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C L Schaub - One of the best experts on this subject based on the ideXlab platform.

  • polydipsia and dopamine behavioral effects of dopamine d1 and d2 receptor Agonists and antAgonists
    Journal of Pharmacology and Experimental Therapeutics, 1994
    Co-Authors: Guy Mittleman, Amy Rosner, C L Schaub
    Abstract:

    Substantial evidence implicates dopaminergic neural systems in the occurrence of polydipsia in both animals and humans. Two experiments were conducted in order to specify the behavioral mechanisms whereby manipulation of dopaminergic neural transmission can affect scheduled-induced polydipsia (SIP). The role of dopamine D1 and D2 receptors was investigated by comparing the behavioral effects of dopamine D1 Agonists (SKF 38393 and SKF 82958) and antAgonists (SCH 23390 and SKF 83566) to those of a dopamine D2 Agonist (quinpirole) and antAgonist (haloperidol) by using an animal model of excessive water consumption, drinking evoked in the SIP paradigm. Additionally, the behavioral effects of these relatively specific compounds were compared to those of the Indirect Agonist d-amphetamine sulfate and the nondopaminergic drug, diazepam. All of the drugs produced dose-related decreases in SIP. With the exception of SKF 38393 and SCH 23390, the decreased drinking appeared to be a behaviorally nonspecific drug effect in that changes in activity consistently preceded or accompanied reductions in water consumption. Some of the drugs tested, including quinpirole, haloperidol and SKF 83566, also produced changes in behavior consistent with decreased hunger, which may have also contributed to the reductions in SIP. These results are generally suggestive that dopamine neural systems are involved mainly in the motor or performance aspects of established SIP and that disruptions in established SIP produced by dopamine Agonists or antAgonists may result from a change in the balance of activation of dopamine D1 and D2 receptors. These results may be relevant to understanding the factors influencing polydipsia in humans.

J B Young - One of the best experts on this subject based on the ideXlab platform.

  • central 5 hydroxytryptamine2 receptors are involved in the adrenal catecholamine releasing and hyperglycemic effects of the 5 hydroxytryptamine Indirect Agonist d fenfluramine in the conscious rat
    Journal of Pharmacology and Experimental Therapeutics, 1992
    Co-Authors: F Chaouloff, S H Gunn, J B Young
    Abstract:

    Stimulation of either the 5-hydroxytryptamine (5-HT)1A, the 5-HT1C or the 5-HT2 receptor subtype triggers adrenal catecholamine release and hyperglycemia. Nonetheless, the identity of the serotonergic receptors that mediate the effects of 5-HT release upon the sympathoadrenal system (and on plasma glucose) is still unknown. Thus, we have examined the effects of the 5-HT uptake inhibitor and releaser d-fenfluramine (d-Fen) on plasma epinephrine (EPI), norepinephrine (NE) and glucose levels in conscious rats. Acute administration of d-Fen (1-8 mg/kg i.v.) promoted early increases in plasma EPI and glucose levels, whereas increases in plasma NE levels were less marked. The effects of a 4-mg/kg dose of d-Fen were then evaluated. Prior adrenalectomy prevented d-Fen-induced hyperglycemia but not d-Fen-induced increases in plasma NE levels. Pretreatment (15 min beforehand) with either the 5-HT1C/5-HT2 receptor antAgonist LY 53857 (0.3 mg/kg i.v.) or the 5-HT2 receptor/alpha-1 adrenoceptor antAgonist ketanserin (0.3 mg/kg i.v.) markedly diminished the EPI-releasing effect of d-Fen. Pretreatment with the 5-HT1C receptor Agonist/5-HT2 receptor antAgonist m-chlorophenylpiperazine (1 mg/kg i.v.) tended to decrease the EPI-releasing effect of d-Fen, whereas that with the peripheral 5-HT1C/5-HT2 receptor antAgonist BW 501C67 (0.5 mg/kg i.v.) did not alter the EPI-releasing effect of d-Fen. In addition, pretreatment with either LY 53857 or ketanserin prevented the hyperglycemic effect of d-Fen.(ABSTRACT TRUNCATED AT 250 WORDS)

Edward D. Levin - One of the best experts on this subject based on the ideXlab platform.

