The effect of 3,4‐methylenedioxymethamphetamine (MDMA, ?ecstasy?) and its metabolites on neurohypophysial hormone release from the isolated rat hypothalamus

Forsling, Mary L.; Fallon, John K.; Shah, Darshna; Tilbrook, Gary S; Cowan, David; Kicman, Andrew T.; Hutt, Andrew J.

doi:10.1038/sj.bjp.0704502

Cited by 72 publications

(50 citation statements)

References 34 publications

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“…Other useful avenues of enquiry could examine changes in the efficacy of 5-HT receptor subtypes, changes in the transcription of 5-HT-related receptors, and alterations of basal and stimulated 5-HT within the synapse. The ability of MDMA to alter endocrine function chronically (Forsling et al, 2002) is another avenue through which anxiety may be affected as well as global effects on brain energy metabolism (Darvesh et al, 2002). Thus, it would be premature to conclude that the present study has isolated the mechanism through which MDMA chronically increases anxiety in rats.…”

Section: Discussionmentioning

confidence: 75%

Increased Anxiety 3 Months after Brief Exposure to MDMA (‘Ecstasy’) in Rats: Association with Altered 5-HT Transporter and Receptor Density

McGregor

Clemens

Plasse

et al. 2003

Neuropsychopharmacol

106

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Male Wistar rats were treated with 3,4-methylenedioxymethamphetamine (MDMA, 'Ecstasy') using either a high dose (4 Â 5 mg/kg over 4 h) or low dose (1 Â 5 mg/kg over 4 h) regimen on each of 2 consecutive days. After 10 weeks, rats were tested in the social interaction and emergence tests of anxiety. Rats previously given either of the MDMA dose regimens were significantly more anxious on both tests. After behavioral testing, and 3 months after the MDMA treatment, the rats were killed and their brains examined. Rats given the high-, but not the low-, dose MDMA treatment regimen exhibited significant loss of 5-hydroxytryptamine (5-HT) and 5-HIAA in the amygdala, hippocampus, striatum, and cortex. Quantitative autoradiography showed loss of SERT binding in cortical, hippocampal, thalamic, and hypothalamic sites with the high-dose MDMA regime, while low-dose MDMA only produced significant loss in the medial hypothalamus. Neither high-nor low-dose MDMA affected 5HT 1A receptor density. High-dose MDMA increased 5HT 1B receptor density in the nucleus accumbens and lateral septum but decreased binding in the globus pallidus, insular cortex and medial thalamus. Low-dose MDMA decreased 5HT 1B receptor density in the hippocampus, globus pallidus, and medial thalamus. High-dose MDMA caused dramatic decreases in cortical, striatal, thalamic, and hypothalamic 5HT 2A / 2C receptor density, while low-dose MDMA tended to produce similar effects but only significantly in the piriform cortex. These data suggest that even brief, relatively low-dose MDMA exposure can produce significant, long-term changes in 5-HT receptor and transporter function and associated emotional behavior. Interestingly, long-term 5-HT depletion may not be necessary to produce lasting effects on anxiety-like behavior after low-dose MDMA.

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Section: Discussionmentioning

confidence: 75%

Increased Anxiety 3 Months after Brief Exposure to MDMA (‘Ecstasy’) in Rats: Association with Altered 5-HT Transporter and Receptor Density

McGregor

Clemens

Plasse

et al. 2003

Neuropsychopharmacol

106

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“…Ecstasy is a potent inducer of the secretion of AVP (57)(58)(59)(60). Henry and colleagues demonstrated that small doses of MDMA (40 mg; common "street dose" is 100 mg) led to a significant increase in AVP levels (from 1.14-1.88 pmol/L to 2.46-9.16 pmol/L) within 1-2 hours after dosing.…”

