The effects of ladasten on dopaminergic neurotransmission and hippocampal synaptic plasticity in rats

Mikhaylova, Marina; Jv, Vakhitova; Rs, Yamidanov; MKh, Salimgareeva; Sb, Seredenin; Behnisch, Thomas

doi:10.1016/j.neuropharm.2007.07.001

Cited by 8 publications

(9 citation statements)

References 24 publications

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“…These findings and our previous results concerning the dynamics of PKA, PKC, CaMKII and ERK1/2 (extracellular signal-regulated kinase) suggest that early (0.5 h after ladasten dosing) increase in pCREB level is possibly associated with the fact that induction of transcriptional factor expression is realized via different signal transduction systems (PKA, PKC, CaMKII and ERK1/2) [1,2,12]. According to modern view, CREB is a central integration link for various signal pathways.…”

Section: Resultssupporting

confidence: 78%

“…Regulation of CREB activity in the hypothalamus most likely depends on CaMKII and ERK1/2 kinases. This statement comes from the data about similar dynamics of protein kinase activity and pCREB level in this structure [1,12]. The same relationship was observed in the hippocampus: peaks of CaMKII and ERK1/2 activation and pCREB level are observed at the same time interval after drug administration.…”

Section: Resultsmentioning

confidence: 52%

“…Systems mediated by calcium ions are the main signaling systems, triggering changes in cell metabolism inducted by this compound [1,2,3,12]. It is known that Ca 2+ -dependent pathways play the principal role at the early phase of target activation and readily respond to extracellular stimuli.…”

Section: Ladastenmentioning

confidence: 99%

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Changes in CREB (SER133) Content and DNA-Binding Activity of Transcriptional Factors in Rat Brain Cells against the Background of Ladasten Exposure

et al. 2009

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Section: Resultssupporting

confidence: 78%

Section: Resultsmentioning

confidence: 52%

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Changes in CREB (SER133) Content and DNA-Binding Activity of Transcriptional Factors in Rat Brain Cells against the Background of Ladasten Exposure

et al. 2009

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“…Transformation of STP to LTP might be a result of priming plasticity related signaling pathways related to cAMP and phospholipase C (PLC). For example modulation of the dopaminergic system before STP induction was found to transform STP to LTP (Mikhaylova et al. 2007).…”

Section: Discussionmentioning

confidence: 99%

MPTP modulates hippocampal synaptic transmission and activity‐dependent synaptic plasticity via dopamine receptors

Zhu¹,

Huang²,

Chen³

et al. 2012

Journal of Neurochemistry

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J. Neurochem. (2012) 122, 582–593. Abstract Parkinson’s disease (PD)‐like symptoms and cognitive deficits are inducible by 1‐methyl‐4‐phenyl‐1, 2, 3, 6‐tetrahydropyridine (MPTP). Since cognitive abilities, including memory formations rely also on hippocampus, we set out to clarify the effects of MPTP on hippocampal physiology. We show that bath‐application of MPTP (25 μM) to acute hippocampal slices enhanced AMPA receptor‐mediated field excitatory postsynaptic potentials (AMPAr‐fEPSPs) transiently, whereas N‐methyl‐D‐aspartate (NMDA) receptor‐mediated fEPSPs (NMDAr‐fEPSPs) were facilitated persistently. The MPTP‐mediated transient AMPAr‐fEPSP facilitation was antagonized by the dopamine D2‐like receptor antagonists, eticlopride (1 μM) and sulpiride (1 and 40 μM). In contrast, the persistent enhancement of NMDAr‐fEPSPs was prevented by the dopamine D1‐like receptor antagonist SCH23390 (10 μM). In addition, we show that MPTP decreased paired‐pulse facilitation of fEPSPs and mEPSCs frequency. Regarding activity‐dependent synaptic plasticity, 25 μM MPTP transformed short‐term potentiation (STP) into a long‐term potentiation (LTP) and caused a slow onset potentiation of a non‐tetanized synaptic input after induction of LTP in a second synaptic input. This heterosynaptic slow onset potentiation required activation of dopamine D1‐like and NMDA‐receptors. We conclude that acute MPTP application affects basal synaptic transmission by modulation of presynaptic vesicle release and facilitates NMDAr‐fEPSPs as well as activity‐dependent homo‐ and heterosynaptic plasticity under participation of dopamine receptors.

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“…L-DOPA, DA, and DOPAC contents were measured using high-performance liquid chromatography (HPLC/UV; Agilent) as described previously [17]. Samples (approximately 100 mg) were homogenized (1 : 10 w/v) in 0.1 M HClO 4 and centrifuged at 12 000 × g for 15 min at 4°C.…”

Section: Hplc Analysismentioning

confidence: 99%

Puerarin Protects Dopaminergic Neurons against 6-Hydroxydopamine Neurotoxicity via Inhibiting Apoptosis and Upregulating Glial Cell Line-Derived Neurotrophic Factor in a Rat Model of Parkinson's Disease

et al. 2010

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Neurodegeneration is one of the primary etiologies in the onset of Parkinson's disease. In the quest for a new antiparkinsonism treatment the potential benefits of puerarin from the roots of Pueraria lobata have been recognized. Thus, we examined whether puerarin is capable to protect dopaminergic neurons of the substantia nigra against 6-hydroxydopamine induced neuronal cell death. Our data showed that the intraperitoneal administration of 0.12 mg/kg/day puerarin over 10 days reduced the 6-hydroxydopamine-induced decrease of tyrosine hydroxylase-positive cell counts. Analysis of apoptosis via DNA fragmentation by the terminal deoxynucleotidyl transferase dUTP nick-end labeling assay proved that puerarin could prevent 6-hydroxydopamine-induced apoptosis. As an additional apoptotic cell death marker, the BAX and BCL-2 expression levels were investigated using immunohistochemistry. Whereas 6-hydroxydopamine increased the level of Bax (p < 0.05), the coadministrated puerarin significantly antagonized this effect in a dose-dependent manner. Bcl-2 expression was not affected. Analysis of the dopamine, dihydroxyphenylacetic acid, and L-dihydroxy-phenyl-alanine contents of 6-hydroxydopamine-treated animals by HPLC revealed that puerarin was capable to restore the contents of dopamine and its metabolites. Moreover, the expression level of glial cell line-derived neurotrophic factor in the striatum was higher in puerarin than in rats treated with 6-hydroxydopamine alone. These results suggest that puerarin develops its neuroprotective effect against 6-hydroxydopamine-induced neurotoxicity in the substantia nigra through the inhibition of apoptotic signaling pathways and upregulation of glial cell line-derived neurotrophic factor expression in the striatum.

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The effects of ladasten on dopaminergic neurotransmission and hippocampal synaptic plasticity in rats

Cited by 8 publications

References 24 publications

Changes in CREB (SER133) Content and DNA-Binding Activity of Transcriptional Factors in Rat Brain Cells against the Background of Ladasten Exposure

Changes in CREB (SER133) Content and DNA-Binding Activity of Transcriptional Factors in Rat Brain Cells against the Background of Ladasten Exposure

MPTP modulates hippocampal synaptic transmission and activity‐dependent synaptic plasticity via dopamine receptors

Puerarin Protects Dopaminergic Neurons against 6-Hydroxydopamine Neurotoxicity via Inhibiting Apoptosis and Upregulating Glial Cell Line-Derived Neurotrophic Factor in a Rat Model of Parkinson's Disease

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