  • PPI deficit induced by amphetamine is attenuated by the histamine H1 antAgonist pyrilamine, but is exacerbated by the serotonin 5-HT2 antAgonist ketanserin
    Psychopharmacology, 2010
    Co-Authors: José A. Larrauri, Edward D. Levin
    Abstract:

    Prepulse inhibition (PPI) of the startle response is a classic model of sensorimotor gating. Robust PPI impairments can be induced by dopamine Agonists such as the Indirect Agonist amphetamine. The antipsychotic clozapine can attenuate PPI impairment induced by dopamine Agonists. Clozapine is a complex drug with antAgonistic effects on a variety of receptors, including serotonin and histamine. The relative contribution of its component actions to its efficacy is still unclear. To better characterize the role of histamine and serotonin receptors in the modulation of PPI in rats, we studied the effects of the H1 histamine antAgonist pyrilamine (10, 20, and 40 mg/kg) on amphetamine-induced (1 mg/kg) PPI deficits (Experiment 1); and the interaction of pyrilamine (20 mg/kg) with the 5-HT2 antAgonist ketanserin (1 and 2 mg/kg) on the amphetamine-induced PPI disruption (Experiment 2). Tactile startle stimuli consisted of 30 PSI air-puffs. Three acoustic prepulse intensity levels were used: 68, 71, and 77 dB, presented on a 65-dB background noise. In both experiments, all animals received all drug doses and combinations with different counterbalanced orders. Pyrilamine (20 mg/kg) was effective in counteracting the PPI impairment caused by amphetamine administration, whereas ketanserin exacerbated the amphetamine-induced PPI deficit. Based on its ability to reverse amphetamine-induced PPI deficits, blockade of histamine H1 receptors seems to contribute to the therapeutic effect of the antipsychotic clozapine. Serotonin 5-HT2-receptor blockade, though, does not appear to contribute to this effect, and may in fact detract from it.

Aigar Ottas - One of the best experts on this subject based on the ideXlab platform.

  • Repeated Administration of D-Amphetamine Induces Distinct Alterations in Behavior and Metabolite Levels in 129Sv and Bl6 Mouse Strains
    Frontiers Media S.A., 2018
    Co-Authors: Taavi Vanaveski, Jane Narvik, Jürgen Innos, Mari-anne Philips, Aigar Ottas
    Abstract:

    The main goal of the study was to characterize the behavioral and metabolomic profiles of repeated administration (for 11 days) of d-amphetamine (AMPH, 3 mg/kg i. p.), Indirect Agonist of dopamine (DA), in widely used 129S6/SvEvTac (129Sv) and C57BL/6NTac (Bl6) mouse strains. Acute administration of AMPH (acute AMPH) induced significantly stronger motor stimulation in Bl6. However, repeated administration of AMPH (repeated AMPH) caused stronger motor sensitization in 129Sv compared acute AMPH. Body weight of 129Sv was reduced after repeated saline and AMPH, whereas no change occurred in Bl6. In the metabolomic study, acute AMPH induced an elevation of isoleucine and leucine, branched chain amino acids (BCAA), whereas the level of hexoses was reduced in Bl6. Both BCAAs and hexoses remained on level of acute AMPH after repeated AMPH in Bl6. Three biogenic amines [asymmetric dimethylarginine (ADMA), alpha-aminoadipic acid (alpha-AAA), kynurenine] were significantly reduced after repeated AMPH. Acute AMPH caused in 129Sv a significant reduction of valine, lysophosphatidylcholines (lysoPC a C16:0, lysoPC a C18:2, lysoPC a C20:4), phosphatidylcholine (PC) diacyls (PC aa C34:2, PC aa C36:2, PC aa C36:3, PC aa C36:4) and alkyl-acyls (PC ae C38:4, PC ae C40:4). However, repeated AMPH increased the levels of valine and isoleucine, long-chain acylcarnitines (C14, C14:1-OH, C16, C18:1), PC diacyls (PC aa C38:4, PC aa C38:6, PC aa C42:6), PC acyl-alkyls (PC ae C38:4, PC ae C40:4, PC ae C40:5, PC ae C40:6, PC ae C42:1, PC ae C42:3) and sphingolipids [SM(OH)C22:1, SM C24:0] compared to acute AMPH in 129Sv. Hexoses and kynurenine were reduced after repeated AMPH compared to saline in 129Sv. The established changes probably reflect a shift in energy metabolism toward lipid molecules in 129Sv because of reduced level of hexoses. Pooled data from both strains showed that the elevation of isoleucine and leucine was a prominent biomarker of AMPH-induced behavioral sensitization. Simultaneously a significant decline of hexoses, citrulline, ADMA, and kynurenine occurred. The reduced levels of kynurenine, ADMA, and citrulline likely reflect altered function of N-methyl-D-aspartate (NMDA) and NO systems caused by repeated AMPH. Altogether, 129Sv strain displays stronger sensitization toward AMPH and larger variance in metabolite levels than Bl6

