Nitric oxide modulates tapentadol antinociceptive tolerance and physical dependence

Wolińska, Renata; Kleczkowska, Patrycja; Corde-Skurska, Anna de; Poznański, Piotr; Sacharczuk, Mariusz; Mika, Joanna; Bujalska‐Zadrożny, Magdalena

doi:10.1016/j.ejphar.2021.174245

Cited by 7 publications

(6 citation statements)

References 55 publications

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“…The exact mechanisms by which Botox relieves CM and NP remains unknown [ 239 , 240 ]. Furthermore, engineering chimeric compounds targeting more moieties responsible for pain sensation are under extensive study [ 241 , 242 , 243 , 244 , 245 ]. In addition, the contribution of sex and stress hormones such as estrogen and cortisol to pain thresholds and pain sensitivity must be taken into consideration, and may not only help personalized pain management but also elucidate unidentified targets [ 246 ].…”

Section: Discussionmentioning

confidence: 99%

Exploring Novel Therapeutic Targets in the Common Pathogenic Factors in Migraine and Neuropathic Pain

Tajti

Delia

Csáti

et al. 2023

IJMS

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Migraine and neuropathic pain (NP) are both painful, disabling, chronic conditions which exhibit some symptom similarities and are thus considered to share a common etiology. The calcitonin gene-related peptide (CGRP) has gained credit as a target for migraine management; nevertheless, the efficacy and the applicability of CGRP modifiers warrant the search for more effective therapeutic targets for pain management. This scoping review focuses on human studies of common pathogenic factors in migraine and NP, with reference to available preclinical evidence to explore potential novel therapeutic targets. CGRP inhibitors and monoclonal antibodies alleviate inflammation in the meninges; targeting transient receptor potential (TRP) ion channels may help prevent the release of nociceptive substances, and modifying the endocannabinoid system may open a path toward discovery of novel analgesics. There may exist a potential target in the tryptophan-kynurenine (KYN) metabolic system, which is closely linked to glutamate-induced hyperexcitability; alleviating neuroinflammation may complement a pain-relieving armamentarium, and modifying microglial excitation, which is observed in both conditions, may be a possible approach. Those are several potential analgesic targets which deserve to be explored in search of novel analgesics; however, much evidence remains missing. This review highlights the need for more studies on CGRP modifiers for subtypes, the discovery of TRP and endocannabinoid modulators, knowledge of the status of KYN metabolites, the consensus on cytokines and sampling, and biomarkers for microglial function, in search of innovative pain management methods for migraine and NP.

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Section: Discussionmentioning

confidence: 99%

Exploring Novel Therapeutic Targets in the Common Pathogenic Factors in Migraine and Neuropathic Pain

Tajti

Delia

Csáti

et al. 2023

IJMS

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“…67 NOS inhibitors can attenuate the development of physical dependence and tolerance to abusive drugs. [68][69][70] T A B L E 1 Effects of the expression of behavioural sensitization to the mephedrone-induced central activity on the protein expression in mice hippocampus and prefrontal cortex. Although the detailed molecular analyses were not within the range of the present study, we guess that the mechanism by which NOS inhibitors attenuated response to the mephedrone challenge dose in our experiment was at least partially associated with modulation of the dopaminergic and glutamatergic neurotransmissions.…”

Section: Discussionmentioning

confidence: 99%

“…self‐administration, 65 drug discrimination 66 or conditioned place preference) 67 . NOS inhibitors can attenuate the development of physical dependence and tolerance to abusive drugs 68–70 …”

Section: Discussionmentioning

confidence: 99%

The L‐arginine‐NO‐cGMP pathway mediates the locomotor activity alterations during the expression of sensitization to mephedrone in mice

Bielecka-Papierz

Poleszak

Listos

et al. 2023

Clin Exp Pharma Physio

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Mephedrone is a representative of synthetic cathinones that is known from its rewarding and psychostimulant effects. It exerts behavioural sensitization after repeated and then interrupted administration. In our study, we investigated a role of the L-arginine-NO-cGMP-dependent signalling in the expression of sensitization to hyperlocomotion evoked by mephedrone. The study was carried out in male albino Swiss mice. The tested mice received mephedrone (2.5 mg/kg) for 5 consecutive days and on the 20th day of the experiment (the 'challenge' day) animals received both mephedrone (2.5 mg/kg) and a given substance that affects the L-arginine-NO-cGMP signalling, that is, L-arginine hydrochloride (125 or 250 mg/kg), 7-nitroindazole (10 or 20 mg/kg), L-NAME (25 or 50 mg/kg) or methylene blue (5 or 10 mg/kg). We observed that 7-nitroindazole, L-NAME and methylene blue inhibited

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“…Nitric oxide (NO) is synthesized from L-arginine via NOS enzymes (iNOS, eNOS, and nNOS) (1). Different studies indicated that NO-NOS/GC (guanylyl cyclase)/cGMP (cyclic guanosine mono phosphate) has contribution into the development of opioids analgesic tolerance and physical dependence (23,24). It was demonstrated that the repeated morphine treatment causes an increase in the secretion of some mediators including NO (17).…”

Section: Discussionmentioning

confidence: 99%

The Expression and Function of Nitric Oxide Synthase Enzyme in Atorvastatin Effects on Morphine-Induced Dependence in Mice

et al. 2021

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Background: Atorvastatin exerts neuroprotective effects on the treatment of central nervous system disorders. Morphine analgesic tolerance and dependence remain as major concerns in medicine. Nitric oxide (NO) pathway mediates the development of opioid analgesic tolerance and dependence, as well as atorvastatin neuroprotection. Objectives: The present study aimed to assess the possible involvement of the NO/cGMP pathway in the process of the effects of atorvastatin on morphine physical dependence. Methods: Dependence was induced by repetitive injection of morphine sulfate. Naloxone was injected at the dose of 4 mg/kg on the last day of the experiment to assess withdrawal signs. Animals received atorvastatin (1, 5, 10, and 20 mg/kg, orally). Nitric oxide synthase (NOS) inhibitors and ODQ were injected before protective dose atorvastatin. The gene expression of NOS isoforms was evaluated by real time-PCR. Thereafter, the hippocampal levels of cGMP and nitrite were measured. Results: Treatment with atorvastatin 10 mg/kg significantly attenuated naloxone-induced withdrawal behaviours. The administration of L-NAME, aminoguanidine, and ODQ before atorvastatin enhanced its effects. The treatment with atorvastatin significantly decreased the nitrite and cGMP levels as well as NOS gene expression in the hippocampus of dependent animals. Conclusions: It can be concluded that atorvastatin, possibly, through inducible NOS, could alleviate morphine dependence and withdrawal signs.

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Nitric oxide modulates tapentadol antinociceptive tolerance and physical dependence

Cited by 7 publications

References 55 publications

Exploring Novel Therapeutic Targets in the Common Pathogenic Factors in Migraine and Neuropathic Pain

Exploring Novel Therapeutic Targets in the Common Pathogenic Factors in Migraine and Neuropathic Pain

The L‐arginine‐NO‐cGMP pathway mediates the locomotor activity alterations during the expression of sensitization to mephedrone in mice

The Expression and Function of Nitric Oxide Synthase Enzyme in Atorvastatin Effects on Morphine-Induced Dependence in Mice

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