Section: Clinical Manifestations Of Ecstasy Use and Underlying Pathogmentioning

confidence: 99%

Nephrotoxic Effects of Common and Emerging Drugs of Abuse

Pendergraft

Herlitz

Thornley‐Brown

et al. 2014

Clinical Journal of the American Society of Nephrology

112

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The kidneys can be injured in diverse ways by many drugs, both legal and illegal. Novel associations and descriptions of nephrotoxic effects of common and emerging drugs of abuse have appeared over the past several years. Anabolic androgenic steroids, illicitly used by athletes and others for decades to increase muscle mass and decrease body fat, are emerging as podocyte toxins given recent descriptions of severe forms of FSGS in long-term abusers. Synthetic cannabinoids, a new group of compounds with marijuana-like effects, recently became popular as recreational drugs and have been associated with an atypical form of AKI. 3,4-Methylenedioxymethamphetamine, commonly known as ecstasy, is a widely used synthetic recreational drug with mood-enhancing properties and a constellation of toxicities that can result in death. These toxic effects include hyperthermia, hypotonic hyponatremia due to its arginine vasopressin secretagogue-like effects, rhabdomyolysis, and cardiovascular collapse. Cocaine, a serotonin-norepinephrine-dopamine reuptake inhibitor that serves as an illegal stimulant, appetite suppressant, and anesthetic, also causes vasoconstriction and rhabdomyolysis. Recent adulteration of much of the world's supply of cocaine with levamisole, an antihelminthic agent with attributes similar to but distinct from those of cocaine, appears to have spawned a new type of ANCAassociated systemic vasculitis. This review discusses the nephrotoxic effects of these common and emerging drugs of abuse, of which both community and health care providers should become aware given their widespread abuse. Future investigation into pathogenetic mechanisms associated with these drugs is critical and may provide a window into ways to lessen and even prevent the nephrotoxic effects of these drugs of abuse and perhaps allow a deeper understanding of the nephrotoxicities themselves.

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“…MDMA administration stimulated ADH release from rat hypothalamus in vitro (26) and in healthy, normally hydrated human male volunteers, with a drop in serum sodium accompanying the rise in serum ADH (27). Additional evidence for MDMA-induced ADH secretion has been provided by determination of elevated levels of ADH in a patient with hyponatremic coma after Ecstasy ingestion (20).…”

Section: Discussionmentioning

confidence: 96%

Patterns of Ecstasy-Associated Hyponatremia in California

Rosenson

Smollin

Sporer

et al. 2007

Annals of Emergency Medicine

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Study objective: To describe the clinical characteristics of patients with Ecstasy (MDMA)-associated hyponatremia (serum sodium less than 130 mmol/L) reported to the California Poison Control System (CPCS) over a five-year period and to determine if a gender difference exists among patients with Ecstasy-associated hyponatremia. Methods:We performed a retrospective review of cases involving Ecstasy intoxication reported to the CPCS and recorded in its computerized database from January 1, 2000 through October 9, 2005 We excluded all "information only" calls, cases managed at home, cases with no gender specified and cases in which the outcome was coded as "no effect", "unrelated -probably not responsible", "confirmed non-exposure", "judged as non-toxic-expect no effect", and "minimal clinical effects possible". Confirmation of exposure to MDMA was based on the history of use and, when available, urine toxicology screen testing positive for MDMA or amphetamine derivatives. Hyponatremia was defined as a measured serum sodium less than 130 mmol/L.Results: A total of 1,436 cases involving Ecstasy were reported to the CPCS over the 5-year study period, of which 891 were excluded based on the criteria described above. Of the 545 cases that met inclusion criteria, 296 (54.3%) were females and 249 (45.7%) were males. There were 188 cases (34.5%) with a documented serum sodium, including 73/188 (38.8%) with hyponatremia (Na < 130 mmol/L). Of the 73 subjects with hyponatremia, there were 55 (75.3%) females and 18 (24.7%) males; of the 115 non-hyponatremic subjects 50 (43.5%) were female and 65 (56.5%) male. There was no observed gender difference in the ascertainment of serum sodium levels. Among patients with a documented serum sodium level, female gender was 3 associated with increased odds of hyponatremia by univariate analysis (OR 3.97; 95% CI 2.08 -7.59). Conclusion:Female gender was associated with increased odds of hyponatremia among persons with Ecstasy intoxication and a documented serum sodium level reported to CPCS from 2000 -2005. Multiple potential study confounders, including spectrum bias, incomplete laboratory data and individual differences in subject characteristics prevent determination of causality regarding gender differences in the incidence of Ecstasy-associated hyponatremia and its complications.

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The effect of 3,4‐methylenedioxymethamphetamine (MDMA, ?ecstasy?) and its metabolites on neurohypophysial hormone release from the isolated rat hypothalamus

Cited by 72 publications

References 34 publications

Increased Anxiety 3 Months after Brief Exposure to MDMA (‘Ecstasy’) in Rats: Association with Altered 5-HT Transporter and Receptor Density

Increased Anxiety 3 Months after Brief Exposure to MDMA (‘Ecstasy’) in Rats: Association with Altered 5-HT Transporter and Receptor Density

Nephrotoxic Effects of Common and Emerging Drugs of Abuse

Patterns of Ecstasy-Associated Hyponatremia in California

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