Relationship between Temperature, Dopaminergic Neurotoxicity, and Plasma Drug Concentrations in Methamphetamine-Treated Squirrel Monkeys

@article{Yuan2006RelationshipBT,
  title={Relationship between Temperature, Dopaminergic Neurotoxicity, and Plasma Drug Concentrations in Methamphetamine-Treated Squirrel Monkeys},
  author={Jie Yuan and George Hatzidimitriou and Pranav Suthar and Melanie Mueller and Una D. McCann and George A. Ricaurte},
  journal={Journal of Pharmacology and Experimental Therapeutics},
  year={2006},
  volume={316},
  pages={1210 - 1218}
}
To examine the relationship between temperature (ambient and core), dopaminergic neurotoxicity, and plasma drug [methamphetamine (METH)] and metabolite [amphetamine (AMPH)] concentrations, two separate groups of squirrel monkeys (n = 4–5 per group) were treated with METH (1.25 mg/kg, given twice, 4 h apart) or vehicle (same schedule) at two different ambient temperatures (26 and 33°C). Core temperatures and plasma drug concentrations were measured during the period of drug exposure; striatal… Expand
Brain Region–Specific Neurodegenerative Profiles Showing the Relative Importance of Amphetamine Dose, Hyperthermia, Seizures, and the Blood–Brain Barrier
TLDR
Recent findings on the neurodegenerative effects of both a single high dose of 40 mg/kg and a 4‐dose exposure to AMPH in the rat suggest that damage may also occur in humans exposed to high doses of AMPH or METH in the absence of status epilepticus or prominent motor manifestations of seizure activity. Expand
Impact of Ambient Temperature on Hyperthermia Induced by (±)3,4-Methylenedioxymethamphetamine in Rhesus Macaques
TLDR
Monkey temperature responses to MDMA appear to be more similar to humans than to rodents and therefore the monkey may offer an improved model of effects related to MDMA-induced hyperthermia. Expand
Pharmacological activation of the neurotensin receptor 1 abrogates the methamphetamine-induced striatal apoptosis in the mouse brain
TLDR
Data indicate that the neuropeptide neurotensin modulates the striatal neuronal apoptosis induced by METH through diverse mechanisms that need to be investigated. Expand
Brain edema and breakdown of the blood–brain barrier during methamphetamine intoxication: critical role of brain hyperthermia
TLDR
Along with a direct destructive action on neural cells and functions, brain hyperthermia, via breakdown of the BBB, may be crucial for both decompensation of brain functions and cell injury following acute METH intoxication, possibly contributing to neurodegeneration resulting from chronic drug use. Expand
Influences of methamphetamine-induced acute intoxication on urinary and plasma metabolic profiles in the rat.
TLDR
Mass spectrometry-based metabolomics experiments performed on Sprague-Dawley rats suggested that high doses of MA inhibit biogenic energy production by glycolysis, oxidative phosphorylation via the TCA cycle, and the beta-oxidation of fatty acids. Expand
Hyperthermic and lethal effects of methamphetamine: Roles of dopamine D1 and D2 receptors
TLDR
Both D1 and D2 receptors play roles in the lethal toxic effects of methamphetamine, and mainly the D2 receptor is involved in the elevation of body temperature. Expand
Amphetamine- and methamphetamine-induced hyperthermia: Implications of the effects produced in brain vasculature and peripheral organs to forebrain neurotoxicity
TLDR
The hyperthermia and the hypertension produced by high doses amphetamines are a primary cause of transient breakdowns in the blood-brain barrier resulting in concomitant regional neurodegeneration and neuroinflammation in laboratory animals. Expand
High doses of methamphetamine that cause disruption of the blood‐brain barrier in limbic regions produce extensive neuronal degeneration in mouse hippocampus
TLDR
High doses of METH can cause damage to the BBB when hyperthermia occurs, resulting in rapid and extensive hippocampal and amygdalar damage, sufficient to compromise learning and memory. Expand
Pharmacology of Methamphetamine
TLDR
Chronic methamphetamine abuse is reported to lead to significant reduction in grey matter in the brain, greater than those in dementia or schizophrenia patients, though this needs further clarification. Expand
Methamphetamine-induced dopamine terminal deficits in the nucleus accumbens are exacerbated by reward-associated cues and attenuated by CB1 receptor antagonism
TLDR
Data suggest that the endocannabinoid system is involved in the subsecond dopaminergic response to METH, and pretreatment with the CB1 receptor antagonist rimonabant would reduce METH-induced alterations at dopamine terminals. Expand
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 77 REFERENCES
Further studies of the role of hyperthermia in methamphetamine neurotoxicity.
