The Experts below are selected from a list of 108 Experts worldwide ranked by ideXlab platform
A.e Medvedev - One of the best experts on this subject based on the ideXlab platform.
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The stimulating effects of ethanol consumption on synthesis of rat brain monoamine oxidases and their sensitivity to the irreversible inhibitor, Pargyline.
Neuroscience letters, 2000Co-Authors: N.g Panova, L.n Axenova, A.e MedvedevAbstract:Administration of a large dose of Pargyline (60 mg/kg) caused total irreversible inhibition of brain monoamine oxidases (MAOs) in both control and alcoholised rats. During the first 50 h the recovery of brain MAO-A (but not MAO-B) activity occurred faster in the alcoholised rats. A low dose of Pargyline (10 mg/kg) produced significantly higher inhibition of MAO-A in the alcoholised rats, whereas the degree of MAO-B inhibition was the same in both groups. Brain MAOs of control and alcoholised rats exhibited similar sensitivity to Pargyline in vitro. Since chronic ethanol feeding reduced the content of reversible endogenous MAO inhibitor, tribulin, higher Pargyline-induced inhibition of MAO-A in alcoholised rats may stem from a tribulin deficit. The data obtained suggest that chronic ethanol consumption increases turnover of MAO-A molecules in the brain and reduces the content of endogenous MAO(A) inhibitors.
N.g Panova - One of the best experts on this subject based on the ideXlab platform.
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The stimulating effects of ethanol consumption on synthesis of rat brain monoamine oxidases and their sensitivity to the irreversible inhibitor, Pargyline.
Neuroscience letters, 2000Co-Authors: N.g Panova, L.n Axenova, A.e MedvedevAbstract:Administration of a large dose of Pargyline (60 mg/kg) caused total irreversible inhibition of brain monoamine oxidases (MAOs) in both control and alcoholised rats. During the first 50 h the recovery of brain MAO-A (but not MAO-B) activity occurred faster in the alcoholised rats. A low dose of Pargyline (10 mg/kg) produced significantly higher inhibition of MAO-A in the alcoholised rats, whereas the degree of MAO-B inhibition was the same in both groups. Brain MAOs of control and alcoholised rats exhibited similar sensitivity to Pargyline in vitro. Since chronic ethanol feeding reduced the content of reversible endogenous MAO inhibitor, tribulin, higher Pargyline-induced inhibition of MAO-A in alcoholised rats may stem from a tribulin deficit. The data obtained suggest that chronic ethanol consumption increases turnover of MAO-A molecules in the brain and reduces the content of endogenous MAO(A) inhibitors.
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The effect of ethanol consumption on the sensitivity of rat brain monoamine oxidases to the inhibition by Pargyline in vivo and in vitro.
Neurobiology (Budapest Hungary), 2000Co-Authors: N.g PanovaAbstract:The effect of ethanol consumption on the sensitivity of rat brain mitochondrial monoamine oxidases to the inhibition by Pargyline in vivo and in vitro was investigated. Administration of Pargyline (10 mg/kg, s.c.) produced significantly higher inhibition of MAO-A in alcoholised rats, whereas MAO-B inhibition did not differ from that observed in control animals. The concentration-response curve for the inhibition of brain mitochondrial MAO-A and MAO-B by Pargyline in vitro did not reveal higher sensitivity of MAO from alcoholised rats to Pargyline. This probably means that more pronounced inhibition by Pargyline of brain MAO-A in alcoholised rats in vivo can be attributed to decreased content of compounds reversibly interacting with the its catalytic site. Taking into consideration some ethanol-induced decrease of brain tribulin content we suggest that the reduced level of endogenous inhibitors (tribulin components?) may have some importance in the development of alcoholism.
Hiroshi Watanabe - One of the best experts on this subject based on the ideXlab platform.
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Central serotonin level-dependent changes in body temperature following administration of tryptophan to Pargyline- and harmaline-pretreated rats.
