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Characterization of beta-adrenergic receptors in duck cerebral cortex

100%
Zawilska H. J. B., Zalewska-Kaszubska J., Marczak G., Gorska D., Woldan-Tambor A.
Acta Neurobiologiae Experimentalis
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2000
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vol. 60
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issue 3
301-307
EN
Beta-adrenoceptor binding sites were characterized in duck cerebral cortex by an in vitro binding technique, using [3H]dihydroalprenolol ([3H]DHA) as a receptor-specific radioligand. The specific binding of [3H]DHA to duck cerebral cortical membranes was found to be rapid, stable, saturable, reversible, and of high affinity. Saturation analysis resulted in a linear Scatchard plot suggesting binding to a single class of receptor binding sites with high affinity (Kd = 1.18 nM) and high capacity (Bmax = 162 fmol/mg protein). Competition studies showed the following relative rank order of potency of various compounds to inhibit the [3H]DHA binding: antagonists - ICI 118,551 > S(-)-propranolol >> betaxolol, yohimbine, WB-4101, prazosin, mianserine; agonists - isoprenaline @ fenoterol > salbutamol >> clonidine, phenylephrine. The obtained data suggest that in duck cerebral cortex beta-adrenergic receptors (like those described in brains of chick and pigeon) are of the beta2 subtype. This is in contrast to what has been reported for the mammalian brain, where - among b-adrenoceptors - the beta1 subtype is predominant.
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Age-related changes in muscarinic receptor and post-receptor mechanisms in brain and ileum strip of rats

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Michalek H., Fortuna S., Pintor A.
Acta Neurobiologiae Experimentalis
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1993
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vol. 53
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issue 1
93-101
EN
Age-related differences in the response of the cerebral cortex and ileum strip to a repeated treatment with an anticholinesterase compound, diisopropyl fluorophosphate (DFP) were evaluated in 3- and 24-month Sprague-Dawley rats. The response was measured in terms of acetylcholinestrase (AChE) inhibition and total muscarinic receptor density (MAChRs, measured as3 H-QNB binding). At the end of DFP treatment there was a 75% inhibition of brain AChE and 30% inchibition of ileal AChE, independently of age. The adaptive down-regulation of brain MAChRs was more pronounced in aged than in young rats (50 and 25%, respectively), while that of ileal MAChRs was greater in young than in aged (50 and 35%). The normalization of cortical MAChRs was delayed in aged rats of ileal MAChRs was delayed in young rats. As regards age-related changes of AChE and MAChRs in untreated rats, there was a 30% decrease of cortical and ileal AChE, no changes in Bmax of cortical MAChRs and a 45% deficit of ileal MAChRs. This was accompanied by only a little age-related decrease in sensitivity of the isolated ileum to cholinergic agonists. Additional experiments on the responsiveness of phosphatidyl inositol syste stimulated with carbachol showed that accumulation of inositol phosphate both in cortical and ileum strip slices was higher in aged than in young rats. The overall data indicate that treatment- and age-related changes of AChR mechanisms in the ileum strip differ considerably from those in the brain. However, the increased efficiency of post-receptor mechanisms in old age is their common feature.
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Ischemia-related alteration of GABAA-operated chloride channel properties in gerbil hippocampus and cerebral cortex

88%
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.
4
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D1 dopamine receptors distribution following photothrombotic stroke in rat cerebral cortex

88%
Rogozinska K., Skangiel-Kramska J.
Acta Neurobiologiae Experimentalis
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2005
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vol. 65
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issue 2
167-172
EN
The effect of focal photothrombotic stroke on the distribution of D1 dopamine receptor (D1R) sites was examined in different cortical areas of rat brain with quantitative receptor autoradiography using [3H]SCH23390 as a ligand. Unilateral cortical stroke was located in the primary somatosensory cortex. After different survival times (1, 7 and 28 days) D1R binding levels were determined in the lesion core, penumbra, frontoparietal motor (FrPaM) and somatosensory (FrPaSS) areas as well as in homotopic regions in the contralateral hemisphere. One day after stroke, D1R density decreased by 36% (P<0.01) in the lesion core relative to sham-operated controls. At 7th day binding density was further reduced by 56% (P<0.002). Twenty-eight days after infarction, D1R binding returned to control level. No alterations in D1R binding levels were found in penumbra and other investigated regions. We suggest that the return of D1R binding to control level in the area initially corresponding to the infarct results from the shrinkage of the lesion volume.
5
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Cholinergic modulation of synaptic transmission in horizontal connections of rat motor cortex

