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Zozulya, A. A.; Кост, Н. В.; Sokolov, O. Yu.; Gabaeva, M. V.; Гривенников, И. А.; Andreeva, L. N.; Zolotarev, Yu. A.; Ivanov, S V; Andryushchenko, A. V.; Myasoedov, N. F.; Ab, Smulevich

doi:10.1023/a:1017979514274

Cited by 13 publications

(3 citation statements)

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“…We previously demonstrated that the anxiolytic action of selank can be explained by its ability to inhibit enkephalin-degrading enzymes [2,3]. In addition to the agonists and antagonists of opioid receptors, the inhibitors of enkephalinases are known to modulate the dopaminergic system [11,13].…”

Section: Resultsmentioning

confidence: 99%

Naloxone-blocked depriming effect of anxiolytic selank on apomorphine-induced behavioral manifestations of hyperfunction of dopamine system

et al. 2006

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Peptide anxiolytic selank (Thr-Lys-Pro-Arg-Pro-Gly-Pro) applied intraperitoneally in doses of 0.01, 0.1, 1.0, and 10.0 mg/kg to mice reduces behavioral manifestations of dopaminergic system induced by apomorphine in the verticalization test. This effect was comparable to that of atypical antipsychotic olanzapine in near-therapeutic doses (0.1 and 1.0 mg/kg, intraperitoneally) and was blocked with nonselective opioid receptor antagonist naloxone (10 mg/kg, intraperitoneally). Radioreceptor assay showed that selank did not displace nonselective D2-dopamine receptor antagonist (3)H-spiperone (EC50>100 microM) and delta- and micro-opioid receptor ligand 3H-DADLE (EC50>40 microM) from specific binding sites on rat brain membranes. It is hypothesized that the revealed behavioral effect of selank is mediated by its modulating effect on the endogenous opioid system and specifically, by its effect on activity of enkephalin-degrading enzymes.

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Section: Resultsmentioning

confidence: 99%

Naloxone-blocked depriming effect of anxiolytic selank on apomorphine-induced behavioral manifestations of hyperfunction of dopamine system

et al. 2006

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“…There appears to be an intricate balance between the memoryenhancing and anxiety-provoking effects of CCK and the amnesic and anxiolytic effects of opioid peptides [46]. A vast amount of data also indicates an interaction between opioid receptors and CCK A and CCK B in the modulation of stress-induced analgesia with antagonistic effects that may be dependent on the anxiety state of the animal [47].…”

Section: The Brain and Interconnecting Circuitriesmentioning

confidence: 99%

“…Inhibition of enkephalinase, which increases enkephalin availability at the synapse, as well as certain CCK antagonists, have antidepressant effects, indicating a possible interaction between these two peptides in mood regulation [47]. While CCK induces relatively protracted behavioral disturbances in both animal and human subjects following stressor applications, opioid receptor activation may change the course of psychopathology.…”

Section: Clinical Translation and Therapeutic Perspectivesmentioning

confidence: 99%

Neuropharmacology of Stress-Induced Mucosal Inflammation: Implications for Inflammatory Bowel Disease and Irritable Bowel Syndrome

Santos

Alonso²,

Vicario³

et al. 2008

CMM

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Inflammatory bowel disease (IBD) and the irritable bowel syndrome (IBS) are common causes of medical consultation and the most frequent diagnosis raised by gastroenterologists. Recent years have witnessed considerable advances in the understanding of the mechanisms involved in the initiation and perpetuation of these chronic and recurrent disorders. However, particularly in IBS, the success of the "bench-to the-bedside medicine" has been rather poor since many affected individuals still experience significant bother and negative impact in their quality of life despite growing investigative and sanitary costs. Besides IBD, several subgroups of IBS patients have been lately identified as carriers of mucosal inflammation throughout the gut. Although multifactorial, life stress has emerged as a critical factor for mucosal inflammation in these conditions. Due to the clinical and biological heterogeneity of IBD and IBS patients, the simplistic hypothesis of a stress-related stepwise progression of gut inflammation may be useful to gain operative knowledge and render better and specific diagnostic markers and improved therapeutic options. Therefore, in this review, we have consciously admitted the possibility of linear evolution of gut inflammation, from the mucosa to the serosa, and assumed a bidirectional progression, from physiological to pathological inflammation. Thus, we have outlined the stress neurocircuitry implicated in the regulation of gut inflammation and the participating pathways (mechanisms, receptors and molecules) and provided with both, evidence and a theoretical-based approach to present and potential drugs that, alone or in combination, might help to prevent, control or regress the stress-induced inflammatory process at different stages.

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Sedative‐Hypnotic Agents That Impact Gamma‐Aminobutyric Acid Receptors: Focus on Flunitrazepam, Gamma‐Hydroxybutyric Acid, Phenibut, and Selank

Doyno

White

2021

The Journal of Clinical Pharma

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There are many nonopioid central nervous system depressant substances that share a gamma‐aminobutyric acid (GABA) receptor–related mechanism of action. These sedatives‐hypnotics can be indicated to treat anxiety, seizures, depression, and insomnia but are also used as substances of abuse and used to facilitate sexual assault. Barbiturates, methaqualone, and glutethimide were among the first type A GABA receptor–mediated sedative‐hypnotics. Their clinical use was limited for most indications by serious adverse events and strong abuse potential but continue to be used illicitly around the world. The benzodiazepines supplanted barbiturates for most indications because they were less likely to cause severe adverse events in monotherapy. Flunitrazepam is a newer benzodiazepine that is preferentially used recreationally and to facilitate sexual assault. Flunitrazepam has greater potency and higher affinity for the type A GABA receptor than most benzodiazepines. Gamma‐hydroxybutyric acid is sought illicitly for its hypnotic, euphoric and anabolic effects as well as to facilitate sexual assault. When any of these GABAergic drugs are used in high doses or with other sedative hypnotic agents, respiratory depression, coma, and death have occurred. Chronic use of these GABAergic drugs can lead to significant withdrawal syndromes. Phenibut and selank are poorly studied Russian drugs with GABAergic mechanisms that are inexplicably sold to US consumers as dietary supplements. Poison control center calls regarding phenibut have increased substantially over the past 5 years. Desired euphoriant effects account for the recreational and illicit use of many GABA‐modulating agents. However, illicit use can lead to significant toxicities related to abuse, dependence, and subsequent withdrawal syndromes. Significant evaluation of developing agents with GABA properties should be conducted to determine abuse potential before public access ensues.

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Cited by 13 publications

References 0 publications

Naloxone-blocked depriming effect of anxiolytic selank on apomorphine-induced behavioral manifestations of hyperfunction of dopamine system

Naloxone-blocked depriming effect of anxiolytic selank on apomorphine-induced behavioral manifestations of hyperfunction of dopamine system

Neuropharmacology of Stress-Induced Mucosal Inflammation: Implications for Inflammatory Bowel Disease and Irritable Bowel Syndrome

Sedative‐Hypnotic Agents That Impact Gamma‐Aminobutyric Acid Receptors: Focus on Flunitrazepam, Gamma‐Hydroxybutyric Acid, Phenibut, and Selank

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