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Ali R Mani - One of the best experts on this subject based on the ideXlab platform.

  • prostaglandin f2α modulates atrial chronotropic hyporesponsiveness to Cholinergic Stimulation in endotoxemic rats
    European Journal of Pharmacology, 2015
    Co-Authors: Vahid Nikoui, Shahram Ejtemaei Mehr, Farahnaz Jazaeri, Sattar Ostadhadi, Golnar Eftekhari, Ahmad Reza Dehpour, Ali R Mani, Azam Bakhtiarian
    Abstract:

    Abstract Endotoxemia induces various physiological adaptive responses such as tachycardia. There is evidence to show that inflammatory tachycardia might be linked to a direct action of prostanoids on the cardiac pacemaker cells. Recent reports have indicated that systemic inflammation may uncouple of cardiac pacemaker from Cholinergic neural control in experimental animals; however, the exact mechanism of this phenomenon is uncertain. This study was aimed to explore the hypothesis that prostanoids modulate atrial chronotropic hyporesponsiveness to Cholinergic Stimulation in endotoxemic rats. Male albino rats were given intraperitoneal injection of either saline or lipopolysaccharide (LPS, 1 mg/kg). 3 h after saline or LPS injection, the atria were isolated and chronotropic responsiveness to Cholinergic Stimulation was evaluated in an organ bath. The expression of atrial cyclooxygenases (COX)-1, COX-2 and COX-3 mRNA was assessed by quantitative real-time RT-PCR and cytosocalcium-dependent phospholipase A 2 (cPLA 2 ) activity was measured in the atria. The expression of atrial COX-2 mRNA and cPLA 2 activity increased significantly in endotoxemic atria ( P 2α (PGF 2α , 100 pM) could significantly decrease chronotropic response to Cholinergic Stimulation in vitro . Likewise, LPS injection could induce a significant hyporesponsiveness to Cholinergic Stimulation, and incubation of isolated atria with either indomethacin (5 µM) or AL-8810 (a PGF 2α antagonist, 10 µM) could reverse it ( P 0.01, P 0.05, respectively), while SQ29548 (a thromboxane A 2 antagonist, 10 nM) was failed ( P >0.05). Our data showed that PGF 2α may contribute to the atrial chronotropic hyporesponsiveness to Cholinergic Stimulation in endotoxemic rats.

  • Prostaglandin F2α modulates atrial chronotropic hyporesponsiveness to Cholinergic Stimulation in endotoxemic rats
    European journal of pharmacology, 2014
    Co-Authors: Vahid Nikoui, Shahram Ejtemaei Mehr, Farahnaz Jazaeri, Sattar Ostadhadi, Golnar Eftekhari, Ahmad Reza Dehpour, Ali R Mani, Azam Bakhtiarian
    Abstract:

    Endotoxemia induces various physiological adaptive responses such as tachycardia. There is evidence to show that inflammatory tachycardia might be linked to a direct action of prostanoids on the cardiac pacemaker cells. Recent reports have indicated that systemic inflammation may uncouple of cardiac pacemaker from Cholinergic neural control in experimental animals; however, the exact mechanism of this phenomenon is uncertain. This study was aimed to explore the hypothesis that prostanoids modulate atrial chronotropic hyporesponsiveness to Cholinergic Stimulation in endotoxemic rats. Male albino rats were given intraperitoneal injection of either saline or lipopolysaccharide (LPS, 1 mg/kg). 3 h after saline or LPS injection, the atria were isolated and chronotropic responsiveness to Cholinergic Stimulation was evaluated in an organ bath. The expression of atrial cyclooxygenases (COX)-1, COX-2 and COX-3 mRNA was assessed by quantitative real-time RT-PCR and cytosocalcium-dependent phospholipase A₂ (cPLA₂) activity was measured in the atria. The expression of atrial COX-2 mRNA and cPLA₂ activity increased significantly in endotoxemic atria (P

