Structural requirements for cocaine congeners to interact with dopamine and serotonin uptake sites in mouse brain and to induce stereotyped behavior

Reith, Maarten E. A.; Meisler, Bernard E.; Sershen, Henry; Lajtha, Ábel

doi:10.1016/0006-2952(86)90148-6

Cited by 298 publications

(189 citation statements)

References 19 publications

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“…A similar involvement of the s 1 receptor was previously observed for the acquisition of cocaine-induced appetitive properties (Romieu et al, 2000. Conceivably, the abused drug seems to misappropriate a natural neuromodulatory system to acquire and amplify its effects, from the subtlest ones, the memory trace (this study), to the most drastic, including hyperlocomotion, convulsions, and lethality (Reith et al, 1986;Menkel et al, 1991;Ujike et al, 1992;Ritz and George, 1993). As such, the receptor appeared as a very important component mediating the neuroplastic changes induced by cocaine.…”

Section: The R 1 Receptor and Cocaine-induced Stdsupporting

confidence: 81%

“…Cocaine self-administration and relapse are also mediated by glutamate neurotransmission in the nucleus accumbens (Cornish et al, 1999;Park et al, 2002). In addition, cocaine interacts with the s 1 receptor at a similar dose range as observed for the dopamine transporter (Sharkey et al, 1988), and the s 1 receptor is implicated in several of cocaine's effects such as locomotor stimulation, sensitization, acquisition and reactivation of conditioned place preference, convulsions, and lethality (Reith et al, 1986;Menkel et al, 1991;Ujike et al, 1992;Ritz and George, 1993;Romieu et al, 2000Romieu et al, , 2002Romieu et al, , 2003Romieu et al, , 2004; for a review, see Maurice et al, 2002). This intracellular protein sharing some characteristics of neuromodulatory receptors is also a target for several neuroactive steroids, including pregnenolone, dehydroepiandrosterone (3b-hydroxy-5a-androsten-17-one (DHEA)), their sulfate esters, or progesterone, but not pregnanolone or allopregnanolone (Su et al, 1988;Monnet et al, 1995;Bergeron et al, 1996;Maurice et al, 1999).…”

Section: Introductionmentioning

confidence: 96%

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σ1 Receptor Ligands and Related Neuroactive Steroids Interfere with the Cocaine-Induced State of Memory

Romieu

Lucas

Maurice

2005

Neuropsychopharmacol

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The present series of experiments examined the involvement of the s 1 receptor and related neuroactive steroids in the memory state induced by a very low dose of cocaine. Using a modified passive avoidance procedure in mice, we examined whether cocaine induces state-dependent (StD) learning. Animals trained and tested with saline or the same dose of cocaine (0.1 or 0.3 mg/kg) showed correct retention, measured using two independent parameters: the retention latency and a ratio between the retention latency and the last training latency. Animals trained with cocaine (0.1 mg/kg) and tested with saline or cocaine (0.03, 0.3 mg/kg), or trained with saline and tested with cocaine, showed altered retention parameters, demonstrating that StD occurred. Therefore, cocaine administered before training produced a chemical state used as an endogenous cue to insure optimal retention. Since s 1 receptor activation is an important event during the acquisition of cocaine reward, we tested several s 1 ligands and related neurosteroids. The s 1 agonist igmesine or antagonist BD1047 failed to produce StD, but modified the cocaine state. Among neuroactive steroids, pregnanolone and allopregnanolone, positive modulators of the g-aminobutyric acid type A (GABA A ) receptor, produced StD. However, steroids also acting as s 1 agonists, dehydroepiandrosterone (3b-hydroxy-5a-androsten-17-one (DHEA)), pregnenolone, or antagonist, progesterone, failed to induce StD but modified the cocaine state. Furthermore, optimal retention was observed with mice trained with (igmesine or DHEA) + cocaine and tested with a higher dose of cocaine, or with mice trained with (BD1047 or progesterone) + cocaine and tested with vehicle. This study demonstrated that: (i) low doses of cocaine induce a chemical state/memory trace sustaining StD; (ii) modulation of the s 1 receptor activation, although insufficient to provoke StD, modulates the cocaine state; (iii) neuroactive steroids exert a unique role in state-dependent vs state-independent learning, via GABA A or s 1 receptor modulation, and are able to affect the cocaine-induced mnesic trace at low brain concentrations.

