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In vertebrates, opiates modulate nociception and opioid receptor antagonists, e.g. naloxone and CTOP, reverse this effect.
Several experiments have shown that opioid receptor antagonists applied directly to the brain block the antinociceptive effects of NO, but these drugs have no effect when injected into the spinal cord.
These effects were reversed with the opioid receptor antagonists naloxone and CTOP, leading the authors to conclude that thermonocifensive behaviour in C. elegans was modulated by opioids.
Pharmacological treatments using selective serotonin reuptake inhibitors (SSRIs), mood stabilizers and opioid receptor antagonists, and other antidepressants along with cognitive behavioral therapy, have yielded positive results.
Opioid receptor antagonists are regarded as practical in lessening urge-related symptoms, which is a central part of impulse control disorders; for this reason, they are used in treatment of substance abuse.
The effects of the drug can be suppressed by the CB receptor antagonist rimonabant (SR141716A) as well as opioid receptor antagonists (opioid blockers) naloxone and naloxonazine.
Biological models explaining the origins of kleptomania have been based mostly on pharmacotherapy treatment studies that used selective serotonin reuptake inhibitors (SSRIs), mood stabilizers, and opioid receptor antagonists.
The toxic effects mediated by the metabolites cannot be countered with opioid receptor antagonists such as naloxone or naltrexone and are probably primarily due to norpethidine's anticholinergic activity probably due to its structural similarity to atropine, though its pharmacology has not been thoroughly explored.