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Aging and beta amyloid peptides decrease cholinergic receptor-mediated calcium increase in brain cortex synaptoneurosomes

100%
Samochocki M.
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vol. 58
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issue 1
3-11
EN
In this study, the muscarinic cholinergic receptor (MAChR)-evoked inositol 1,4,5-trisphosphate (IP3)-mediated increase of cytosolic calcium concentration ([Ca]i) in synaptoneurosomes from brain cortex of adult and aged rats was investigated. In addition, the effect of two beta-amyloid (A beta) peptides, 1-28 and 25-35, on the resting and MAChR-induced increase of [Ca]i in brain cortex synaptoneurosomes of adult rats was evaluated. Release of IP3 was measured after prelabeling of synaptoneurosomal phosphoinositides withmyo-[2-3H]inositol. Changes in [Ca]i were monitored by using fura-2 indicator. The effect of A beta peptides was evaluated following their preincubation with synaptoneurosomal protein for 1, 5, 30 and 60 min. It was observed that in brain cortex synaptoneurosomes from aged rats, Ca2+-dependent and MAChR-mediated IP3 production was not changed in comparison with that estimated in adult brain, over 60 min of incubation. Activation of MAChR in synaptoneurosomes from brain cortex of adult rats for 10 min increased [Ca]i by about 60% over its resting level (240 nM). This increase was completely blocked by muscarinic antagonists, atropine and pirenzepine, as well as by the antagonist of IP3 receptor,8-(diethylamino)-octyl-3,4,5-trimethoxybenzoate (TMB-8). In aged brain, there was no detectable change in resting [Ca]i (165 nM) due to MAChR stimulation. The 25-35 A beta peptide caused a time-dependent significant increase of resting [Ca]i in synaptoneurosomes from brain cortex of adult rats, which was almost five-fold after 60 min. In the same conditions, the action of 1-28 A beta peptide was statistically insignificant up to 30 min, then a rapid increase of resting [Ca]i by two-fold was observed up to 60 min. Both A beta peptides decreased markedly the MAChR-dependent elevation of [Ca]i in respect to control (resting [Ca]i in synaptoneurosomes from brain cortex of adult rats. These results indicate that beta-amyloid 1-28 and 25-35 peptides may be involved in alteration of muscarinic receptor-mediated signal transduction during brain aging.
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Ischemia-related alteration of GABAA-operated chloride channel properties in gerbil hippocampus and cerebral cortex

51%
Strosznajder J., Koladkiewicz I., Chalimoniuk M., Samochocki M.
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issue 2
95-102
EN
The properties of GABA-gated chloride (Cl^-) channels in ischemia-reperfusion injury were studied by determination of the binding and dissociation kinetics of a specific Cl^- channel ligand, tert-butylbicyclophosphoro[^35S]thionate (TBPS) and by determination of ^36Cl^- uptake in the presence of the GABAA receptor agonist, muscimol. Four days after ischemia a small but insignificant decrease of [^35S]TBPS binding to synaptic plasma membranes (SPM) was observed in the hippocampus and cerebral cortex as compared to control. The effect of ischemia was larger and statistically significant after the first and second month of reperfusion, constituting 20% inhibition of [^35S]TBPS binding to SPM of sham-operated gerbils. On the other hand, the half-life of fast phase [^35S]TBPS dissociation four days after ischemia was markedly diminished by about 40%-50% as compared to its control value and persisted during the first and second month of reperfusion in the hippocampal SPM. A similar but less potent reduction of the half-life of the fast phase of [^35S]TBPS dissociation (about 30% versus control) appeared one and two months after ischemia in cerebral cortex SPM. One month after ischemia muscimol-stimulated ^36Cl^- uptake into cerebral cortex synaptoneurosomes was lowered as compared with control uptake, but remained statistically insignificant in the whole range of muscimol concentrations tested. Our results indicated that ischemia-reperfusion injury significantly decreases opening time of GABAA receptor-gated Cl^- channels in the hippocampus and cerebral cortex, which may lower the hyperpolarization ability of this receptor complex leading to an imbalance between excitatory and inhibitory neurotransmitter pathways in these brain areas, and in consequence to neuronal dysfunction or degeneration.
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