Neurochemical effects of cocaine following acute and repeated injection

Taylor, Dorothy; Ho, Beng T.

doi:10.1002/jnr.490030203

Cited by 105 publications

(23 citation statements)

References 17 publications

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“…Hyperactivity is one of the striking effects of cocaine in doses that generate moderate plasma levels, on the order of 2 M (Taylor and Ho, 1977;Benowitz, 1993). Blockade of this effect by a modified BChE is consistent with other evidence that sequestration or metabolic conversion of circulating cocaine lessens behavioral effects in rodents (Baird et al, 2000;Mets et al, 1998).…”

Section: Discussionsupporting

confidence: 84%

Re-engineering Butyrylcholinesterase as a Cocaine Hydrolase

et al. 2002

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To address the problem of acute cocaine overdose, we undertook molecular engineering of butyrylcholinesterase (BChE) as a cocaine hydrolase so that modest doses could be used to accelerate metabolic clearance of this drug. Molecular modeling of BChE complexed with cocaine suggested that the inefficient hydrolysis (k cat ϭ 4 min Ϫ1 ) involves a rotation toward the catalytic triad, hindered by Tyr332. To eliminate rotational hindrance and retain substrate affinity, we introduced two amino acid substitutions (Ala328Trp/Tyr332Ala). The resulting mutant BChE reduced cocaine burden in tissues, accelerated plasma clearance by 20-fold, and prevented cocaine-induced hyperactivity in mice. The enzyme's kinetic properties (k cat ϭ 154 min Ϫ1

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Section: Discussionsupporting

confidence: 84%

Re-engineering Butyrylcholinesterase as a Cocaine Hydrolase

et al. 2002

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“…In fact, even though antiserotoninergic properties have been attributed to co caine [18][19][20][21], some authors suggested that cocaine di rectly activates scrotoninergic receptors at the post-synaptic level [20],…”

Section: Discussionmentioning

confidence: 99%

Diurnal Variations in Plasma ACTH, Cortisol and Beta-Endorphin Levels in Cocaine Addicts

et al. 1992

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In order to establish possible alterations in the hypothalamic pituitary-adrenal axis and in ACTH-related opioids in cocaine addicts, plasma ACTH, cortisol and β-endorphin levels were measured throughout the day in 9 cocaine addicts [age: 27 ± 5 years (mean ± SE); weight: 72 ± 6.1 kg, duration of cocaine addiction: at least 2 years] on the day of their admission to a recovery community for drug abusers (first test) and after 15 days of abstinence (second test). Nine normal controls (age: 28 + 6 years; weight: 73 ± 3.2 kg) were tested only once in a similar manner. Blood samples were taken at 06.00, 08.00, 10.00, 12.00, 18.00 and 20.00 h and served for hormonal assays. Urine samples were taken from cocaine addicts at 08.00 h on the experimental day and on the following day. Results of both urine assays were positive for cocaine catabolites, indicating cocaine administration during the day before the experimental test. From the day of their admission in the community (1st experimental day), the patients were forbidden to use cocaine. For 4 days after admission, they were treated with symptomatics to attenuate withdrawal symptoms. Thereafter, the patients underwent a washout period of pharmacological treatments for 10 days before being retested (second test). Urine samples taken at 08.00 h on this second experimental day and on the next day were negative for the presence of drug catabolites. During the first test, cocaine addicts showed higher plasma ACTH, cortisol and β-endorphin levels than normal controls at all examined time points. However, maximal and minimal secretory periods and the general temporal structure of all hormonal secretions coincided in the two groups. No significant quantitative or qualitative differences in the secretory pattern of ACTH, cortisol and β-endorphin were observed between normal controls and cocaine addicts as tested after 15 days of abstinence. The results fail to show alterations in the diurnal hormonal secretory rhythms of ACTH, cortisol and β-endorphin in cocaine addicts. The enhancement in the overall ACTH, cortisol and β-endorphin secretions in cocaine addicts during the first, but not the second test, may be supposed to depend on recent cocaine self-administration.

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“…Some authors reported that tissular levels of DA and its metabolites measured in the striatum were not affected in the short term after multiple injections of cocaine (Hanson et al, 1987;Taylor and Ho, 1977). On the other hand, Karoum et al (1990) reported a decrease in DOPAC without change in DA and HVA in the striatum, while in the nucleus accumbens, both DA and DOPAC were decreased immediately after chronic cocaine administration.…”

Section: Discussionmentioning

confidence: 92%

Invariance of the density of dopamine uptake sites and dopamine metabolism in the rat brain after a chronic treatment with the dopamine uptake inhibitor GBR 12783

Boulay

Leroux-Nicollet

Duterte-Boucher

et al. 1994

J. Neural Transmission

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Summary.A chronic treatment (10 mg/kg, twice daily during 9 days) with the dopamine uptake inhibitor GBR 12783 was performed in rats at a dose increasing their locomotor activity.Forty-eight hours after the last administration, animals were sacrificed and 3H mazindol binding was performed on brain slices. Autoradiographic analysis revealed no change in this binding relatively to control animals in regions with high dopamine contents: striatum, nucleus accumbens, olfactory tubercle, substantia nigra and ventral tegmentum area. The treatment did not either modify the levels of dopamine (DA) and metabolites (HVA, DOPAC) both in the striatum and the nucleus accumbens. Thus, early after the end of the treatment, the chronic blockade of the dopamine uptake complex regulates neither the dopamine uptake complex nor the dopamine metabolism.

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Neurochemical effects of cocaine following acute and repeated injection

Cited by 105 publications

References 17 publications

Re-engineering Butyrylcholinesterase as a Cocaine Hydrolase

Re-engineering Butyrylcholinesterase as a Cocaine Hydrolase

Diurnal Variations in Plasma ACTH, Cortisol and Beta-Endorphin Levels in Cocaine Addicts

Invariance of the density of dopamine uptake sites and dopamine metabolism in the rat brain after a chronic treatment with the dopamine uptake inhibitor GBR 12783

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