Opposite effects of glutamate antagonists and antiparkinsonian drugs on the activities of DOPA decarboxylase and 5-HTP decarboxylase in the rat brain

Fisher, Andrew; Starr, Michael S.

doi:10.1016/s0006-8993(00)02339-8

Cited by 18 publications

(13 citation statements)

References 37 publications

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“…Although these drugs have been reported to bind with low affinity to the NMDA channel site (Reynolds and Miller 1988;Kornhuber et al 1995), they also have a variety of actions at other receptors that may modulate their NMDA antagonist effects. For example, amantadine is an indirect dopamine agonist (Fisher and Starr 2000). Swerdlow et al (1998) have shown that 100 mg/kg amantadine (compared with 56 mg/ kg, the highest dose tested in our study) produced a moderate disruption of prepulse inhibition, an effect that they attribute to its dopaminergic effects.…”

Section: Discussionmentioning

confidence: 51%

Affinity and specificity of N-methyl-D-aspartate channel blockers affect their ability to disrupt prepulse inhibition of acoustic startle in rats

et al. 2003

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Section: Discussionmentioning

confidence: 51%

Affinity and specificity of N-methyl-D-aspartate channel blockers affect their ability to disrupt prepulse inhibition of acoustic startle in rats

et al. 2003

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“…These studies have largely focused on the effects of these drugs on the dopaminergic system due to their clinical role in Parkinson's disease. Both have been shown to potentiate the activity of L ‐DOPA decarboxylase as well as inhibiting monoamine oxidase B (Eltze, 1999; Fisher & Starr, 2000) and to increase extracellular DA. Fisher & Starr (2000) have also reported regional effects of these drugs on the activity 5‐hydroxy‐tryptophan decarboxylase in the substantia nigra and striatum of rats.…”

Section: Discussionmentioning

confidence: 99%

Effects of amantadine and budipine on antidepressant drug‐evoked changes in extracellular 5‐HT in the frontal cortex of freely moving rats

Owen

Whitton

2005

British J Pharmacology

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1 Evidence has recently suggested that NMDA receptors may play a role in the aetiology and possible treatment of depression and that weak noncompetitive NMDA receptor antagonists such as amantadine can synergize with conventional antidepressants in a model of the illness. 2 To try to obtain a neurochemical rationale for these findings, we have studied the effects of acute and chronic administration of amantadine or the related drug budipine on cortical release of 5-hydroxytryptamine (5-HT) following the antidepressants reboxitine (REB), paroxetine (PAROX) and clomipramine (CLOM) in freely moving rats by using microdialysis. ) all failed to significantly alter extracellular 5-HT in the cortex. However, when either amantadine or budipine was administered 30 min prior to any of the three antidepressants, a significant rise in 5-HT was observed. 4 For chronic studies, the effects of the drugs were studied at 4, 7, 14 and 21 days. Amantadine and budipine did not significantly alter extracellular 5-HT at any time point. The three antidepressant drugs all elicited a gradual increase in 5-HT, which became significant after 14 days and tended to plateau thereafter. When either amantadine (20 mg kg À1 ) or budipine (5 mg kg À1 ) was coadministered with any of the three antidepressants, two differences were seen compared with the effects of the antidepressants alone. Firstly, the time required for significant increases in cortical 5-HT was reduced with elevated levels now being observed by 7 days. Secondly, the absolute magnitude of the increase in extracellular 5-HT was markedly greater in these rats from day 7 until the end of the experiment. 5 If, as is widely considered, an increase in extracellular 5-HT represents a critical step in the mechanism of action of antidepressants, these data suggest that combined treatment with clinically tolerated NMDA antagonists such as amantadine could reduce the delay in therapeutic onset of antidepressants as well as possibly enhance their efficacy.

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“…It is reported that high levels of 5-HTP reduce serum dopamine and that serotonin counterregulates dopamine (35,43). It is also reported that dopamine regulates Th17 and mast cell responses (67,68,89).…”

Section: -Htp Diets Did Not Alter Total Tissue Levels Of 5-htp and Imentioning

confidence: 99%

Inhibition of allergic inflammation by supplementation with 5-hydroxytryptophan

Abdala-Valencia¹,

Berdnikovs²,

McCary³

et al. 2012

American Journal of Physiology-Lung Cellular and Molecular Phys

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Clinical reports indicate that patients with allergy/asthma commonly have associated symptoms of anxiety/depression. Anxiety/depression can be reduced by 5-hydroxytryptophan (5-HTP) supplementation. However, it is not known whether 5-HTP reduces allergic inflammation. Therefore, we determined whether 5-HTP supplementation reduces allergic inflammation. We also determined whether 5-HTP decreases passage of leukocytes through the endothelial barrier by regulating endothelial cell function. For these studies, C57BL/6 mice were supplemented with 5-HTP, treated with ovalbumin fraction V (OVA), house dust mite (HDM) extract, or IL-4, and examined for allergic lung inflammation and OVA-induced airway responsiveness. To determine whether 5-HTP reduces leukocyte or eosinophil transendothelial migration, endothelial cells were pretreated with 5-HTP, washed and then used in an in vitro transendothelial migration assay under laminar flow. Interestingly, 5-HTP reduced allergic lung inflammation by 70-90% and reduced antigen-induced airway responsiveness without affecting body weight, blood eosinophils, cytokines, or chemokines. 5-HTP reduced allergen-induced transglutaminase 2 (TG2) expression and serotonylation (serotonin conjugation to proteins) in lung endothelial cells. Consistent with the regulation of endothelial serotonylation in vivo, in vitro pretreatment of endothelial cells with 5-HTP reduced TNF-α-induced endothelial cell serotonylation and reduced leukocyte transendothelial migration. Furthermore, eosinophil and leukocyte transendothelial migration was reduced by inhibitors of transglutaminase and by inhibition of endothelial cell serotonin synthesis, suggesting that endothelial cell serotonylation is key for leukocyte transendothelial migration. In summary, 5-HTP supplementation inhibits endothelial serotonylation, leukocyte recruitment, and allergic inflammation. These data identify novel potential targets for intervention in allergy/asthma.

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Opposite effects of glutamate antagonists and antiparkinsonian drugs on the activities of DOPA decarboxylase and 5-HTP decarboxylase in the rat brain

Cited by 18 publications

References 37 publications

Affinity and specificity of N-methyl-D-aspartate channel blockers affect their ability to disrupt prepulse inhibition of acoustic startle in rats

Affinity and specificity of N-methyl-D-aspartate channel blockers affect their ability to disrupt prepulse inhibition of acoustic startle in rats

Effects of amantadine and budipine on antidepressant drug‐evoked changes in extracellular 5‐HT in the frontal cortex of freely moving rats

Inhibition of allergic inflammation by supplementation with 5-hydroxytryptophan

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