  • interleukin 6 impairs chronotropic responsiveness to Cholinergic Stimulation and decreases heart rate variability in mice
    European Journal of Pharmacology, 2011
    Co-Authors: Khalil Hajiasgharzadeh, Javad Mirnajafizadeh, Ali R Mani
    Abstract:

    Heart rate variability is reduced in several clinical settings associated with systemic inflammation. The underlying mechanism of decreased heart rate variability during systemic inflammation is unknown. It appears that the inflammatory cytokines might play a role, since epidemiologic studies has shown that circulating levels of interleukine-6 (IL-6) correlate significantly with indexes of depressed heart rate variability in various clinical conditions. The present investigation was carried out to study the peripheral and central effects of IL-6 on heart rate dynamic in mice. Adult male BALB/c mice were used in the study. RT-PCR was performed to study the expression of IL-6 receptor in mouse atrial and the results showed that gp130 mRNA was detectable in the atrium. The effect of IL-6 was also studies on chronotropic responsiveness of isolated atria to adrenergic and Cholinergic Stimulations. Incubation of isolated atria with 10 ng/ml of IL-6 was associated with a significant hypo-responsiveness to Cholinergic Stimulation (log IC₅₀ of carbacholine changed from -6.26±0.10 in controls to -5.59±0.19 following incubation with IL-6, P<0.05). The chronotropic responsiveness to adrenergic Stimulation was identical with or without incubation with IL-6. Intraperitoneal injection of IL-6 (200 ng/mouse) was associated with a significant decrease in heart rate variability parameters (SDNN, SD1, and SD2). While intracerebroventricular injection of IL-6 (50 ng/mouse) had no significant effect on heart rate variability parameters. These data are in line with a peripheral role for IL-6 in the genesis of decreased heart rate variability during systemic inflammation.

  • Interleukin-6 impairs chronotropic responsiveness to Cholinergic Stimulation and decreases heart rate variability in mice
    European Journal of Pharmacology, 2011
    Co-Authors: Khalil Hajiasgharzadeh, Javad Mirnajafi-zadeh, Ali R Mani
    Abstract:

    Heart rate variability is reduced in several clinical settings associated with systemic inflammation. The underlying mechanism of decreased heart rate variability during systemic inflammation is unknown. It appears that the inflammatory cytokines might play a role, since epidemiologic studies has shown that circulating levels of interleukine-6 (IL-6) correlate significantly with indexes of depressed heart rate variability in various clinical conditions. The present investigation was carried out to study the peripheral and central effects of IL-6 on heart rate dynamic in mice. Adult male BALB/c mice were used in the study. RT-PCR was performed to study the expression of IL-6 receptor in mouse atrial and the results showed that gp130 mRNA was detectable in the atrium. The effect of IL-6 was also studies on chronotropic responsiveness of isolated atria to adrenergic and Cholinergic Stimulations. Incubation of isolated atria with 10 ng/ml of IL-6 was associated with a significant hypo-responsiveness to Cholinergic Stimulation (log IC₅₀ of carbacholine changed from -6.26±0.10 in controls to -5.59±0.19 following incubation with IL-6, P

Philip Winn - One of the best experts on this subject based on the ideXlab platform.

  • Additivity of nicotinic and muscarinic Cholinergic Stimulation of substantia nigra.
    Neuroreport, 1992
    Co-Authors: Graham C. Parker, Philip Winn
    Abstract:

    Microinjection of Cholinergic agonists into the anterior substantia nigra increases behaviours for which there is a pre-existing tendency and a low current rate. Rats received microinjections of carbachol, nicotine or a combination of both into the anterior substantia nigra. Carbachol and nicotine both stimulated consumption of palatable food in a dose-dependent manner (F(3,24) = 3.99, p < 0.02 and F(3,33) = 7.07, p < 0.01 respectively). Addition of carbachol to each dose of nicotine caused a significant increase in feeding compared with nicotine alone (F(1,23) = 7.01, p < 0.015). This suggests muscarinic or nicotinic Cholinergic Stimulation of the anterior substantia nigra can have behaviourally similar effects and, at the doses used here, the effects of nicotinic and muscarinic Stimulation are additive.

