Catecholamines and drug—behavior interactions

Seiden, Lewis S.; MacPhail, Robert C.; Oglesby, Michael

doi:10.1007/978-1-4684-2634-2_11

Cited by 32 publications

(26 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Exposure to a chronic high dose of METH produced depletion of dopamine (up to 80%) in the caudate nucleus of rhesus monkeys for up to six months post-treatment (Seiden et al, 1975). The same study reported loss of some noradrelanin as well.…”

Section: Introductionmentioning

confidence: 72%

Methamphetamine-induced striatal apoptosis in the mouse brain: Comparison of a binge to an acute bolus drug administration

Zhu

Angulo

et al. 2006

NeuroToxicology

View full text Add to dashboard Cite

Methamphetamine (METH) is a psychostimulant that induces neural damage in experimental animals and humans. A binge (usually in the 5-10 mg/kg dose range 4× at 2 h intervals) and the acute bolus drug administration (20-40 mg/kg) of METH have been employed frequently to study neurotoxicity in the brain. In this study we have compared these drug delivery schedules to determine their efficacy to induce striatal apoptosis. Exposure of male mice to a binge of METH at 10 mg/kg 4× at 2 h intervals (cumulative dose of 40 mg/kg) was approximately four times less effective in inducing apoptotic cell death (TUNEL staining) 24 h after METH treatment in the striatum than a single bolus administration of 30 mg/kg of METH. The residual TUNEL staining observed three days after METH treatment is proportionately equivalent between a binge and the acute bolus drug administration. Interestingly, a binge of METH induces a hyperthermic response of longer duration. This study demonstrates that an acute bolus drug administration of METH is more effective inducing striatal apoptosis in mice, and therefore, is more suitable for studies assessing the impact of METH on sites post-synaptic to the striatonigral dopamine terminals.

show abstract

Section: Introductionmentioning

confidence: 72%

Methamphetamine-induced striatal apoptosis in the mouse brain: Comparison of a binge to an acute bolus drug administration

Zhu

Angulo

et al. 2006

NeuroToxicology

View full text Add to dashboard Cite

show abstract

“…Exposure to METH produces deleterious effects on DA levels [30] and on the rate-limiting enzyme of catecholamine biosynthesis TH [16]. Rats given one single injection of METH (40 mg/kg) displayed decreased levels of TH protein at 6 h (29% decrease) with the lowest depletion reached at 72 h (76% decrease) after METH [6].…”

Section: Discussionmentioning

confidence: 99%

“…The work of Escalante and Ellinwood [9] showed that chronic exposure to amphetamine induced chromatolysis in neurons of the cat brain. Soon after this finding, another group reported that exposure to a chronic high dose of METH produced depletion of DA (up to 80%) in the caudate nucleus of rhesus monkeys for up to 6 months post-treatment [30]. That same study reported loss of some noradrelanin as well.…”

Section: Introductionmentioning

confidence: 91%

Disparity in the temporal appearance of methamphetamine-induced apoptosis and depletion of dopamine terminal markers in the striatum of mice

Zhu

Angulo

2005

Brain Research

View full text Add to dashboard Cite

Methamphetamine (METH) causes damage in the striatum at pre-and post-synaptic sites. Exposure to METH induces long-term depletions of dopamine (DA) terminal markers such as tyrosine hydroxylase (TH) and DA transporters (DAT). METH also induces neuronal apoptosis in some striatal neurons. The purpose of this study is to demonstrate which occurs first, apoptosis of some striatal neurons or DA terminal toxicity in mice. This is important because the death of striatal neurons leaves the terminals in a state of deafferentation. A bolus injection (i.p.) of METH (30 mg/kg) induces apoptosis (TUNEL staining) in approximately 25% of neurons in the striatum at 24 h after METH. However, in contrast to apoptosis, depletion of TH (Western blotting) begins to appear at 24 h after METH in dorsal striatum while the ventral striatum is unaffected. The peak of TH depletion (approximately 80% decrease relative to control) occurs at 48 h after METH. Autoradiographic analysis of DAT sites showed that depletion begins to appear 24 h after METH and peaks at 2 days (approximately 60% depletion relative to control). Histological analysis of the induction of glial fibrillary acidic protein (GFAP) by METH in striatal astrocytes revealed an increase at 48 h after METH that peaked at 3 days. These data demonstrate that striatal apoptosis precedes the depletion (toxicity) of DA terminal markers in the striatum of mice, suggesting that the ensuing state of deafferentation of the DA terminals may contribute to their degeneration.

show abstract

“…In sufficient doses, exposure to mAMPH produces long-lasting damage to the dopaminergic [18,38] and serotonergic systems [1,32] as well as to cells in somatosensory cortex [14,29]. The injury to monoaminergic terminals and to nonmonoaminergic cell bodies has been most extensively reported in animals, but convergent evidence suggests that humans may also be subject to the neurotoxic effects of mAMPH [24, 46, 47; however, see 49].…”

mentioning

confidence: 99%

A sensitizing regimen of methamphetamine causes impairments in a novelty preference task of object recognition

Belcher¹,

O’Dell²,

Marshall³

2006

Behavioural Brain Research

View full text Add to dashboard Cite

Catecholamines and drug—behavior interactions

Cited by 32 publications

References 53 publications

Methamphetamine-induced striatal apoptosis in the mouse brain: Comparison of a binge to an acute bolus drug administration

Methamphetamine-induced striatal apoptosis in the mouse brain: Comparison of a binge to an acute bolus drug administration

Disparity in the temporal appearance of methamphetamine-induced apoptosis and depletion of dopamine terminal markers in the striatum of mice

A sensitizing regimen of methamphetamine causes impairments in a novelty preference task of object recognition

Contact Info

Product

Resources

About