Extracellular dopamine in rat striatum following uptake inhibition by cocaine, nomifensine and benztropine

Church, William H.; Justice, Joseph B.; Byrd, Larry D.

doi:10.1016/0014-2999(87)90592-9

Cited by 214 publications

(89 citation statements)

References 3 publications

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“…The effects of GBR-12909 or cocaine treatment on GP firing rate and pattern, prevented and reversed by DA receptor antagonists, are consistent with the marked increases in DA overflow caused by these drugs at or around the presently tested doses (Church et al 1987;Baumann et al 1994;Fink-Jensen et al 1994;Engberg et al 1997). However, our observations indicate that other transmitter systems are involved in these electrophysiological effects.…”

Section: Discussioncontrasting

confidence: 43%

Cocaine or Selective Block of Dopamine Transporters Influences Multisecond Oscillations in Firing Rate in the Globus Pallidus

Ruskin

Bergstrom

Baek

et al. 2001

Neuropsychopharmacology

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Previous studies have shown that direct-acting dopamine agonists modulate the multisecond oscillations which are present in globus pallidus spike trains in vivo inPeriodicities in brain electrical activity occur in many nuclei and in many frequency ranges, and have been described in the electroencephalogram, in field potentials, and in the spiking activity of single neurons. Much of the attention that brain periodicities have received has been directed to the range of frequencies from 1 Hz (the slow end of the delta rhythm) up to roughly 60 Hz (the fast end of the gamma rhythm). However, recent studies have demonstrated that much slower periodic oscillations are commonly present in the spike trains of tonically firing neurons in the basal ganglia. The firing rates of a majority of neurons in the globus pallidus (GP), the subthalamic nucleus, the substantia nigra pars reticulata and the entopeduncular nucleus oscillate in vivo with slow periods, most often in the range of 10-60 s (0.1-0.017 Hz) (Ruskin et al. 1999a;Ruskin et al. 1999c;Wichmann et al. 1999;Allers et al. 2000). These multisecond periodicities in tonic activity are present in awake rats, but are markedly attenuated by general anesthesia (Ruskin et al. 1999a).One of the most striking characteristics of these slow oscillations is their strong modulation by dopamine

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Section: Discussioncontrasting

confidence: 43%

Cocaine or Selective Block of Dopamine Transporters Influences Multisecond Oscillations in Firing Rate in the Globus Pallidus

Ruskin

Bergstrom

Baek

et al. 2001

Neuropsychopharmacology

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“…At doses similar to those employed here, the effects of amphetamine, cocaine, nomensifine and GBR 12909 on extracellular DA were reported to peak between 20 and 40 min after treatment and to remain elevated at 60 min, with concentrations ranging between 50% and 80% of the maximal levels (Church et al, 1987;Westerink et al, 1987;Carboni et al, 1989;Callaway et al, 1989;Pettit et al, 1990; Kuczenski & Segal, 1992). Time course studies on the effects of 5 mg kg-' of amphetamine on striatal 3MT and DOPAC demonstrated maximal effects of the drug at 60 min.…”

Section: Discussionmentioning

confidence: 99%

Regional effects of amphetamine, cocaine, nomifensine and GBR 12909 on the dynamics of dopamine release and metabolism in the rat brain