  • Cholinergic Stimulation of substantia nigra: effects on feeding, drinking and sexual behaviour in the male rat.
    Psychopharmacology, 1991
    Co-Authors: Philip Winn
    Abstract:

    Previous studies have shown that Cholinergic Stimulation of the substantia nigra increases food intake but not other activities. The present experiments were undertaken to determine whether or not activities other than feeding could be stimulated if conditions were appropriate. Microinjections of the Cholinergic agonist carbachol (0.5 micrograms/0.5 microliters each side) bilaterally into substantia nigra increased the consumption of dry spaghetti, and, in subsequent tests, changed sexual behaviour in male rats. Ejaculation, mount and intromission latencies were unaffected but intromission frequency (though not mount frequency) was reduced following Cholinergic Stimulation (experiment 1). In a second experiment, an increase in the consumption of 2.0% saccharin solution and lab chow was stimulated by intranigral carbachol while the intake of tap water, and locomotion, gnawing, grooming, rearing and sniffing were all unaffected. These data indicate that Cholinergic Stimulation of substantia nigra can affect activity for which there is a pre-existing tendency, regardless of its form. A possible role for nigral acetylcholine in the control of pars compacta dopamine containing neurones is discussed.

Godfried M. Roomans - One of the best experts on this subject based on the ideXlab platform.

  • Changes in calcium concentrations in subcellular compartments of rat submandibular gland acinar cells induced by Cholinergic Stimulation.
    Histochemistry and cell biology, 1999
    Co-Authors: A.-l. Zhang, J. R. Martinez, Godfried M. Roomans
    Abstract:

    The effects of Cholinergic and alpha-adrenergic Stimulation on calcium concentrations in rat submandibular gland acinar cells were evaluated at the subcellular level by electron probe X-ray microanalysis, and the subcellular distribution of receptors for inositol 1,4,5-trisphosphate (IP(3)Rs) was investigated by electron microscopic immunohistochemistry. For measurement of calcium concentrations, experiments were carried out both in vivo and in vitro. In in vivo experiments, fragments of glands were removed and slam-frozen 3 min after intraperitoneal injection of an agonist. In in vitro experiments, the gland tissue was enzymatically dispersed, treated with an agonist in the presence or absence of extracellular Ca(2+), and slam-frozen. The frozen specimens were cut into ultrathin cryosections, which were then freeze dried. Spectra were collected from secretory granules, the perinuclear cytoplasm containing endoplasmic reticulum (ER), and the nucleus of the acinar cells. A clear decrease in calcium content in secretory granules was observed after Cholinergic Stimulation both in vivo and in vitro in the presence or absence of extracellular Ca(2+). In the presence of extracellular Ca(2+), Cholinergic Stimulation following alpha-adrenergic Stimulation reduced the calcium content in secretory granules to the same extent as Cholinergic Stimulation alone. No significant changes in the calcium content of the perinuclear cytoplasm and the nucleus were noticed after Cholinergic Stimulation. alpha-adrenergic Stimulation did not significantly affect the calcium concentrations in any of the three compartments studied. IP(3)Rs were localized to ER lamellae, but not to secretory granule membranes or to nuclear membranes. Our findings suggest that: (1) in rat submandibular acini, Ca(2+) can be released from secretory granules by exposure to Cholinergic, but not alpha-adrenergic, stimuli, (2) there are, however, no IP(3)Rs present in the granular membrane and the trigger for the Ca(2+) release remains under study, and (3) the response to either type of stimulus does not involve changes in the Ca(2+) content of the nucleus or of the perinuclear cytoplasm/ER, despite the presence of IP(3)Rs in the latter structure. This may be the result of limitation in the technique used, which cannot measure changes in the proper compartment of the ER.

