Magnetic cells: stuff of legend?
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Animals↗
Biomedical subjects
M Mertl
Publications and source records attributed to M Mertl.
Cognitive performance in (+/-) 3,4-methylenedioxymethamphetamine (MDMA, "ecstasy") users: a controlled study.
RATIONALE: (+/-) 3,4-Methylenedioxymethamphetamine (MDMA, "ecstasy") is an amphetamine analog and drug of abuse. In animals, MDMA damages brain serotonin (5-HT) neurons at doses that overlap with those used recreationally by some humans. To date, few functional sequelae of MDMA-induced 5-HT damage have been identified. OBJECTIVE: Since serotonin is thought to be involved in cognitive processes, and since previous studies have reported verbal and visual memory deficits in MDMA users, the present study sought to determine whether other cognitive processes are influenced by previous exposure to MDMA. METHODS: Twenty-two MDMA users who had not used MDMA for at least 3 weeks and 23 control subjects were tested repeatedly with a computerized cognitive performance assessment battery while participating in a 5-day controlled inpatient study. Cerebrospinal fluid (CSF) measures of monoamine metabolites were also collected as an index of brain monoaminergic function. RESULTS: MDMA users and controls were found to perform similarly on several cognitive tasks. However, MDMA subjects had significant performance deficits on a sustained attention task requiring arithmetic calculations, a task requiring complex attention and incidental learning, a task requiring short term memory and a task of semantic recognition and verbal reasoning. MDMA users also had significant selective decreases in CSF 5-HIAA. CONCLUSIONS: The present CSF data provide further evidence that MDMA is neurotoxic to brain 5-HT neurons in humans, and the behavioral data suggest that brain 5-HT injury is associated with subtle, but significant, cognitive deficits.
Adult↗
Altered neuroendocrine and behavioral responses to m-chlorophenylpiperazine in 3,4-methylenedioxymethamphetamine (MDMA) users.
RATIONALE: (+/-) 3,4-Methylenedioxymethamphetamine (MDMA, "Ecstasy") is a popular drug of abuse and a brain serotonin neurotoxin in animals. Growing evidence indicates that humans are also susceptible to MDMA's neurotoxic effects, although few functional consequences of MDMA-induced 5-HT damage have been identified. OBJECTIVE: The present study sought to determine whether possible differences between MDMA users and control subjects could be unmasked by utilizing a pharmacological challenge with the mixed 5-HT agonist, meta-chlorophenylpiperazine (m-CPP). It was postulated that 5-HT neurotoxicity in MDMA users would be associated with altered 5-HT responsivity, exemplified by altered physiological and behavioral responses to m-CPP. METHODS: Twenty-five MDMA users who had not taken MDMA for at least 3 weeks and 25 controls received intravenous placebo (normal saline) and m-CPP (0.08 mg/kg) in a fixed order, single blind design. Repeated measures of mood, physical symptoms, and blood samples for neuroendocrine analyses were collected during the 90 min after each infusion. RESULTS: MDMA users reported more positive and fewer negative emotions and physical symptoms following m-CPP than controls, and were significantly less likely to report an m-CPP-induced panic attack. Male MDMA users had diminished cortisol and prolactin responses to m-CPP. CONCLUSIONS: The present data indicate that MDMA users have alterations in 5-HT neuronal function, possibly as a consequence of MDMA-induced brain serotonin neural injury.
Adult↗
[The equilibrium of nitrogen, potassium and phosphate and renal excretion of creatinine and creatinine over the course of 3 weeks following severe trauma].
In 19 patients after accidental trauma and with intact renal function during an observation time of 21 days we found a cumulated negative balance of nitrogen (N), phosphate (P) and potassium (K) amounting to a mean of 214g, 357 and 447 mmol, respectively. Median daily potassium balance was positive on day 2 to 5 and this was interpreted as an increased extrarenal potassium deposition due to increased levels of circulating catecholamines. Median renal creatinine excretion was about 120% of predicted normal till day 10 and continuously decreased thereafter to values lower than predicted normal. Three patients did not show creatinuria (greater than 200 mg/day) during the whole observation time. In 15 patients after a "free interval" with a mean duration of 7 days creatinuria frequently developed rather quickly and maximal excretion of creatine was as high as 4 g/day. In 7 patients creatinuria persisted to the end of the 21 days observation time. During the phase of creatinuria the median cumulated excretion of creatine amounted to 14.4 g. The "free interval" of creatinuria after severe trauma is remarkable. Most of the N, K and P, which is lost from the body during this time obviously stems from tissues other than sceletal muscle. During the phase of creatinuria, however, the negative balance of N, K and P seems to be mainly due to muscle wasting. Hypophosphatemia was prominent during the first 5 days after trauma and obviously was caused by a decrease in renal phosphate threshold (TmPO4/GFR). The underlying mechanism of this primary change in renal function after severe trauma could not yet be identified.
Adolescent↗