  • Data_Sheet_1_Repeated Administration of D-Amphetamine Induces Distinct Alterations in Behavior and Metabolite Levels in 129Sv and Bl6 Mouse Strains.docx
    2018
    Co-Authors: Taavi Vanaveski, Jane Narvik, Jürgen Innos, Mari-anne Philips, Aigar Ottas, Mario Plaas, Liina Haring, Mihkel Zilmer, Eero Vasar
    Abstract:

    The main goal of the study was to characterize the behavioral and metabolomic profiles of repeated administration (for 11 days) of d-amphetamine (AMPH, 3 mg/kg i. p.), Indirect Agonist of dopamine (DA), in widely used 129S6/SvEvTac (129Sv) and C57BL/6NTac (Bl6) mouse strains. Acute administration of AMPH (acute AMPH) induced significantly stronger motor stimulation in Bl6. However, repeated administration of AMPH (repeated AMPH) caused stronger motor sensitization in 129Sv compared acute AMPH. Body weight of 129Sv was reduced after repeated saline and AMPH, whereas no change occurred in Bl6. In the metabolomic study, acute AMPH induced an elevation of isoleucine and leucine, branched chain amino acids (BCAA), whereas the level of hexoses was reduced in Bl6. Both BCAAs and hexoses remained on level of acute AMPH after repeated AMPH in Bl6. Three biogenic amines [asymmetric dimethylarginine (ADMA), alpha-aminoadipic acid (alpha-AAA), kynurenine] were significantly reduced after repeated AMPH. Acute AMPH caused in 129Sv a significant reduction of valine, lysophosphatidylcholines (lysoPC a C16:0, lysoPC a C18:2, lysoPC a C20:4), phosphatidylcholine (PC) diacyls (PC aa C34:2, PC aa C36:2, PC aa C36:3, PC aa C36:4) and alkyl-acyls (PC ae C38:4, PC ae C40:4). However, repeated AMPH increased the levels of valine and isoleucine, long-chain acylcarnitines (C14, C14:1-OH, C16, C18:1), PC diacyls (PC aa C38:4, PC aa C38:6, PC aa C42:6), PC acyl-alkyls (PC ae C38:4, PC ae C40:4, PC ae C40:5, PC ae C40:6, PC ae C42:1, PC ae C42:3) and sphingolipids [SM(OH)C22:1, SM C24:0] compared to acute AMPH in 129Sv. Hexoses and kynurenine were reduced after repeated AMPH compared to saline in 129Sv. The established changes probably reflect a shift in energy metabolism toward lipid molecules in 129Sv because of reduced level of hexoses. Pooled data from both strains showed that the elevation of isoleucine and leucine was a prominent biomarker of AMPH-induced behavioral sensitization. Simultaneously a significant decline of hexoses, citrulline, ADMA, and kynurenine occurred. The reduced levels of kynurenine, ADMA, and citrulline likely reflect altered function of N-methyl-D-aspartate (NMDA) and NO systems caused by repeated AMPH. Altogether, 129Sv strain displays stronger sensitization toward AMPH and larger variance in metabolite levels than Bl6.

Lin Jian-sheng - One of the best experts on this subject based on the ideXlab platform.

