Amphetamine-induced stereotyped behaviour and brain concentrations of amphetamine and its hydroxylated metabolites in mice

Brien, J. F.; Peachey, John E.; Rogers, Bairbre; Kitney, J C

doi:10.1111/j.2042-7158.1977.tb11239.x

Cited by 31 publications

(19 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…While dose, strain, and type of administration all affect pharmacokinetics, our estimates of cocaine and methamphetamine concentrations in the brain and blood are within the range observed in other studies for methamphetamine (Brien et al 1978;Fornai et al 1999;Hendrickson et al 2004;Won et al 2001) and cocaine (Azar et al 1998;Benuck et al 1987;Miller et al 1996;Pan and Hedaya 1998;Reith et al 1987). Additionally, the primary routes of metabolism in mice (Boyer and Petersen 1992;Shuster et al 1983) are similar to those in rats (Estevez et al 1977) and humans (Bencharit et al 2003;Brzezinski et al 1997).…”

Section: Limitationssupporting

confidence: 73%

See 1 more Smart Citation

Evaluation of a pharmacokinetic hypothesis for reduced locomotor stimulation from methamphetamine and cocaine in adolescent versus adult male C57BL/6J mice

2008

View full text Add to dashboard Cite

show abstract

Section: Limitationssupporting

confidence: 73%

“…Drugs were dissolved in 0.9% saline and administered in a volume of 5 ml/kg. Doses and time points were chosen based on the literature (Azar et al 1998;Benuck et al 1987;Brien et al 1978 …”

Section: Drugsmentioning

confidence: 99%

Evaluation of a pharmacokinetic hypothesis for reduced locomotor stimulation from methamphetamine and cocaine in adolescent versus adult male C57BL/6J mice

2008

View full text Add to dashboard Cite

show abstract

“…SB and self-injurious biting (SIB) occur after large doses or repeated administration of drugs that promote dopamine release, such as amphetamine [Brien et al, 1977;Lara-Lemus et al, 1997], methamphetamine [Kita et al, 2000;Shishido et al, 2000;Halladay et al, 2003], or pemoline Mueller et al, 1986;King et al, 1995;Cromwell et al, 1999;Turner et al, 1999]. They also emerge after repeated administration of high doses of the dopamine reuptake blocker, GBR-12909 [Sivam, 1995;Loupe et al, 2002].…”

Section: Introductionmentioning

confidence: 99%

The Role of Dopamine Receptors in the Neurobehavioral Syndrome Provoked by Activation of L-Type Calcium Channels in Rodents

et al. 2006

View full text Add to dashboard Cite

In rodents, activation of L-type calcium channels with ±BayK 8644 causes an unusual behavioral syndrome that includes dystonia and self-biting. Prior studies have linked both of these behaviors to dysfunction of dopaminergic transmission in the striatum. The current studies were designed to further elucidate the relationship between ±BayK 8644 and dopaminergic transmission in the expression of the behavioral syndrome. The drug does not appear to release presynaptic dopamine stores, since microdialysis of the striatum revealed dopamine release was unaltered by ±BayK 8644. In addition, the behaviors were preserved or even exaggerated in mice or rats with virtually complete dopamine depletion. On the other hand, pretreatment of mice with D₃ or D_1/5 dopamine receptor antagonists attenuated the behavioral effects of ±BayK 8644, while pretreatment with D₂ or D₄ antagonists had no effect. In D₃ receptor knockout mice, ±BayK 8644 elicited both dystonia and self-biting, but these behaviors were less severe than in matched controls. In D₁ receptor knockout mice, behavioral responses to ±BayK 8644 appeared exaggerated. These results argue that the behavioral effects of ±BayK 8644 are not mediated by a presynaptic influence. Instead, the behaviors appear to result from a postsynaptic activation of the drug, which does not require but can be modified by D₃ or D_1/5 receptors.

