Publications by authors named "Carman-Krzan M"

Neurotrophin-3 (NT-3) is produced by astrocytes, in addition to neurons, and monoamine neurotransmitters play a role in controlling NT-3 synthesis. The impact of histamine (HA) on the regulation of NT-3 synthesis in cultured astrocytes has not been studied. We evaluated the involvement of histamine receptors and intracellular mechanisms in the regulation of NT-3 production by HA.

View Article and Find Full Text PDF

Astrocytes actively control neuronal activity and synaptic transmission and by producing various neurotrophic factors represent an important local cellular source of trophic support in the normal and diseased brain. Our present study showed the ability of astrocytes to synthesize neurotrophin-3 (NT-3) and the active involvement of the monoamine neurotransmitters noradrenaline, adrenaline, dopamine, and serotonin, as well as basic intracellular second messenger systems, in the regulation of NT-3 production in neonatal rat cortical astrocytes. Using a new NT-3 specific enzyme-immunoassay, we showed that neonatal rat cortical and, for comparison, cerebellar astrocytes in primary culture can synthesize NT-3; the basal cellular content of NT-3 protein was 23.

View Article and Find Full Text PDF

Brain-derived neurotrophic factor (BDNF) synthesis in astrocytes induced by noradrenaline (NA) is a receptor-mediated process utilizing two parallel adrenergic pathways: beta1/beta2-adrenergic/cAMP and the novel alpha1-adrenergic/PKC pathway. BDNF is produced by astrocytes, in addition to neurons, and the noradrenergic system plays a role in controlling BDNF synthesis. Since astrocytes express various subtypes of alpha- and beta-adrenergic receptors that have the potential to be activated by synaptically released NA, we focused our present study on the mediatory role of adrenergic receptors in the noradrenergic up-regulation of BDNF synthesis in cultured neonatal rat cortical astrocytes.

View Article and Find Full Text PDF

Astrocytes as an active part of the tripartite synapse can respond to the synaptically released neurotransmitters. Because brain-derived neurotrophic factor (BDNF) is produced by astrocytes, in addition to neurons, we focused our present study on the regulatory effects of monoamines noradrenaline (NA), serotonin (5-HT), and dopamine (DA) on the synthesis of BDNF protein in rat neonatal astrocytes from specific brain regions (cortex, cerebellum). All tested neurotransmitters are able to potently and transiently increase BDNF cellular contents; their maximal effects are dose and time dependent and differ between the two brain regions.

View Article and Find Full Text PDF

Objective: Histamine stimulates nerve growth factor (NGF) secretion from cultured astrocytes. Histamine H(1)-receptor antagonists completely block its effect. In the present study, we determined the involvement of histamine-receptor subtypes in this process.

View Article and Find Full Text PDF

Using a new brain-derived neurotrophic factor (BDNF) specific enzyme-immunoassay, we determined the basal cellular content of BDNF protein in neonatal rat astrocytes in primary culture, thus confirming the ability of astrocytes to synthesize BDNF in addition to nerve growth factor (NGF). We subsequently monitored the influence of different pharmacological agents: neurotransmitter receptor agonists, cytokines, and second messenger up-regulators, on the synthesis of BDNF and NGF. Marked differences in the regulation of their synthesis by the above pharmacological agents were observed in our study.

View Article and Find Full Text PDF

We determined the molecular properties of the selective and potent H(1)-receptor agonist histaprodifen and its N(alpha) substituted analogues: methyl-, dimethyl-, and imidazolylethyl-histaprodifen (suprahistaprodifen). All derivatives show high affinity for (3)H-mepyramine labeled bovine aortic H(1)-receptor binding sites with the following order of potency: suprahistaprodifen > dimethylhistaprodifen > methylhistaprodifen > histaprodifen > histamine. Suprahistaprodifen and dimethylhistaprodifen were the most potent displacers of (3)H-mepyramine binding (K(i)=4.

View Article and Find Full Text PDF

Objective And Design: This study was aimed to investigate effects of extracellular Na+ and Ca2+ ions on nerve growth factor (NGF) induced histamine release from mast cells.

Material: Isolated peritoneal mast cells were obtained from male Wistar rats.

Methods: Cells were suspended in solution with different concentration of Na+ and Ca2+ ions and stimulated with NGF.

View Article and Find Full Text PDF

It has been demonstrated that the release of histamine from mast cells by cytokines is strongly dependent on extracellular Ca2+ and Na+ ions. The results of our current research indicate that the removal of extracellular Na+ enhances NGF induced histamine release, but reduces induction by compound 48/80, suggesting that different mechanisms are involved in the secretory process induced by these agents.