  • Role of histamine H1-receptor on behavioral states and wake maintenance during deficiency of a brain activating system: A study using a knockout mouse model
    'Elsevier BV', 2016
    Co-Authors: Parmentier Régis, Zhao Yan, Perier Magali, Akaoka Hidéo, Lintunen Minnamaija, Hou Yiping, Panula Pertti, Watanabe Takeshi, Franco Patricia, Lin Jian-sheng
    Abstract:

    International audienceUsing knockout (KO) mice lacking the histamine (HA)-synthesizing enzyme (histidine decarboxylase, HDC), we have previously shown the importance of histaminergic neurons in maintaining wakefulness (W) under behavioral challenges. Since the central actions of HA are mediated by several receptor subtypes, it remains to be determined which one(s) could be responsible for such a role. We have therefore compared the cortical-EEG, sleep and W under baseline conditions or behavioral/pharmacological stimuli in littermate wild-type (WT) and H1-receptor KO (H1-/-) mice. We found that H1-/- mice shared several characteristics with HDC KO mice, i.e. 1) a decrease in W after lights-off despite its normal baseline daily amount; 2) a decreased EEG slow wave sleep (SWS)/W power ratio; 3) inability to maintain W in response to behavioral challenges demonstrated by a decreased sleep latency when facing various stimuli. These effects were mediated by central H1-receptors. Indeed, in WT mice, injection of triprolidine, a brain-penetrating H1-receptor antAgonist increased SWS, whereas ciproxifan (H3-receptor antAgonist/inverse Agonist) elicited W; all these injections had no effect in H1-/- mice. Finally, H1-/- mice showed markedly greater changes in EEG power (notably in the 0.8-5 Hz band) and sleep-wake cycle than in WT mice after application of a cholinergic antAgonist or an Indirect Agonist, i.e., scopolamine or physostigmine. Hence, the role of HA in wake-promotion is largely ensured by H1-receptors. An upregulated cholinergic system may account for a quasi-normal daily amount of W in HDC or H1-receptor KO mice and likely constitutes a major compensatory mechanism when the brain is facing deficiency of an activating system. This article is part of the Special Issue entitled 'Histamine Receptors'

  • Role of histamine H1-receptor on behavioral states and wake maintenance during deficiency of a brain activating system : A study using a knockout mouse model
    'Elsevier BV', 2016
    Co-Authors: Parmentier Régis, Zhao Yan, Perier Magali, Akaoka Hidéo, Lintunen Minnamaija, Hou Yiping, Panula Pertti, Watanabe Takeshi, Franco Patricia, Lin Jian-sheng
    Abstract:

    Using knockout (KO) mice lacking the histamine (HA)-synthesizing enzyme (histidine decarboxylase, HDC), we have previously shown the importance of histaminergic neurons in maintaining wakefulness (W) under behavioral challenges. Since the central actions of HA are mediated by several receptor subtypes, it remains to be determined which one(s) could be responsible for such a role. We have therefore compared the cortical-EEG, sleep and W under baseline conditions or behavioral/pharmacological stimuli in littermate wild-type (WT) and H1-receptor KO (H1-/-) mice. We found that H1-/- mice shared several characteristics with HDC KO mice, i.e. 1) a decrease in W after lights-off despite its normal baseline daily amount; 2) a decreased EEG slow wave sleep (SWS)/W power ratio; 3) inability to maintain W in response to behavioral challenges demonstrated by a decreased sleep latency when facing various stimuli. These effects were mediated by central H1-receptors. Indeed, in WT mice, injection of triprolidine, a brain-penetrating H1-receptor antAgonist increased SWS, whereas ciproxifan (H3-receptor antAgonist/inverse Agonist) elicited W; all these injections had no effect in H1-/- mice. Finally, H1-/- mice showed markedly greater changes in EEG power (notably in the 0.8-5 Hz band) and sleep-wake cycle than in WT mice after application of a cholinergic antAgonist or an Indirect Agonist, i.e., scopolamine or physostigmine. Hence, the role of HA in wake-promotion is largely ensured by H1-receptors. An upregulated cholinergic system may account for a quasi-normal daily amount of W in HDC or H1-receptor KO mice and likely constitutes a major compensatory mechanism when the brain is facing deficiency of an activating system. This article is part of the Special Issue entitled 'Histamine Receptors'. Copyright (C) 2015 Elsevier Ltd. All rights reserved.Peer reviewe