Dopaminergic involvement in the mechanism of action of pentazocine
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Pentazocine
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Opiate
Dopaminergic pathways
Caudate nucleus
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Drug addiction is a brain disease with complex genetic, psychological and social factors. The dopaminergic system of the brain plays a central role in natural reward and motivation and is the main neural substrate for the actions of abusive drugs. The analysis of mice with mutations in their dopamine receptor genes has provided new information regarding the influence of individual dopamine receptors on drug actions. The use of genetic manipulation of dopamine receptors, and related intracellular signaling molecules, in mice will help to enhance our understanding of the molecular and cellular mechanisms underlying compulsive drug-seeking and drug-taking behaviors, reasons for relapse into drug addiction and persistent neuronal changes in response to repeated drug use. These studies will provide new insights for improved therapeutic strategies for the prevention and treatment of drug addiction.
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Tardive dyskinesia
Dopaminergic pathways
Tetrabenazine
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Pentazocine
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The synaptic deficit of brain dopaminergic activity involves a complex pattern of changes both at presynaptic and at postsynaptic level. The aged dopaminergic nuclei present a reduced number of dopamine terminals, a decreased ability to synthesize and reuptake dopamine and defective recognition sites both in terms of absolute number of D2 receptors and of transducing mechanisms linked to D1 receptors. These changes suggest that the dopaminergic system may be particularly sensitive during aging to environmental, iatrogenic and toxic factors, which may easily make the elderly develop symptoms of central dopamine deficiency.
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Opiate-adrenomimetic interaction was investigated by studying the effect of the adrenomimetic agent, ephedrine, on the analgesia produced by intravenous placebo and that produced by the predominantly kappa opiate agonist, pentazocine, in patients with dental postoperative pain. Ephedrine did not significantly affect the analgesia of intravenous placebo or of pentazocine. These results contrast with earlier studies demonstrating enhancement of opiate analgesia by other adrenomimetics. Further clinical studies are needed to delineate the specificity of opiate-adrenomimetic interaction.
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Racemate pentazocine was found to induce stereotyped behaviour (SB) in rats. Pretreatment with haloperidol and alpha-methyl-p-tyrosine significantly antagonised dl-pentazocine induced SB. This indicates that dl-pentazocine induces SB by releasing dopamine (DA) from the nigrostriatal and mesolimbic dopaminergic neurones with resultant activation of the postsynaptic striatal and mesolimbic D2 DA receptors by the released DA. However, pretreatment with naloxone failed to significantly modify dl-pentazocine induced SB indicating thereby that opioid mechanisms are not involved in the DA releasing action of dl-pentazocine. Our findings are explained on the basis of recent reports that the d-isomer of pentazocine releases DA by stimulating sigma receptors located on the nigrostriatal and mesolimbic dopaminergic neurones.
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Pentazocine
Pethidine
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Abstract Most opioid receptor agonists have abuse potential, and the rewarding effects of opioids can be reduced in the presence of pain. While each of the enantiomers of pentazocine has a differential pharmacologic profile, (±)‐pentazocine has been used clinically for the treatment of pain. However, little information is available regarding which components of pentazocine are associated with its rewarding effects, and whether the (±)‐pentazocine‐induced rewarding effects can be suppressed under pain. Therefore, the present study was performed to investigate the effects of pain on the acquisition of the rewarding effects of (±)‐pentazocine, and to examine the mechanism of the rewarding effects of (±)‐pentazocine using the conditioned place preference paradigm. (±)‐Pentazocine and (−)‐pentazocine, but not (+)‐pentazocine, produced significant rewarding effects. Even though the rewarding effects induced by (±)‐pentazocine were significantly suppressed under pain induced by formalin, accompanied by increase of preprodynorphin mRNA levels in the nucleus accumbens, a high dose of (±)‐pentazocine produced significant rewarding effects under pain. In the normal condition, (±)‐pentazocine‐induced rewarding effects were blocked by a low dose of naloxone, whereas the rewarding effects induced by high doses of pentazocine under pain were suppressed by naltrindole (a δ ‐opioid receptor antagonist). Interestingly, (±)‐pentazocine did not significantly affect dopamine levels in the nucleus accumbens. These findings suggest that the rewarding effects of (−)‐pentazocine may contribute to the abuse potential of (±)‐pentazocine through μ ‐ as well as δ ‐opioid receptors, without robust activation of the mesolimbic dopaminergic system. We also found that neural adaptations can reduce the abuse potential of (±)‐pentazocine under pain.
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Objective To review the neurochemical substrates of opiate reinforcement.Methods The related papers were consulted and the neurochemical mechanisms of opiate reinforcement were reviewed.Results and conclusions Dopamine and non-dopamine substrates,including opiate,Gamma-aminobutyric acid(GABA),glutamate and serotonin are well involved in the opiate reinforcement.The activities of dopamine and GABA ergic neurons in the ventral tegmental area and the nucleus accumbens play critical roles.
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