). Spontaneous bursting activity was induced in slices prepared 3 days after the last drug administration by perfusion with a medium devoid of Mg2+ ions and with added picrotoxin (30 mM). The application of 2-3 µM 8-OH-DPAT, acting through 5-HT1A receptors, resulted in a reversible decrease of bursting frequency. In the presence of 1 µM DOI, the 5-HT2 agonist, or 5 µM zacopride, the 5-HT4 agonist, bursting frequency increased. Chronic clozapine treatment resulted in an attenuation of the effect of the activation of 5-HT2 receptors, while the effects related to 5-HT1A and 5-HT4 receptor activation were unchanged. Treatment with haloperidol did not influence the reactivity to the activation of any of the three 5-HT receptor subtypes. These data are consistent with earlier findings demonstrating a selective downregulation of 5-HT2A receptors by clozapine and indicate that chronic clozapine selectively attenuates the 5-HT-mediated excitation in neuronal circuitry of the frontal cortex while leaving the 5-HT-mediated inhibition intact.
9
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Apomorphine-induced upregulation of serotonin 5-HT2A receptors in male rats is independent from development of aggressive behaviour

84%
Matto V., Skrebuhhova T., Allikmets L.
Journal of Physiology and Pharmacology
|
1999
|
tom 50
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nr 2
10
Content available remote

The 5-HT7 receptor antagonist SB 269970 counteracts restraint stress-induced attenuation of long-term potentiation in rat frontal cortex

67%
Tokarski K., Bobula B., Kusek M., Hess G.
Journal of Physiology and Pharmacology
|
2011
|
tom 62
|
nr 6
11
Content available remote

Repeated blockade of 5-HT7 receptors depresses glutamatergic transmission in the rat frontal cortex

67%
Tokarski K., Kusek M., Hess G.
Journal of Physiology and Pharmacology
|
2012
|
tom 63
|
nr 2
12

Bicuculline administration into ventromedial hypothalamus: effects on fear and regional brain monoamines and GABA concentrations in rats

67%
Zagrodzka J., Romaniuk A., Wieczorek M., Boguszewski P.
Acta Neurobiologiae Experimentalis
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2000
|
tom 60
|
nr 3
13

Cortical projections of the thalamic mediodorsal nucleus in the rat. Definition of the prefrontal cortex

67%
Divac I., Mogensen J., Petrovic-Minic B., Zilles K., Regidor J.
Acta Neurobiologiae Experimentalis
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1993
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tom 53
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nr 2
14

Effect of acute hepatic encephalopathy on [3 H]dopamine release from rat cerebral cortex and striatum in vitro: role of Ca2plus

59%
Borkowska H. D., Oja S. S., Hilgier W., Saransaari P., Albrecht J.
Acta Neurobiologiae Experimentalis
|
2000
|
tom 60
|
nr 1
Hepatic encephalopathy (HE) is characterized by motor symptoms associated with disturbed functions of the dopaminergic systems, but the underlying mechanisms are not clear. A previous study from our laboratories revealed that HE, induced in rats by repeated treatment with thioacetamide, enhanced the 50 mM potassium (KC1) -stimulated release of newly loaded [3H]dopamine in both striatal and frontal cerebral cortical slices in the presence of Ca2+. In the present study we compared the effects of HE on dopamine release in striatal and frontal cerebral cortical slices and synaptosomes in the presence and absence of Ca2+. HE enhanced the KCl-stimulated [3H]dopamine release from striatal and frontal cortical synaptosomes in the presence of Ca2+ to the same extent as in slices prepared from the respective brain regions. In the absence of Ca2+ a slight reduction in dopamine release was observed in frontal cortical synaptosomes from HE rats when compared to control rats, while no effect of HE on the release was discernible in frontal cortical and striatal slices and striatal synaptosomes. We conclude that in both brain regions studied HE stimulates dopamine exocytosis triggered by Ca2+ influx without affecting the release mediated by means of plasma membrane transporters or exocytosis involving intraterminal Ca2+.
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