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Results for “Amphetamine”

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At least 19 recordsLinked to original sources
PubMed1977

Comparative effects of d-amphetamine, l-amphetamine, and methylphenidate on mood in man.

The comparative effects of d-amphetamine, l-amphetamine, and methylphenidate were assessed in 16 normal subjects, using a double-blind, crossover placebo-controlled design. Within the dose range tested, the efficacy ratio of d-amphetamine:l-amphetamine was about 2:1, and graphic presentation of dose response scores indicated a relatively small difference in potency between the amphetamine isomers. Methylphenidate was intermediate in efficacy between d-amphetamine and l-amphetamine. The efficacy ratios for d-amphetamine:l-amphetamine on increasing euphoric mood in man were similar to the previously reported ratios of there two isomers in inducing or exacerbating psychosis in humans. These findings do not support the suggestion, made by Snyder and others, that the differential effects of d-amphetamine vs. l-amphetamine on a specific type of behavior in man could be utilized to infer the predominance of noradrenergic vs. dopaminergic mediation of amphetamine's effects on this behavior.

Adult↗
PubMed1992

Sensitization and individual differences to IP amphetamine, cocaine, or caffeine following repeated intracranial amphetamine infusions.

Rats that have a high locomotor response to novelty (HR) sensitize more readily to IP-administered amphetamine than rats with a low locomotor response (LR) to novelty. This experiment compared sensitization in HR and LR rats following amphetamine (3.0 micrograms/side for 5 days) infused bilaterally into either the nucleus accumbens (NACC), ventral tegmental area (VTA), or the medial frontal cortex (MFC). The subsequent locomotor response to IP-administered d-amphetamine sulfate (1 mg/kg), cocaine HCl (15 mg/kg), and caffeine benzoate (20 mg/kg) was also examined. No differences were observed between HR and LR rats following amphetamine infusion into either the MFC, NACC, or VTA. However, HR rats showed greater locomotor activity compared to LR rats following either IP amphetamine, cocaine, or caffeine for subjects cannulated in the NACC, MFC, or the VTA. Repeated infusions of amphetamine into the VTA increased the locomotor response to both IP amphetamine and cocaine, but not to IP caffeine, while repeated infusions of amphetamine into the NACC or MFC had no effect on locomotor response to any drug subsequently administered IP. The results support previous findings that changes induced by intra-VTA infusions, but not intra-NACC or MFC infusions, of amphetamine induce sensitization to IP-administered amphetamine and cocaine. Findings from the present experiment indicate the ability of the dopamine cell body region, but not the dopamine terminal fields, to produce locomotor sensitization to amphetamine and cocaine. The results from the present experiment also indicate the lack of localization to one of studied regions of individual differences.(ABSTRACT TRUNCATED AT 250 WORDS)

Amphetamine↗
PubMed1979

Paradoxical effect of amphetamine in an endogenous model of the hyperkinetic syndrome in a hybrid dog: correlation with amphetamine and p-hydroxyamphetamine blood levels.

A telomian-beagle hybrid has been studied as a possible model for the hyperkinetic syndrome in children. Behavior tests showed that hybrids, like children, exhibit hyperactivity, impulsiveness, and impaired learning. Two groups of hybrid could be differentiated; the behaviour of one improved after amphetamine (responders) while that of the other did not (nonresponders). Moreover hybrids were less responsive than beagles to other effects of amphetamine such as stereotyped behaviour and hyperthermia. Measurement of blood levels of amphetamine and its active metabolite p-hydroxyamphetamine (pOA) showed that hybrids form less pOA. We propose that the lesser response of hybrids to toxic effects of amphetamine is due to this difference in amphetamine metabolism. Responders showed higher peak blood levels of amphetamine than nonresponders and their improvement on amphetamine correlated with blood levels of amphetamine. Therefore high levels of amphetamine appear to be necessary for its 'paradoxical' effect in this model. This suggests that amphetamine acts by activating both noradrenergic and dopaminergic neuronal systems in the CNS.

Amphetamine↗
PubMed1976

A comparison of dextro-amphetamine and racemic-amphetamine in the treatment of the hyperkinetic syndrome or minimal brain dysfunction.

In a double-blind trial of placebo, dextro-amphetamine, racemic-amphetamine, and methylphenidate, each used for a week, in 48 children with the diagnosis of Minimal Brain Dysfunction or Hyperkinetic Syndrome, it was found that although on the average dextro-amphetamine as well as methylphenidate was significantly superior to racemic-amphetamine, with side effects about the same, in some cases racemic-amphetamine was superior to both dextro-amphetamine and methylphenidate. In 20 cases, improvement was about the same for both the dextro and racemic forms; of these 20, side effects were absent for both in 10 patients; dextro-amphetamine showed fewer side effects in 3 patients, and racemic-amphetamine showed fewer side effects in 7 patients. In 20 other patients, dextro-amphetamine resulted in greater clinical improvement than racemic-amphetamine, while in 7 cases the reverse was true.