Karoum

Chrapusta

Brinjak

et al. 1994

British J Pharmacology

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1 The effects of single-dose regimens of amphetamine, cocaine, nomifensine and GBR 12909 on the dynamics of dopamine (DA) release and metabolism were evaluated in the frontal cortex, hypothalamus, nucleus accumbens and striatum. The regimens selected are known to produce substantial behavioural effects. 2 3-Methoxytyramine (3MT) and 3,4-dihydroxyphenylacetic acid (DOPAC) rates of formation were used to assess DA metabolism by catechol-O-methyltransferase and monoamine oxidase respectively. The rate of formation of 3MT was used as an index of synaptic DA. The ratio and sum, respectively, of 3MT and DOPAC rates of formation were used to assess DA reuptake inhibition and turnover. 3 The effects of amphetamine on 3MT production and DOPAC steady-state levels were similar in all regions, suggesting similar pharmacodynamic actions. Amphetamine increased 3MT formation and steady-state levels, and reduced DOPAC steady-state levels. DOPAC formation was significantly reduced only in the nucleus accumbens and striatum. Total DA turnover remained unchanged except in the nucleus accumbens. Apparently, the amphetamine-induced increase in DA release occurred at the expense of intraneuronal DA metabolism and did not require stimulation of synthesis. 4 Nomifensine elevated 3MT formation in all regions. A similar effect was produced by cocaine except in the nucleus accumbens. GBR 12909 elevated 3MT production only in the hypothalamus, the striatum and the nucleus accumbens. 5 Cocaine selectively reduced DOPAC formation in the frontal cortex. Nomifensine increased and reduced, respectively, DOPAC formation in striatum and hypothalamus. GBR 12909 elevated DOPAC formation in all regions except the cortex, where pargyline did not reduce DOPAC levels in GBR 12909-treated rats. 6 Ratios and sum of 3MT and DOPAC rates of formation also exhibited wide regional variations for each drug. In contrast to the other drugs, the ratio was not increased after GBR 12909. Apparently, the DA uptake properties of this drug are poorly related to its in vivo effects on the ratio of 3MT production to that of DOPAC, which should increase when DA reuptake is inhibited. 7 Total DA turnover was increased by GBR 12909 in the hypothalamus, nucleus accumbens and striatum, while cocaine and nomifensine increased it only in the nucleus accumbens and striatum respectively. 8 It is concluded that: (a) 3MT and DOPAC rates of formation provide better indices of DA release and metabolism than do their steady-state concentrations. (b) Some effects of DA uptake blockers on DA transmission, especially those of nomifensine and cocaine, may be attributed to increased DA release. (c) Patterns of regional effects of psychostimulants on the dynamics of DA release and metabolism may be better biochemical correlates of stimulant-induced behaviours than would changes in any single region.

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“…Probes were tested in vitro to determine the suitability of probe efficiency and performance before and after in vivo experiments. Microbore HPLC and electrochemical detection quantitated extracellular levels of dopamine according to well-established analytical procedures (Church et al, 1987;Skirboll et al, 1990;Parsons and Justice, 1993).…”

Section: In Vivo Microdialysis Methodsmentioning

confidence: 99%

Olanzapine-Induced Suppression of Cocaine Self-Administration in Rhesus Monkeys

Howell

Wilcox

Lindsey

et al. 2005

Neuropsychopharmacol

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The neuropharmacological profile of the atypical antipsychotic, olanzapine, is consistent with a potentially useful medication for cocaine abuse. The present study utilized an i.v. drug self-administration paradigm in nonhuman primates to obtain definitive evidence regarding the effectiveness of olanzapine to modulate the reinforcing effects of cocaine. The effects of olanzapine were compared directly to those of the neuroleptic, haloperidol. Rhesus monkeys (n ¼ 7) were trained to self-administer cocaine (0.03-0.3 mg/kg/injection) under a second-order, fixed-interval 600-s schedule with fixed ratio 20 components. Experimental sessions comprised five consecutive fixed intervals, each followed by a 1-min timeout. In drug-interaction experiments, a single dose of olanzapine (0.03-0.3 mg/kg) or haloperidol (0.01-0.03 mg/kg) was administered i.v. 15 min presession for at least three consecutive sessions. In drug-substitution experiments, different doses of olanzapine (0.01-0.1 mg/kg/injection) were substituted for cocaine until responding stabilized. Olanzapine caused doserelated decreases in cocaine self-administration at pretreatment doses that had no overt behavioral effects indicative of sedation. A dose of 0.1 mg/kg eliminated cocaine self-administration in all subjects. In contrast, doses of haloperidol that suppressed cocaine selfadministration induced marked sedation and catalepsy. Olanzapine failed to maintain self-administration behavior above saline extinction levels over a range of unit doses. In vivo microdialysis experiments in a second group of awake rhesus monkeys (n ¼ 3) confirmed previous reports in rodents that olanzapine effectively increases extracellular dopamine in ventral striatum. The dose of olanzapine that markedly suppressed cocaine self-administration behavior increased dopamine to approximately 190% of control values. Lastly, pretreatment with fluoxetine had no systematic effect on olanzapine-induced increases in striatal dopamine. The results indicate that olanzapine can effectively suppress cocaine self-administration behavior in nonhuman primates at doses that enhance dopamine release but do not maintain drug self-administration.

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Extracellular dopamine in rat striatum following uptake inhibition by cocaine, nomifensine and benztropine

Cited by 214 publications

References 3 publications

Cocaine or Selective Block of Dopamine Transporters Influences Multisecond Oscillations in Firing Rate in the Globus Pallidus

Cocaine or Selective Block of Dopamine Transporters Influences Multisecond Oscillations in Firing Rate in the Globus Pallidus

Regional effects of amphetamine, cocaine, nomifensine and GBR 12909 on the dynamics of dopamine release and metabolism in the rat brain

Olanzapine-Induced Suppression of Cocaine Self-Administration in Rhesus Monkeys

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