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Phosphorylation of Protein Kinase C substrate proteins in rat hippocampal slices - effect of calpain inhibition

100%
Domanska-Janik K., Zablocka B., Zalewska T., Zajac H.
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vol. 58
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issue 4
247-252
EN
Incubation of the acutely dissected rat hippocampal slices in calcium-containing media resulted in spontaneous activation-translocation of classical PKC isoforms and their subsequent (especially g- type) proteolytic degradation. These changes were blocked by calpain inhibitor MDL 28 170 in 100 mM concentration. Rat hippocampal slices were metabolically prelabelled with 32Pi and stimulated with NMDA/glycine, depolarization or phorbol dibutyrate (PDBu) treatment. The basal phosphorylation of specific PKC substrates (MARCKS, neuromodulin and neurogranin) was significantly reduced in non-stimulated slices by MDL pretreatment. In contrast, only the slices where calpain activity was inhibited responded to further NMDA or phorbol dibutyrate stimulation by a substantial increase of PKC-dependent protein phosphorylation. It is concluded that the PKC phosphorylation system is severely affected by non-specific activation and a subsequent, calpain-dependent proteolysis in the acutely prepared hippocampal slices. Calpain inhibition by 100 mM MDL partially prevented these changes and increased stimulus-dependent phosphorylation of PKC-specific protein substrates.
2

The effect of chronic treatment with imipramine, ECS and nifedipine on the beta-andrenergic function in the rat hippocampal slices

88%
Frankiewicz T., Legutko B., Czyrak A., Pilc A.
Polish Journal of Pharmacology
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1993
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vol. 45
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issue 2
207-212
EN
Nifedipine administered for either 10 or 28 dayz did not affect the cAMP response to noradrenalina or isoproterenol; however it decreased the inhibitory effect of ECS on the noradrenaline-stimulated cAMP generation.
3
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Enhancement of [3H]D-aspartate release during ischemia like conditions in rat hippocampal slices:source of excitatory amino acids

88%
Zablocka B., Domanska-Janik K.
Acta Neurobiologiae Experimentalis
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1996
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vol. 56
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issue 1
63-70
EN
Ischemic neuronal injury is supposed to be caused in part by the extracellular accumulation of excitatory amino acids (EAA). Neurotransmitter and metabolic EAA can be released from synaptic vesicles and cytoplasm of neurones and glial cells. In this study the release of the glutamate analogue [3H]D-aspartate (3[H]D-ASP), loaded into 500 mugm slices of rat hippocampus, was investigated. The efflux of the label was measured during anoxic - aglycemic ("ischemic") and normoxic K+ depolarization. To identify the pools from which [3H]D-ASP is released we have estimated its calcium dependence and the effects of inhibitors of: (1) Na+ - dependent transporter of amino acids (100 mugM L-trans-pyrrolidine-2,4-dicarboxylic acid /L-trans-PDC/), (2) sodium channel (1 mugM tetrodotoxin TTX), and (3) anion channel (1mM furosemide). [3H]D-ASP released upon normoxic depolarization was 40% inhibited by TTX,nearly 40% by L-trans-PDC and over 50% by furosemide. The "ischemic" release was in 40% calcium dependent, completely TTX independent and in approximately 50% blocked by furosemide treatment. Our data suggest that EAA accumulated in the synaptic cleft during ischemia are mainly released from the cytosolic compartment by mechanisms wich are connected with the ischemic increase of extracellular potassium concentration.
4
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Measurement of nitric oxide in hippocampal slices: induction with nitroso compounds and the effect of depolarization

88%
Haklar G., Saybasili H., Yuksel M., Yalcyn S.
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EN
Nitric oxide not only acts as a messenger for different physiological processes, but also mediates neurotoxicity associated with a variety of neurological disorders including epilepsy. The molecular mechanisms behind these actions are unclear. In this study, we aimed to detect relative amounts of NO released from rat hippocampal slices by chemiluminescence measurements under NMDA stimulation and spontaneous depolarization conditions. Hippocampal slices were preferred because of their functional integrity useful in simulating in vivo conditions. The reliability of the system was verified by administering increasing concentrations of a NO donor sodium nitroprusside in different redox milieu and a NO scavenger, carboxy-2-phenyl-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxide (carboxy PTIO). The redox versatility of NO allows interconversion from neuroprotective to neurotoxic species by a change in the ambient redox milieu. We have quantitated NO formed under NMDA stimulation and spontaneous depolarization conditions, and showed that depolarization increased NO formation and was excitotoxic for the neural tissue.
5
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Effects of DAGO on the rodent hippocampal evoked potentials using different perfusion solutions

88%
San_ M. S., Menendez L., Gutierrez M., Hidalgo A., Baamonde A.
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EN
Opioid receptor agonists exert excitatory effects in the hippocampus by inhibiting GABA release. We report that the mu-opioid agonist, DAGO, increases the amplitude of the population spikes (PS) measured in the stratum pyramidale of the CA1 cell layer in mouse and rat hippocampal slices perfused with an artificial cerebrospinal fluid (ACSF), but not when perfused in Krebs solution. The GABA A agonist, 3-APS, induces inhibitory responses when perfused in either ACSF or Krebs. Also, the field excitatory postsynaptic potentials (EPSP) measured on stratum radiatum do not differ when the slice is perfused with either ACSF or Krebs. The increase in the amplitude of the PS induced by DAGO is not obtained when perfused in a modified ACSF whose concentration of MgSO4 was lowered to its concentration in the Krebs solution (from 2.4 mM to 1.2 mM). Thus, changes in the concentration of MgSO4 seem to be responsible for the different responses induced by DAGO.
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