Adolescent↗
PubMed1992

In vivo microdialysis reveals a diminished amphetamine-induced DA response corresponding to behavioral sensitization produced by repeated amphetamine pretreatment.

In vivo microdialysis procedures were used to assess the effects of repeated amphetamine administration on behavior and regional brain DA dynamics in freely moving rats. Pretreatment with amphetamine (2.5 or 3.0 mg/kg) for 4-6 days did not alter baseline DA or its metabolites in caudate or accumbens 48 h or 6 days after the last injection. However, whereas this dosage regimen revealed a profound behavioral sensitization in response to challenge with amphetamine (2.5 mg/kg), including a more rapid onset and intensification of stereotypy, the DA response was significantly diminished in both brain regions. In addition, the ratio of caudate to accumbens DA, either before or after amphetamine challenge, was not altered by the pretreatment regimen. These results are consistent with our previous suggestion that there is a dissociation between the DA and behavioral responses to amphetamine, and therefore that other neurotransmitter systems and/or mechanisms significantly contribute to the amphetamine response profile. Furthermore, DA effects may represent only one, albeit critical, aspect in a time-dependent sequence of changes underlying stimulant sensitization.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1991

The effects of conditioning with amphetamine on the thermic effects of amphetamine and pentobarbital.

1. Rats were injected with amphetamine (1.5 mg/kg) in the presence of a distinctive set of environmental stimuli (CS1) and saline in the presence of a different set of environmental stimuli (CS2) on different days for a total of 10 amphetamine and 20 saline injections. 2. The hyperthermic effect of amphetamine first increased but then declined to levels seen during the very first drug administration. 3. Following the conditioning phase, half the rats were injected with amphetamine in CS1 and half in CS2. Although there was little thermic effect of amphetamine injected in CS1, there was pronounced hyperthermia following amphetamine in CS2. 4. Next, pentobarbital (30 mg/kg) was administered to half the rats in CS1 and half in CS2. The hypothermic effect of pentobarbital was attenuated in CS2.

Amphetamine↗
PubMed1976

Distribution and occurrence of amphetamine and p-hydroxyamphetamine in tissues of the rat after injection of d-amphetamine sulfate.

The distribution of amphetamine and the formation and distribution of its principal metabolite p-hydroxyamphetamine after the injection of relatively small amounts of d-amphetamine was examined in the rat. Amphetamine entered all organs readily and was rapidly eliminated. p-Hydroxyamphetamine was rapidly synthesised and it is suggested that substrate inhibition of hepatic hydroxylating enzymes occurs. In the brain, amphetamine was homogeneously distributed between the seven brain regions examined whereas p-hydroxyamphetamine was predominantly concentrated in the striatum.

Amphetamine↗
PubMed1991

Presynaptic dopaminergic neurotransmission mediates amphetamine-induced unconditioned but not amphetamine-conditioned locomotion and defecation in the rat.

A series of experiments were conducted to investigate the role of presynaptic dopamine (DA) and noradrenaline (NA) neurotransmission in stimulant-unconditioned and conditioned locomotion and defecation. (+)-Amphetamine (AMP, 1.5 mg/kg, s.c.) increased both locomotion and defecation in rats, and both of these effects were conditioned to environmental stimuli. Some groups of rats were treated with DSP4 (50 mg/kg, i.p.), a selective, long-lasting NA neurotoxin, given 7 days prior to conditioning with AMP. This treatment depleted forebrain NA to between 1% and 54% of control levels, depending on the brain region, but did not attenuate either AMP-unconditioned or conditioned locomotion. These results indicate that NA does not mediate either AMP unconditioned or conditioned locomotion. alpha-Methyl-para-tyrosine methyl ester (alpha MPT, 25-50 mg/kg, s.c.), a selective inhibitor of catecholamine synthesis given during conditioning with AMP, attenuated unconditioned AMP-induced locomotion and defecation but did not influence AMP-conditioned locomotion and defecation. Thus, alpha MPT blocked AMP-induced unconditioned locomotion, supporting the hypothesis that the locomotor and defecation stimulant effects of AMP are mediated by DA release. In spite of the attenuation of the direct effects of AMP, alpha MPT did not attenuate AMP-conditioned locomotion or defecation. It is concluded that AMP-induced release of dopamine is responsible for the unconditioned behavioral effects of amphetamine but not for the conditioning of amphetamine-induced locomotion and defecation.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1978

Stimulus properties of d-amphetamine as compared to l-amphetamine.

Rats were trained to discriminate between d-amphetamine and saline. The discriminable ED50 values for amphetamine isomers were calculated from dose--response curves and the potency ration was 4.9 Co-administration of the ED50s was shown to produce synergistic effects suggesting that the amphetamine isomers may share a common site of action.

