Neuropathic Pain Model, Diabetic Neuropathy Model

2008 ◽

Vol 62 (3) ◽

pp. 85-90

Author(s):

Vija Kluša ◽

Juris Rumaks ◽

Ñina Karajeva

Keyword(s):

Neuropathic Pain ◽

Diabetic Neuropathy ◽

Diabetic Neuropathic Pain ◽

Cholinergic Mechanism ◽

Peripheral Neuropathic Pain ◽

Pain Model ◽

Diabetes Model ◽

Neuropathic Pain Model ◽

New Type ◽

Anticholinesterase Drug

Neuromidin Attenuates Neuropathic Pain in the Streptozocin-Induced Diabetes Model in Rats Diabetic neuropathy, which affects all peripheral nerves and may cause dramatic pain, is one of the most severe pathologies associated with hyperglycaemia, damage in the blood vessels, and inflammation in nerves. Anticonvulsants and antidepressants are still the most commonly used options to manage diabetic neuropathy. However, to improve clinical benefit in the treatment of diabetic neuropathies, as well as to minimize side effects, search for a new type of drugs to protect/treat neuropathic pain is still important. The aim of this study was to investigate neuromidin (ipidacrine, amiridin, NIK-247), an anticholinesterase drug of tetrahydroaminoacridine series, in the streptozocin (STZ)-induced diabetic neuropathic pain model in rats. Neuromidin was administered per os at daily doses 0.3, 1.0 and 3.0 mg/kg for ten days. The dynamics in the development of hyperalgesia (pain threshold) was measured by algesimeter for five weeks. The data obtained show that neuromidin considerably protects the development of peripheral neuropathic pain caused by STZ. The most active dose was the lowest—0.3 mg/kg. Neuromidin did not affect STZ-hyperglycemia, nor the weight gain in animal groups. Neuromidin per se at the doses 0.3 and 1.0 mg/kg showed a short-term analgesic activity. The cholinergic mechanism of neuromidin may be considered as essential in attenuating of diabetic neuropathic pain; other mechanisms remain to be elucidated.

Download Full-text

Neuropathic Pain Model, Diabetic Neuropathy Model

Encyclopedia of Pain ◽

10.1007/978-3-642-28753-4_2679 ◽

2013 ◽

pp. 2075-2079

Author(s):

Nigel A. Calcutt ◽

Sandra Chaplan

Keyword(s):

Neuropathic Pain ◽

Diabetic Neuropathy ◽

Pain Model ◽

Neuropathic Pain Model

Download Full-text

Neuropathic Pain Model, Diabetic Neuropathy Model

10.1007/springerreference_122702 ◽

2012 ◽

Keyword(s):

Neuropathic Pain ◽

Diabetic Neuropathy ◽

Pain Model ◽

Neuropathic Pain Model

Download Full-text

Faculty Opinions recommendation of Modulation of the anti-nociceptive effects of 2-arachidonoyl glycerol by peripherally administered FAAH and MGL inhibitors in a neuropathic pain model.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1126773.583854 ◽

2008 ◽

Author(s):

Roger Pertwee ◽

Maria Grazia Cascio

Keyword(s):

Neuropathic Pain ◽

Pain Model ◽

Neuropathic Pain Model ◽

Arachidonoyl Glycerol

Download Full-text

The activation of galanin receptor 2 plays an antinociceptive effect in nucleus accumbens of rats with neuropathic pain

The Journal of Physiological Sciences ◽

10.1186/s12576-021-00790-5 ◽

2021 ◽

Vol 71 (1) ◽

Author(s):

Yan Dong ◽

Chong-Yang Li ◽

Xiao-Min Zhang ◽

Ya-Nan Liu ◽

Shuang Yang ◽

...

Keyword(s):

Neuropathic Pain ◽

Nucleus Accumbens ◽

Pain Threshold ◽

Antinociceptive Effect ◽

Galanin Receptor ◽

Pain Model ◽

Withdrawal Threshold ◽

Neuropathic Pain Model ◽

Galanin Receptors ◽

Intact Rats

AbstractOur previous research has shown that galanin plays an antinociceptive effect via binding to galanin receptors (GalRs) in nucleus accumbens (NAc). This study focused on the involvement of GalR2 in galanin-induced antinociceptive effect in NAc of neuropathic pain rats. The chronic constriction injury of sciatic nerve (CCI) was used to mimic neuropathic pain model. The hind paw withdrawal latency (HWL) to thermal stimulation and hind paw withdrawal threshold (HWT) to mechanical stimulation were measured as the indicators of pain threshold. The results showed that 14 and 28 days after CCI, the expression of GalR2 was up-regulated in bilateral NAc of rats, and intra-NAc injection of GalR2 antagonist M871 reversed galanin-induced increases in HWL and HWT of CCI rats. Furthermore, intra-NAc injection of GalR2 agonist M1145 induced increases in HWL and HWT at day 14 and day 28 after CCI, which could also be reversed by M871. Finally, we found that M1145-induced antinociceptive effect in NAc of CCI rats was stronger than that in intact rats. These results imply that the GalR2 is activated in the NAc from day 14 to day 28 after CCI and GalR2 is involved in the galanin-induced antinociceptive effect in NAc of CCI rats.

Download Full-text

Pharmacological Evidence on Augmented Antiallodynia Following Systemic Co-Treatment with GlyT-1 and GlyT-2 Inhibitors in Rat Neuropathic Pain Model

International Journal of Molecular Sciences ◽

10.3390/ijms22052479 ◽

2021 ◽

Vol 22 (5) ◽

pp. 2479

Author(s):

Amir Mohammadzadeh ◽

Péter P. Lakatos ◽

Mihály Balogh ◽

Ferenc Zádor ◽

Dávid Árpád Karádi ◽

...

Keyword(s):

Neuropathic Pain ◽

Animal Studies ◽

Acute Administration ◽

Pain Model ◽

Therapeutic Value ◽

Small Doses ◽

Function Test ◽

Neuropathic Pain Model ◽

First Time ◽

Glycine Content

The limited effect of current medications on neuropathic pain (NP) has initiated large efforts to develop effective treatments. Animal studies showed that glycine transporter (GlyT) inhibitors are promising analgesics in NP, though concerns regarding adverse effects were raised. We aimed to study NFPS and Org-25543, GlyT-1 and GlyT-2 inhibitors, respectively and their combination in rat mononeuropathic pain evoked by partial sciatic nerve ligation. Cerebrospinal fluid (CSF) glycine content was also determined by capillary electrophoresis. Subcutaneous (s.c.) 4 mg/kg NFPS or Org-25543 showed analgesia following acute administration (30–60 min). Small doses of each compound failed to produce antiallodynia up to 180 min after the acute administration. However, NFPS (1 mg/kg) produced antiallodynia after four days of treatment. Co-treatment with subanalgesic doses of NFPS (1 mg/kg) and Org-25543 (2 mg/kg) produced analgesia at 60 min and thereafter meanwhile increased significantly the CSF glycine content. This combination alleviated NP without affecting motor function. Test compounds failed to activate G-proteins in spinal cord. To the best of our knowledge for the first time we demonstrated augmented analgesia by combining GlyT-1 and 2 inhibitors. Increased CSF glycine content supports involvement of glycinergic system. Combining selective GlyT inhibitors or developing non-selective GlyT inhibitors might have therapeutic value in NP.

Download Full-text