View Article and Find Full Text PDF

In astrocytes, nerve growth factor (NGF) synthesis and secretion is stimulated by the cytokine interleukin-1 beta (IL-1 beta). In the present study, the role of IL-1 receptor binding sites in the regulation of NGF release was evaluated by determining the pharmacological properties of astroglially localized IL-1 receptors, and, by comparing the effects of both the agonists (IL-1 alpha and IL-1 beta) and the antagonist (IL-1ra)-members of the IL-1 family on NGF secretion from rat neonatal cortical astrocytes in primary culture. Using receptor-binding studies, binding of [(125)I] IL-1 beta to cultured astrocytes was saturable and of high affinity.

View Article and Find Full Text PDF

The influence of neurotransmitter histamine and cytokine interleukin-6 (IL-6) on nerve growth factor (NGF) release was studied in rat neonatal cortical astrocytes in primary culture. Exposure of astrocytes to either histamine or IL-6 resulted in the stimulation of NGF release. Maximal stimulation of NGF release was obtained using histamine at concentration 100 nM after 24 h of treatment (2.

View Article and Find Full Text PDF

Interactions involved in the regulation of nerve growth factor (NGF) release by inflammatory cytokines: interleukin-1beta (IL-1beta), interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta1 (TGF-beta1) were examined in rat neonatal cortical astrocytes in primary culture. Exposure of cultured astrocytes to IL-1beta, IL-6, and TGF-beta1 resulted in the stimulation of NGF secretion. Treatment of cells for 24 h with IL-1beta (10 U/ml), IL-6 (5 ng/ml) and TGF-beta1 (5 ng/ml) caused 3-, 1.

View Article and Find Full Text PDF

We identified and characterised histamine H1 and H2 receptor subtypes on rat cortical astrocytes in primary culture with radioligand binding studies and compared their molecular properties with peripheral (bovine vascular smooth muscle and endothelial cells) histamine H1 and H2 receptors. Our results showed the existence of a homogenous population of high affinity binding sites for 3H-mepyramine (Bmax = 281 fmol/mg protein, K(D) = 3.5 +/- 0.

View Article and Find Full Text PDF

We identified and characterised histamine H1 and H2 receptor subtypes on rat cortical astrocytes in primary culture with radioligand binding studies and compared their molecular properties with peripheral (bovine vascular smooth muscle and endothelial cells) histamine H1 and H2 receptors. Our results showed the existence of a homogenous population of high affinity binding sites for H-mepyramine (B = 281 fmol/mg protein, K= 3.5 +/- 0.

View Article and Find Full Text PDF

The influence of neurotransmitter histamine and cytokine interleukin-6 (IL-6) on nerve growth factor (NGF) release was studied in rat neonatal cortical astrocytes in primary culture. Exposure of astrocytes to either histamine or IL-6 resulted in the stimulation of NGF release. Maximal stimulation of NGF release was obtained using histamine at concentration 100 nM after 24 h of treatment (2.

View Article and Find Full Text PDF

Interactions involved in the regulation of nerve growth factor (NGF) release by inflammatory cytokines: interleukin-1β (IL-1β), interleukin-6 (IL-6), tumour necrosis factor-α (TNF-α) and transforming growth factor-β1 (TGF-β1) were examined in rat neonatal cortical astrocytes in primary culture. Abstract Exposure of cultured astrocytes to IL-1β, IL-6, and TGF-β1 resulted in the stimulation of NGF secretion. Treatment of cells for 24 h with IL-1β (10 U/ml), IL-6 (5 ng/ml) and TGF-β1 (5 ng/ml) caused 3-, 1.

View Article and Find Full Text PDF

We determined and compared the molecular properties of histamine H1 receptor binding sites in bovine thoracic aorta smooth muscle and guinea pig myocardial membranes from ventricles with saturation and inhibition binding assay, using 3H-mepyramine to label the receptor and specific and selective H1 receptor agonists of the 2-phenylhistamine group as displacers of specific 3H-mepyramine binding. 3H-mepyramine binds in a saturable manner to a homogenous population of binding sites with a K(D) of 5.6 nM and a Bmax of 57 fmol/mg of protein in bovine aorta vascular smooth muscle membranes, whereas in the guinea pig myocardium high and low affinity 3H-mepyramine binding sites exist having the following molecular characteristics: a K(D) of 1.

View Article and Find Full Text PDF