TLDR
It was concluded that short- and long-term decreases in striatal DA levels depend on the degree of hyperthermia produced during METH exposure but cannot be produced byhyperthermia alone. Expand
Methamphetamine-induced hyperthermia and dopaminergic neurotoxicity in mice: pharmacological profile of protective and nonprotective agents.
TLDR
It is demonstrated that hyperthermia per se contributes to but is not solely responsible for the METH-induced neuropathology, and studies with reserpine, a compound which dramatically lowers core temperature, demonstrated that the hypothermic state produced in the reserpinized mice did not provide protection from Meth-induced toxicity. Expand
Elevated environmental temperature and methamphetamine neurotoxicity.
TLDR
It is shown how a relatively minor change in ambient temperature can have a major impact on the degree of neurotoxicity induced by d-METH. Expand
Effect of Temperature on Dopamine Transporter Function and Intracellular Accumulation of Methamphetamine: Implications for Methamphetamine-Induced Dopaminergic Neurotoxicity
TLDR
It is suggested that relatively small, physiologically relevant changes in temperature significantly alter DAT function and intracellular METH accumulation, and suggest that the effect of temperature on METH-induced DA neurotoxicity is mediated, at least in part, at the level of the DAT. Expand
Low environmental temperatures or pharmacologic agents that produce hypothermia decrease methamphetamine neurotoxicity in mice
TLDR
Whether a cold environment (4 degrees C) or drugs which chloride and glutamate ion channel function block METH neurotoxicity in mice is evaluated and a significant depletion of dopamine (DA) in striatum at 24, 72 h, 1 and 2 weeks is produced. Expand
Recovery of striatal dopamine function after acute amphetamine- and methamphetamine-induced neurotoxicity in the vervet monkey
TLDR
The results indicate that in vervet monkey striatum, an acute Amp or MeAmp drug dosage produces extensive striatal dopamine system neurotoxicity, however, these effects were reversible; observed time-dependent recovery in both FDOPA Ki and dopamine concentrations indicates that neurochemical plasticity remains active in the adult primate striatum. Expand
A single dose model of methamphetamine-induced neurotoxicity in rats: effects on neostriatal monoamines and glial fibrillary acidic protein
TLDR
It is demonstrated that a single-dose of MA can be as effective as the widely used four-dose every 2 h regimen and mortality can be minimized by monitoring core body temperature and preventing MA-induced hyperthermia from exceeding 41.5 degrees C. Expand
Dizocilpine and reduced body temperature do not prevent methamphetamine-induced neurotoxicity in the vervet monkey: [11C]WIN 35,428 - positron emission tomography studies
TLDR
In this non-human primate species, the combination of MK-801 pretreatment and reduced body temperature did not provide protection from the MeAmp-induced loss of DAT, and the absence of an elevated body temperature during the acute MeAMP exposure period indicated that hyperthermia, per se, was not a necessary concomitant of the Me amp neurotoxicity profile as has been previously demonstrated in rodents. Expand
Tolerance to the neurotoxic effects of methamphetamine in young rats.
TLDR
Results confirm that high-dose methamphetamine administration decreases striatal dopamine uptake and transporter ligand binding in post-natal day 90 rats and attenuated the hyperthermia caused by the neurotoxic methamphetamine regimen; a phenomenon that may have contributed to the neuroprotection. Expand
The influence of environmental temperature on the transient effects of methamphetamine on dopamine levels and dopamine release in rat striatum.
TLDR
A cold environmental temperature (4 degrees C) reduced the effects of METH on striatal DA levels and striatal TH activity. Expand
...
1
2
3
4
5
...