General pharmacology, 1997Co-Authors: Abdel-fattah Mohamed Abdel-fattah, Kinzo Matsumoto, Yukihisa Murakami, Moustafa Fayez Mohamed, Hatim Abdel-khalek Gammaz, Hiroshi WatanabeAbstract:1. The effect of tryptophan on body temperature was studied in rats pretreated with Pargyline, an irreversible monoamine oxidase inhibitor (MAOI), and harmaline, a reversible MAOI. 2. Tryptophan (100 mg/kg IP) produced hypothermia followed by hyperthermia in Pargyline-pretreated rats, and hypothermia in harmaline-pretreated rats, but tryptophan did not cause body temperature changes by itself. 3. The tryptophan-induced hypo- and hyperthermic effects, which peaked at about 1 and 6 hr after tryptophan administration, respectively, were accompanied by a significant increase in serotonin (5-HT) levels in the Pargyline-pretreated rat brain (75%-138.7% and 207%-240.9% increase, respectively), and the 5-HT levels in the hyperthermic state were significantly higher than those in the hypothermic state. 4. In harmaline-pretreated rats, tryptophan also increased the central 5-HT levels (80.5%-95.5% increase) in the hypothermic state, and the effect peaked at about 1 hr after tryptophan administration. The central 5-HT levels in harmaline-pretreated rats slightly decreased at 6 hr after tryptophan administration and were significantly lower than those in the hyperthermic state in the Pargyline-pretreated rats. 5. Tryptophan (100 mg/kg IP) administration decreased 5-hydroxy indole acetic acid (5-HIAA) levels, 5-HT turnover, and dopamine (DA) turnover in the brain of Pargyline-pretreated rats, but these parameters were not significantly different between the hypothermic and hyperthermic states (i.e., at 1 and 6 hr after tryptophan administration, respectively). 6. These results suggest that the tryptophan-induced body temperature change depends on the different 5-HT levels in the brain and that the 5-HT level needed to induce hyperthermia is higher than that needed to induce hypothermia.
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Facilitatory and inhibitory effects of harmaline on the tryptophan-induced 5-hydroxytryptamine syndrome and body temperature changes in Pargyline-pretreated rats.
Japanese journal of pharmacology, 1996Co-Authors: Abdel-fattah Mohamed Abdel-fattah, Kinzo Matsumoto, Yukihisa Murakami, Kawther Abdel-wahed El-hady, Moustafa Fayez Mohamed, Hiroshi WatanabeAbstract:The effects of harmaline on tryptophan-induced 5-hydroxytryptamine (5HT) syndrome and body temperature changes in Pargyline-pretreated rats were investigated. When administered i.p. 60 min after Pargyline treatment (50 mg/kg, i.p.), tryptophan, at 100 mg/kg but not 10 mg/kg, induced the 5-HT syndrome. Tryptophan at 100 mg/kg also produced hypothermia followed by hyperthermia in Pargyline-pretreated rats. Administration of harmaline (10 mg/kg, i.p.) 30 min after Pargyline not only potentiated the 100 mg/kg tryptophan-induced 5-HT syndrome and body temperature changes, but also produced the syndrome following administration of 10 mg/kg tryptophan in Pargyline-pretreated rats. In contrast, when administered 30 min before parygline, 10 mg/kg harmaline completely suppressed the syndrome and body temperature changes caused by mg/kg tryptophan. Tryptophan (100 mg/kg, i.p.) administration significantly increased 5-HT levels and decreased 5-hydroxyindole acetic and levels and 5-HT turnover in the brain of Pargyline-pretreated rats. Harmaline administration 30 min after Pargyline did not significantly affect the tryptophan-induced changes in 5-HT levels and 5-HT turnover, whereas when administered 30 min before Pargyline, harmaline significantly blocked the effect of tryptophan. These results suggest that mechanisms underlying the inhibitory action of harmaline on the tryptophan-induced 5-HT syndrome and body temperature changes in Pargyline-pretreated rats differ from those by which harmaline potentiates the effects of tryptophan.
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5-HT1A and 5-HT2 receptors mediate hypo- and hyperthermic effects of tryptophan in Pargyline-pretreated rats.
