Enhancement in extracellular serotonin levels by 5-hydroxytryptophan loading after administration of way 100635 and fluoxetine

Dreshfield-Ahmad, Laura J.; Thompson, Dennis C.; Schaus, John M.; Wong, David T.

doi:10.1016/s0024-3205(00)00530-0

Cited by 10 publications

(3 citation statements)

References 19 publications

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“…WAY-100,635 has been reported to increase extracellular 5-HT level 25 and might suggest another hypothesis for its anticonvulsant effect of WAY-100,635 and opposite/negligible effect of 8-OH-DPAT, in our study. Behavioural findings of this study suggested that the 8-OH-DPAT treatment improves memory function by reducing transfer latency in elevated plus maze and by increasing step-down latency in the passive shock avoidance paradigm.…”

supporting

confidence: 67%

Modulatory Effect of Serotonergic System in Pentylenetetrazole-Induced Seizures and Associated Memory Deficit: Role of 5-HT1A and 5-HT2A/2C

Mishra¹,

Goel²

2020

J Epilepsy Res

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Recent studies have recognised the memory deficit as one of the most common psychiatric issues in the patients with epilepsy, which severely affects the quality of life. Our previous studies have demonstrated the possible involvement of serotonergic system in the pathogenesis of epilepsy and associated memory deficit. The possible involvement of 5-HT1A and 5-HT2A/2C receptor has not been explored yet. Therefore, this study has been envisaged to explore the effect of 5-HT1A and 5-HT2A/2C receptor modulation on epilepsy and memory deficit in pentylenetetrazole-kindled mice. Methods: In the present experimental approach, we examined the efficacy of modulation of 5-HT1A and 5-HT2A/2C receptor in pentylenetetrazole-induced kindling in male Swiss mice (n=75). Mice were kindled by sub-convulsive dose of pentylenetetrazole (35 mg/kg, intraperitoneal injection), at the interval of 48±2 hours). Successfully kindled animals were treated with 5-HT1A and 5-HT2A/2C receptor modulators. The effect of different treatments on seizure severity score and memory impairment was analysed. Results: 5-HT1A receptor agonist improved the memory functions while seizure severity was not improved, and the opposite effect was observed with 5-HT1A receptor antagonist. On the other hand, 5-HT2A/2C receptor agonist significantly improved memory deficit as well as seizure severity in the kindled animals. Conclusions: The outcome of the study indicates the possible involvement of 5-HT2A/2C receptor in the pathogenesis of epilepsy and associated memory deficit, which can be further explored for its management.

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confidence: 67%

Modulatory Effect of Serotonergic System in Pentylenetetrazole-Induced Seizures and Associated Memory Deficit: Role of 5-HT1A and 5-HT2A/2C

Mishra¹,

Goel²

2020

J Epilepsy Res

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“…Although it is quite clear that acute pretreatment with 5-HTP increases the net amount of released 5-HT and its synaptic availability (Dreshfield-Ahmad et al, 2000;Fickbohm and Katz, 2000), the antipanic mechanism of 5-HTP requires further study. The increase in plasma cortisol and prolactin following 5-HTP administration in man is modulated by at least three different postsynaptic receptors, the 5-HT1A, 5-HT2A, 5-HT2C, and 5-HT3 receptors (Meltzer and Maes, 1994;Meltzer et al, 1997).…”

Section: Challenge Studiesmentioning

confidence: 99%

Serotonin Function in Panic Disorder: Important, But Why?

Maron

Shlik

2005

Neuropsychopharmacol

109

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The essential role of serotonin (5-hydroxytryptamine (5-HT)) system in the neurobiology and pharmacotherapy of panic disorder (PD) continues to be a topic of intensive interdisciplinary research. Interest in the involvement of 5-HT in PD has been fuelled by clinical studies demonstrating that medications increasing the synaptic availability of 5-HT, such as selective 5-HT re-uptake inhibitors, are effective in the treatment of PD. Rival theories of 5-HT deficiency vs excess have attempted to explain the impact of 5-HT function in PD. In the past decade, knowledge of the role of 5-HT in the neurobiology of PD has expanded dramatically due to much new research including experimental, treatment, brain-imaging, and genetic studies. The current review attempts to summarize the new data and their implications. The challenge and treatment studies generally confirm the specific inhibitory influence of 5-HT on panicogenesis. The brainimaging studies in PD patients demonstrate functional and clinically relevant alterations in various elements of 5-HT system affecting the neurocircuitry of panic. The findings of genetic association studies suggest that certain 5-HT-related genes may contribute to the susceptibility to PD; however, these data are rather limited and inconsistent. It appears that, even if not the primary etiological factor in PD, the 5-HT function conveys important vulnerability, as well as adaptive factors. A better understanding of these processes may be critical in achieving progress in the treatment of patients suffering from PD.