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Section: The R 1 Receptor and Cocaine-induced Stdsupporting

confidence: 81%

Section: Introductionmentioning

confidence: 96%

σ1 Receptor Ligands and Related Neuroactive Steroids Interfere with the Cocaine-Induced State of Memory

Romieu

Lucas

Maurice

2005

Neuropsychopharmacol

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“…However, the molecular events through which dopamine concentrations are increased in the NA markedly differ between the various drugs of abuse. Stimulants like amphetamine or cocaine increase dopamine release in the NA either directly or by blockade of the dopamine transporter (Reith et al, 1986;Pierce and Kalivas, 1997). Nicotine increases the firing rate of the dopaminergic neurons in the VTA via nicotinic acetylcholine receptors located on the cell bodies of these neurons (Mereu et al, 1987).…”

Section: Brain Metabolic Ethanol Effectsmentioning

confidence: 99%

Acute Alcohol Effects on Neuronal and Attentional Processing: Striatal Reward System and Inhibitory Sensory Interactions under Acute Ethanol Challenge

Schreckenberger

Amberg

Scheurich

et al. 2004

Neuropsychopharmacol

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The acute influence of ethanol on cerebral activity induces complex psycho-physiological effects that are considerably more pronounced during acute ethanol influx than during maximal blood alcohol concentration (elimination phase). Despite the psychiatric and forensic relevance of these different ethanol effects, the underlying neuronal mechanisms are still unclear. In total, 20 male healthy volunteers were investigated each with three different experimental conditions in a randomized order using an intravenous ethanol challenge (40 g bolus infusion): during influx phase, elimination phase, and under placebo condition. During and after the ethanol (or placebo) infusion, neuropsychological testing of divided attention for visual and auditory stimuli was performed with subsequent 18-FDG PET acquisition. The PET data were analysed using SPM99. Ethanol influx and elimination phase showed focal activations in the bilateral striatum and frontal cortex and deactivations in the occipital cortex. The comparison of influx phase vs elimination phase revealed activations in the anterior cingulate and right prefrontal cortex, relevant deactivations were found in the left superior temporal cortex including Wernicke's area. Neuropsychological testing showed an attentional impairment under ethanol influx compared to ethanol elimination and placebo with an inverse correlation of the attentional performance for auditory stimuli to occipital activity and for visual stimuli to the left temporal (including auditory) cortex. Acute ethanol administration in healthy volunteers stimulates those striatal regions that are considered to have a particular relevance for alcohol craving ('reward system'). Modality specific reciprocal inhibition of sensory cortex activity seems to be relevant for attentional performance during acute alcohol impact.

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“…Cocaine is a nonselective inhibitor of monoamine transporters, including dopamine, serotonin, and norepinephrine, and also binds to sodium channels (Kennedy and Hanbauer, 1983;Madras et al, 1989;Reith et al, 1986;Schoemaker et al, 1985). However, the behavioral effects of cocaine have been attributed primarily to its actions at the dopamine transporter (DAT) (Ritz et al, 1987).…”

Section: Introductionmentioning

confidence: 99%

Faster onset and dopamine transporter selectivity predict stimulant and reinforcing effects of cocaine analogs in squirrel monkeys

Kimmel

O’Connor

Carroll

et al. 2007

Pharmacology Biochemistry and Behavior

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Although the behavioral-stimulant and reinforcing effects of cocaine and related psychomotor stimulants have been attributed to their actions at the dopamine transporter (DAT), the reinforcing effectiveness of these compounds varies. The properties that confer these differences are important considerations when developing agonist pharmacotherapies for the treatment of stimulant abuse. The present studies focused on the time course of action and pharmacological specificity of six 3-phenyltropane analogs of cocaine (RTI-112, RTI-126, RTI-150, RTI-171, RTI-177, and RTI-336) by observing their behavioral-stimulant, neurochemical, and reinforcing effects in squirrel monkeys. The faster-onset analogs (RTI-126, RTI-150, and RTI-336), and one of the slower-onset DAT selective analogs (RTI-177 and RTI-171) produced behavioral-stimulant effects, while the sloweronset nonselective analog RTI-112 did not. The time to the peak behavioral-stimulant effect and the peak caudate dopamine levels was strongly correlated, but the area under the curve of the time course of behavioral-stimulant effect and dopamine levels was not correlated. These results suggest that the rate of onset plays a more important role than duration of action in the stimulant effect of these analogs. In addition, the slower-onset nonselective analog (RTI-112) clearly did not exhibit any reinforcing effects while the faster-onset nonselective (RTI-126) and all the DAT-selective analogs showed robust reinforcing effects (RTI-150, and RTI-177) or showed trends towards reinforcing effects (RTI-336 and RTI-171). Hence, there was a general trend for compounds that had a faster onset and/or DAT selectivity to produce significant behavioral-stimulant and reinforcing effects.

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Structural requirements for cocaine congeners to interact with dopamine and serotonin uptake sites in mouse brain and to induce stereotyped behavior

Cited by 298 publications

References 19 publications

σ1 Receptor Ligands and Related Neuroactive Steroids Interfere with the Cocaine-Induced State of Memory

σ1 Receptor Ligands and Related Neuroactive Steroids Interfere with the Cocaine-Induced State of Memory

Acute Alcohol Effects on Neuronal and Attentional Processing: Striatal Reward System and Inhibitory Sensory Interactions under Acute Ethanol Challenge

Faster onset and dopamine transporter selectivity predict stimulant and reinforcing effects of cocaine analogs in squirrel monkeys

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