show abstract

“…This method cannot distinguish between MA and amphetamine. It has been shown that MA is demethylated to am phetamine in the liver (7) and the brain amphetamine/MA+amphetamine concentra tion ratio is 0.11 to 0.14 during 90 min after the administration of MA in mice (8). However, the two compounds may be equipotent in the stereotypy-producing action since the potency of catecholamine-releasing action of MA and amphetamine In vitro is similar (9).…”

Section: Methodsmentioning

confidence: 99%

“…However, the two compounds may be equipotent in the stereotypy-producing action since the potency of catecholamine-releasing action of MA and amphetamine In vitro is similar (9). Furthermore, total level of MA +amphetamine in the brain declines exponen tially after MA administration in rats and mice (10,8). Therefore we considered it suitable for the purpose of the present experi ments to measure the total tissue levels of MA and amphetamine.…”

Section: Methodsmentioning

confidence: 99%

Further studies on the potentiating effect of lithium chloride on methamphetamine-induced stereotypy in mice.

1981

View full text Add to dashboard Cite

Abstract-To study the mechanism of the potentiating effect of lithium chloride (LiCI) on methamphetamine (MA)-induced stereotypy in mice, effects of various drugs on the action of LiCI on the stereotypy and phar macokinetics of MA in different brain regions and liver were examined. The potentiating effect of LiCI disappeared in mice pretreated with atropine or scopolamine whereas LiCl potentiated the stereotypy in mice pretreated with p-chlorophenylalanine, a-methyl-p-tyrosine, nialamide, physostigmine or butylscopolamine. The concentrations of MA in the striatum, brainstem and liver were increased and the half-life of MA in these tissues was prolonged by LiCI. The effect of LiCl on the kinetics of MA in the brain, but not that in the liver, was blocked by scopolamine. LiCI prolonged the half-life of MA in the brain and liver in mice treated with physostigmine or butylscopolamine. The inhibition of MA elimination from the brain and its blockade by scopolamine seem to explain the potentiating action of LiCI on the stereotypy and the antagonism by scopolamine of the behavioural action of LiCI, respectively. Lithium salt is a potent agent in the therapy and prophylaxis of affective disorders although the exact mode of action is unknown (1). We examined the effects of lithium chloride (LiCI) on methamphetamine (MA) induced stereotypy in mice to investigate the action of LiCI on central dopaminergic system (2) since it has generally been considered that amphetamines produce a stereotypy by an indirect activation of dopamine receptors in the striatum (3). We have reported that the stereotypy was potentiated by LiCl, and LiCI had no sig nificant effect on either MA concentration and elevated 3-methoxytyramine level in whole brain observed after the administration of MA.To clarify the mechanism of the potentiating action of LiCI on MA-induced stereotypy, effects of other drugs on the action of LiCI on either the stereotypy and the phar macokinetics of MA in the brain regions and liver were examined in the present experi ments. MATERIALS AND METHODSMale ddl mice (23-30 g) were used in the first experiments (Fig. 1). Data in other experiments were obtained using male ddY mice (23-30 g) since ddl strain mice could not be procured at the time.Behavioural experiments: Mice were placed individually in wire cages (15 x 17 x 11 cm) in a sound proof room maintained at a

show abstract

Amphetamine-induced stereotyped behaviour and brain concentrations of amphetamine and its hydroxylated metabolites in mice

Cited by 31 publications

References 11 publications

Evaluation of a pharmacokinetic hypothesis for reduced locomotor stimulation from methamphetamine and cocaine in adolescent versus adult male C57BL/6J mice

Evaluation of a pharmacokinetic hypothesis for reduced locomotor stimulation from methamphetamine and cocaine in adolescent versus adult male C57BL/6J mice

The Role of Dopamine Receptors in the Neurobehavioral Syndrome Provoked by Activation of L-Type Calcium Channels in Rodents

Further studies on the potentiating effect of lithium chloride on methamphetamine-induced stereotypy in mice.

Contact Info

Product

Resources

About