Pharmacology biochemistry and behavior, 1995Co-Authors: Abdel-fattah Mohamed Abdel-fattah, Kinzo Matsumoto, Kawther Abdel-wahed El-hady, Hiroshi WatanabeAbstract:Abstract Mechanisms of tryptophan (a 5-HT precursor)-induced changes in body temperature were investigated in rats pretreated with Pargyline, a monoamine oxidase inhibitor (MAO-I). Tryptophan (100 mg/kg, IP) did not affect the body temperature in rats, but it produced significant hypothermia followed by marked hyperthermia and higher mortality in the Pargyline-pretreated rats. 5-HT depletion with p-chlorophenylalanine (p-CPA, 100 mg/kg/day for 3 days) significantly suppressed not only the body temperature change but also the mortality and 5-HT syndrome following tryptophan plus Pargyline administration. Although propranolol (10 mg/kg, IP), a β-adrenoceptor antagonist, did not alter the hypothermia caused by tryptophan in the Pargyline-pretreated rats, pindolol (2 mg/kg, SC), a 5-HT 1A receptor and β-adrenoceptor antagonist, suppressed the hypothermia but not the hyperthermia or mortality caused by the same treatment. On the other hand, spiperone and ketanserin, 5-HT 2 receptor antagonists, at doses of 3 mg/kg, potentiated the hypothermia and completely suppressed the hyperthermia and mortality caused by tryptophan in the Pargyline-pretreated rats. These results suggest that tryptophan-induced hypo- and hyperthermia are mediated by 5-HT 1A and 5-HT 2 receptors, respectively, in the Pargyline-pretreated rats.
Victoria N. Luine - One of the best experts on this subject based on the ideXlab platform.
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Pargyline-induced increase in serotonin levels: Correlation with inhibition of lordosis in rats
Pharmacology biochemistry and behavior, 1993Co-Authors: Donald L. Allen, Kenneth J. Renner, Victoria N. LuineAbstract:Abstract The effect of intrahypothalamic infusion of the monoamine oxidase inhibitor Pargyline on lordosis behavior and monoamine levels in the preoptic area and hypothalamus was examined. Progesterone-facilitated lordosis was blocked by Pargyline in half the treated rats. The inhibition of lordosis was correlated with increases in serotonin and dopamine levels in the ventromedial nucleus of the hypothalamus and serotonin levels in the arcuate nucleus-median eminence when compared to controls or Pargyline-treated rats with high levels of lordosis responding. Changes in norepinephrine levels were not correlated with changes in behavior. The results provide further evidence for an inhibitory role of basomedial hypothalamic serotonin in the control of female sexual behavior.
Dale E Edmondson - One of the best experts on this subject based on the ideXlab platform.
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topological probes of monoamine oxidases a and b in rat liver mitochondria inhibition by tempo substituted Pargyline analogues and inactivation by proteolysis
Biochemistry, 2011Co-Authors: Jin Wang, Dale E EdmondsonAbstract:TEMPO-substituted Pargyline analogues differentially inhibit recombinant human monoamine oxidase A (MAO A) and B (MAO B) in intact yeast mitochondria, suggesting these membrane-bound enzymes are located on differing faces of the mitochondrial outer membrane [Upadhyay, A., and Edmondson, D. E. (2009) Biochemistry 48, 3928]. This approach is extended to the recombinant rat enzymes and to rat liver mitochondria. The differential specificities exhibited for human MAO A and MAO B by the m- and p-amido TEMPO Pargylines are not as absolute with the rat enzymes. Similar patterns of reactivity are observed for rat MAO A and B in mitochondrial outer membrane preparations expressed in Pichia pastoris or isolated from rat liver. In intact yeast mitochondria, recombinant rat MAO B is inhibited by the Pargyline analogue whereas MAO A activity shows no inhibition. Intact rat liver mitochondria exhibit an inhibition pattern opposite to that observed in yeast where MAO A is inhibited and MAO B activity is unaffected. Protease inactivation studies show specificity in that MAO A is sensitive to trypsin whereas MAO B is sensitive to β-chymotrypsin. In intact mitochondrial preparations, MAO A is readily inactivated in rat liver but not in yeast upon trypsin treatment and MAO B is readily inactivated by β-chymotrypsin in yeast but not in rat liver. These data show MAO A is oriented on the cytosolic face and MAO B is situated on the surface facing the intermembrane space of the mitochondrial outer membrane in rat liver. The differential mitochondrial outer membrane topology of MAO A and MAO B is relevant to their inhibition by drugs designed to be cardioprotectants or neuroprotectants.