Amphetamine↗
PubMed1978

Interactions of catecholaminergic receptor blockers with lethal doses of amphetamine or substituted amphetamines in mice.

Lethality to both isolated and aggregated mice was determined for graded i.p. doses of d-amphetamine, dl-4-methoxyamphetamine (PMA), dl-2,5-dimethoxyamphetamine (DMA), dl-2,5-dimethoxy-4-bromoamphetamine (DOB), dl-2,5-dimethoxy-4-methylamphetamine (DOM) and d1-3,4-methylenedioxyamphetamine (MDA). Haloperidol (2.0 mg/kg), propranolol (10 mg/kg) and phenoxybenzamine (30 mg/kg) were tested for ability to antagonize the lethal effects of amphetamine and its derivatives. Considerable protection against amphetamine lethality was produced by haloperidol in both isolated and aggregated mice and by phenoxybenzamine in isolated mice, but propranolol was ineffective. An equivalent degree of protection was not achieved by use of any of the three agents before PMA, DMA or DOB. Protection against DOM was achieved only with phenoxybenzamine and only for isolated mice. Extensive protection against MDA was supplied by both phenoxybenzamine and propranolol for either condition of housing. Despite close structural relationships between the toxicants, the antidotal effectiveness of the receptor-blocking agents seemed quite limited and specific, and did not support any generalizations.

Amphetamines↗
PubMed1975

Supersensitivity to d-amphetamine- and apomorphine-induced stereotyped behavior induced by chronic d-amphetamine administration.

Guinea pigs exhibit an increased sensitivity to both d-amphetamine- and apomorphine-induced stereotyped behavior following chronic pretreatment with d-amphetamine. This chronic agonist or "innervation" supersensitivity is believed to be a reflection of an increased sensitivity of dopamine receptor sites within the corpus striatum to dopaminergic agonists. The appearance of dyskinetic movement disorders in humans following the chronic use of levodopa or amphetamine may be a manifestation of similarly increased dopamine receptor site sensitivity within the striatum. It is suggested that the animal model of "innervation" supersensitivity may be useful in the investigation of these human movement disorders.

Animals↗
PubMed1976

Amantadine decreases d-amphetamine stimulation and increases d-amphetamine anorexia in mice.

Amantadine hydrochloride (Symmetrel), an antiviral, antiparkinson agent that is most frequently used clinically at oral doses of 2 to 3 mg/kg, significantly decreased d-amphetamine-induced CNS stimulation (motor activity) and simultaneously increased d-amphetamine-induced anorexia (milk intake) in mice. Amantadine did this at oral doses of 2.5 and 5 mg/kg, which alone had no effect on either motor activity or milk intake.

Amantadine↗
PubMed1992

Amphetamine or haloperidol 2 weeks earlier antagonized the plasma corticosterone response to amphetamine; evidence for the stressful/foreign nature of drugs.

We inquired whether a single exposure to amphetamine (AM) or haloperidol (HALO) could modify the plasma corticosterone (CORT) response to a second injection of AM 2 weeks later. Male rats were injected with 4 mg/kg d-AM sulfate and tested for water intake for 5 h before sacrifice. Overall, AM induced water intake but none of the pretreatments altered this effect. By contrast, preexposure to AM, HALO or its vehicle 2 weeks earlier prevented the elevation of plasma CORT obtained when AM was administered without pretreatment. A combined pretreatment of HALO or its vehicle with AM produced an even greater blockade of AM-induced CORT elevation. Manipulations which prevented AM-induced drinking reduced the effectiveness of AM pretreatment in attenuating AM-induced elevation in CORT, suggesting that the pretreatment may have been sensitizing the effectiveness of a coping response--drinking--in reducing the CORT effect. Our findings also indicate that a dopamine agonist (AM), a dopamine antagonist (HALO) and a nonspecific stressor (acidic vehicle) can all induce the same, long-lasting action on CORT. This strongly suggests that the effects of AM and HALO in this instance cannot be explained in terms of their pharmacological actions, which are opposite to one another, but instead relate to their properties as stressful/foreign agents to the organism.

Amphetamine↗
PubMed1977

Intracranial hemorrhage and amphetamine usage. Review of the effects of amphetamines on the central nervous system.

A 25-year-old man died after an intravenous injection of 100 mg of methedrine. Postmortem studies showed visceral congestion, lung edema, pericardial petechiae, centrolobular necrosis of the liver, and diffuse subarachnoid blood, intracranial vasculitis and cerebritis in the absence of aneurysms, arteriovenous malformations or chronic hypertension. A review of the English-language literature produced 3 other cases of fatal amphetamine-induced intracranial hemorrhage and seven nonfatal cases. Some were the result of overdose, others of hypersensitivity. Angiographic evidence suggests that such hemorrhages result from the development of fibrinoid necrosis and the formation of microaneurysms in the small intracerebral vessels.

Adult↗