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“…Notably, the use of higher doses of 5-HTP demonstrated more prominent anti-panic effects. Although it is quite clear that acute pre-treatment with 5-HTP increases the net amount of released 5-HT and its synaptic availability (Dreshfield-Ahmad et al 2000; Fickbohm and Katz, 2000), the possible antipanic action mode of 5-HTP requires further scrutiny. The increase in plasma cortisol and prolactin following 5-HTP administration is modulated by different postsynaptic receptors, including 5-HT1A, 5-HT2A, 5-HT2C, and 5-HT3 (Meltzer and Maes, 1994; Meltzer et al 1997).…”

Section: Experimental Studiesmentioning

confidence: 99%

Tryptophan Research in Panic Disorder

Maron

Shlik

Nutt

2008

Int J�Tryptophan�Res

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A considerable body of evidence suggests the involvement of serotonin neurotransmission in the pathogenesis of panic disorder. Research on pathways and functions of tryptophan, an essential amino acid converted into serotonin, may advance our understanding of serotonergic actions in panic disorder and related phenomena. The investigative approaches in this fi eld include manipulations of tryptophan availability as well as genetic association and functional brain imaging studies. In this review we examine the principle fi ndings of these studies and propose further research directions.Keywords: tryptophan, panic disorder, anxiety, challenge, gene Panic disorder (PD) is a prevalent and serious illness in need of a better understanding of its neurobiological basis to improve treatment outcomes. The pathogenesis, clinical manifestations and treatment effects of PD are thought to be substantially related to the functions of serotonin or 5-hydroxytryptamine (5-HT) neurotransmission. The crucial role of 5-HT in PD has been suggested by clinical studies demonstrating that medications specifi cally increasing the synaptic availability of 5-HT, especially the selective 5-HT re-uptake inhibitors (SSRIs), are particularly effective in the treatment of PD (Nutt, 1998). Extensive experience with SSRIs in the treatment of PD and the effect of tryptophan depletion (TD) to undermine this action underscored the necessity of increased synaptic availability of 5-HT for achieving remission. Furthermore, growing data from experimental and neuroimaging studies have suggested that altered availability of brain 5-HT is associated with PD; however the exact mechanisms of a possible disturbance in 5-HT metabolism are not fully understood . 5-HT is synthesized from the essential amino acid tryptophan via intermediate metabolite, 5-hydroxytryptophan (5-HTP), and stored in reserpine-sensitive vesicles until released into the synaptic cleft by nerve impulses. The conversion of tryptophan into 5-HTP is regulated by tryptophan hydroxylase (TPH), the rate limiting enzyme in biosynthesis of 5-HT. In the next step, 5-HTP is decarboxylated by aromatic acid decarboxylase to 5-HT. Unlike 5-HTP, tryptophan can be shunted into kynurenine via tryptophan 2,3-dioxygenase, making tryptophan unavailable for 5-HT production (Birdsall, 1998;Ruddick et al. 2006). TPH can be inhibited by numerous factors, including stress, insulin resistance, vitamin B6 deficiency, and insuffi cient magnesium, that may increase the conversion of tryptophan to kynurenine. Under normal conditions, the enzyme TPH is only about 50% saturated in brain, therefore the synthesis of 5-HT is dependent on the availability of free plasma tryptophan, whereas alterations in its availability correlate with the amount of synthesized 5-HT (Schaechter and Wurtman, 1990). Presently, the central 5-HT pathways remain the main targets in the research on the neurobiology of PD. In this paper we review the studies focusing on the role of tryptophan and discuss research directions in this are...

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Enhancement in extracellular serotonin levels by 5-hydroxytryptophan loading after administration of way 100635 and fluoxetine

Cited by 10 publications

References 19 publications

Modulatory Effect of Serotonergic System in Pentylenetetrazole-Induced Seizures and Associated Memory Deficit: Role of 5-HT<sub>1A</sub> and 5-HT<sub>2A/2C</sub>

Modulatory Effect of Serotonergic System in Pentylenetetrazole-Induced Seizures and Associated Memory Deficit: Role of 5-HT<sub>1A</sub> and 5-HT<sub>2A/2C</sub>

Serotonin Function in Panic Disorder: Important, But Why?

Tryptophan Research in Panic Disorder

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