88%
Hess G., Krawczyk R.
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EN
The influence of compounds interacting with cholinergic systems on field potentials evoked in layer II/III horizontal connections was investigated in rat motor cortex in vitro. The cholinesterase inchibitor eserine (10 mM) decreased field responses by 20?2%. This inhibito effect could be prevented by preincubation with atropine (10 mM) Application of 5 mM carbachol resulted in reduction of the responses by 30?1% These reductions were reversible, repeatable and independent of stimulus intensity; they could be blocked by the M1 muscarinic receptor antagonist pirenzepine (3 mM) but not by the M2 ,muscarinic receptor antagonist gallamine (10 mM). During carbachol application, paired-pulse facilitation (40 ms interpulse interval) was increased. The results indicate that endogenous acetylcholine may modulate excitatory synaptic transmission in horizontal connections of rat motor cortex, most likely by acting upon M1 receptors located presynaptically on glutamatergic terminals, and may contribute both to information processing and synaptic plasticity within the motor cortex
6
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Effects of pituitary adenylate cyclase-activating polypeptide (PACAP) on cyclic AMP formation in the duck and goose brain

75%
Nowak J. Z., Kuba K., Zawilska J. B.
Acta Neurobiologiae Experimentalis
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2000
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vol. 60
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issue 2
209-214
EN
Two molecular forms of pituitary adenylate cyclase-activating polypeptide (PACAP), i.e., PACAP27 and PACAP38 (0.0001-1 muM), as well as vasoactive intestinal polypeptide (VIP; 0.1-3 muM), have been studied for their effects on cyclic AMP formation in the hypothalamus and cerebral cortex of duck and goose. All three peptides concentration-dependently stimulated cyclic AMP production in the tested brain regions of 2-3-weeks-old (young) ducks, with VIP showing at least one order of magnitude weaker activity than PACAP. This characteristics suggests the existence in the duck's brain of adenylyl cyclase-linked PAC1 receptors. Both forms of PACAP also stimulated the nucleotide formation in the cerebral cortex and hypothalamus of 5-6-months-old (adult) ducks or geese grown under natural environment. The peptides-evoked effects in adult and young ducks were comparable, and clearly greater than those found in adult geese. The present data extend our recent observations made on chicks, and suggest PACAP to be a potent stimulator of the cyclic AMP generation in the avian central nervous system.
7
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Carnitine - a known compound, a novel function in neural cells

75%
Nalecz K., Nalecz M.
Acta Neurobiologiae Experimentalis
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1996
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vol. 56
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issue 2
597-609
EN
Carnitine (4-N-trimethylammonium-3-hydroxybutyric acid) seems to fullfil in the brain a different role than in peripheral tissues.Carnitine is accumulated by neural cells in a sodium-dependent way.The existence of a novel rtansporter in plasma membrane, specific to compounds with a polar group in the beta-position with respect to carboxyl group, has been postulated.The presence of carnitine carrier in the inner mitochondrial membrane has been proven and the protein has been purified.It is postulated that its major role in adult brain would be rtanslocation of acetyl moieties from mitochondria into the cytoplas for acetylocholine synthesis.The latter process is stimulated by carnitine and choline in a synergistic way in cells utilizing glucose as a main energetic substrate.Carnitine metabolism in neural cells leads to accumulation of different acyl derivatives of carnitine.Palmitoylcarnitine can influence directly the activity of protein kinase C.An involvment of carnitine in a decrease of palmitate pool used for palmitoylation of regulatory proteins has been postulated.
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