N C Tkacs - One of the best experts on this subject based on the ideXlab platform.

  • Identification of pressor regions activated by central Cholinergic Stimulation in rat brain.
    European journal of pharmacology, 1997
    Co-Authors: H E Brezenoff, N C Tkacs
    Abstract:

    The acetylcholinesterase inhibitor neostigmine (2 microg) was microinjected into the lateral cerebral ventricle (i.c.v.) of unanesthetized rats to activate central Cholinergic receptors. Changes in arterial blood pressure were correlated with changes in Fos-like immunoreactivity in the hypothalamus and forebrain following Cholinergic Stimulation. Neostigmine increased mean arterial pressure by 39 +/- 3 mmHg at peak (P < 0.05) from a pretreatment level of 104 +/- 4 mmHg. Blood pressure remained elevated for more than 30 min. Distinct Fos-like immunoreactivity was found in the posterior hypothalamic nucleus, the paraventricular nucleus and the supraoptic nucleus of the hypothalamus, the ventral premamillary nucleus, the central nucleus of amygdala, the lateral septum and the medial preoptic area. In contrast, only a very small amount of Fos-like immunoreactivity was scattered in those regions in a control group injected i.c.v. with saline. Pretreatment with the muscarinic receptor antagonist methylatropine (i.c.v., 0.5 microg) prevented the pressor response to neostigmine and evoked a reduced Fos-like immunoreactivity compared to animals given neostigmine without methylatropine. The pressor response to neostigmine was blocked after pretreatment with phenoxybenzamine, however, this did not prevent the development of Fos-like immunoreactivity. These results indicate that the pressor response induced by central Cholinergic Stimulation may result from muscarinic receptor activation in specific regions of the hypothalamus and the forebrain that are implicated in regulating cardiovascular activity.

Jorge Aceves - One of the best experts on this subject based on the ideXlab platform.

  • Cholinergic Stimulation of rostral and caudal substantia nigra pars compacta produces opposite effects on circling behavior and striatal dopamine release measured by brain microdialysis
    Neuroscience, 1994
    Co-Authors: Salvador Hernández-lópez, José Luis Góngora-alfaro, Daniel Martinez-fong, M.g. Rosales, Jorge Aceves
    Abstract:

    Abstract Turning in circles is among the behaviors elicited by unilateral Cholinergic Stimulation of the substantia nigra. Recent studies have shown that microinjection of Cholinergic agonists into the substantia nigra pars compacta increases dopamine release and turnover in the striatum of anesthetized rats [Hernandez-Lopez et al . (1992) Brain. Res. 598 , 114-120; Blaha and Winn (1993) J. Neurosci . 13, 1035–1044]. In this study, the relationship between circling behavior and striatal dopamine release following Cholinergic Stimulation of the substantia nigra pars compacta neurons was assessed by brain microdialysis in awake rats. The results indicate that Cholinergic Stimulation of the substantia nigra pars compacta with the mixed nicotinic-muscarinic Cholinergic agonist carbachol modulates striatal dopamine release, and this effect is accompanied by circling behavior and stereotypies. Microinjection of carbachol (109nmol) in the caudal portions of the substantia nigra pars compacta induced contralateral circling associated with an increase of dopamine release in neostriatum. On the contrary, ipsilateral circling and reduction of striatal dopamine release was elicited when the same dose of the drug was applied in the rostral portions of the substantia nigra pars compacta. The above findings are in accordance with recent electrophysiological studies suggesting the existence of sub-populations of nigrostriatal dopaminergic neurons, and indicate that the substantia nigra pars compacta is functionally compartmentalized. We conclude that the Cholinergic input to the substantia nigra pars compacta could modulate the motor behavior through regulating the firing rate of nigrostriatal dopaminergic neurons and dopamine releasin the neostriatum.