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:: Search published articles ::
Showing 4 results for Neuropathic Pain

Gholam Ali Hamidi, Homa Manaheji, Mahmoud Salami, Hossein Ali Safakhah, Sayed Mohammad Noorbakhsh,
Volume 9, Issue 3 (10-2005)
Abstract

Background: Neuropathic pain syndromes are changes resulted from damage to neuronal pathways which is characterized by spontaneous burning pain with accompanying allodynia and hyperalgesia. The mechanisms underlying neuropathic pain are poorly understood. The present study explores behavioral characteristics of the neuropathic pain models chronic constriction injury (CCI) and spared nerve injury (SNI).

Materials and Methods: Experiments were performed on four groups (n= 8) of male Sprague-Dawley rats (230-280 g). Anesthesia was initially induced with sodium pentobarbital (i.p.) at a dose of 50 mg/kg. The CCI model was made by loose ligation of the sciatic nerve. Also a lesion of two of three terminal branches of the sciatic nerve leads to a SNI model. The animals were tested for behavioral responses cold-and mechano-allodynia and heat-and mechano-hyperalgesia. The cold and mechanical stimulations in the cold- and mechano-allodynia phenomena were applied through acetone and von Frey filament respectively. Pin-prick and radiant heat were applied as thermal and mechanical stimulations in the heat- and mechano-hyperalgesia respectively. Behavioral tests were conducted on the animals prior to surgery (the day 0), and 3, 7, 14, 21 and 28 days post-operation.

Results: Our results indicate that, in comparison to the controlled group, the rats in both SNI and CCI groups reveal an obvious difference in behavioral responses. Although the SNI, compared to the CCI group were more sensitive to mechano-allodynia shortly after surgery (p<0.5) however, both groups share a similar pattern of behavior. In the heat-hyperalgesia testing, again, the animals in the CCI and SNI groups behaved differently than those in the controlled group, but no variation was evident among the test groups, themselves.

Conclusion : These findings clearly show that the two neuropathic models produce abnormal pain-related disorders in the rats. A major feature of the SNI model was the very marked hypersensitivity to normally innocuous mechanical stimuli.


Zahra Bahari, Homa Manaheji, Narges Hosseinmardi , Gholam Hosein Meftahi , Mehdi Sadeghi, Seyyed Mohammad Noorbakhsh,
Volume 18, Issue 4 (8-2014)
Abstract

Background: The underlying central mechanisms for the development and maintenance of neuropathic pain are unknown. The current study aimed to evaluate the long-term potentiation (LTP) changes in spinal dorsal horn wide dynamic range (WDR) neurons following a peripheral neuropathy model.

Materials and Methods: This study was conducted on 26 male Wistar rats. The spinal nerve ligation (SNL) model was performed to induce neuropathy. After surgery, thermal hyperalgesia and mechanical allodynia were evaluated one day before neuropathy, and then on days 2, 5, 7, 14, 21 and 28 after neuropathy. Single-unit recording was used to study the changes of LTP. The changes of LTP and Aδ- and C-fiber evoked responses by high-frequency stimulation (100 Hz and current intensity six times that of the threshold for activation of C- fibers) of sciatic nerve in spinal WDR synapses were studied on day 14 after surgery up to 2 hours.

Results: Neuropathy was induced thermal hyperalgesia and mechanical allodynia on day 2 and persisted for 28 days after neuropathy. Electrophysiological recording revealed that HFS induced LTP either in the Aδ- or in the C-fibers in both sham and neuropathy groups up to 2 hr on day 14 after neuropathy. Neuropathy also significantly decreased the threshold of these fibers.

Conclusion: LTP-induced HFS in spinal WDR neurons can be one of the underlying central mechanisms in the maintenance of neuropathic pain.


Monir Naderi Tehrani, Azhdar Heydari, Gholamali Hamidi, Saeedeh Nasrollahi,
Volume 23, Issue 3 (5-2019)
Abstract

Background: Neuropathic pain is a chronic pain caused by damage to the central nervous system and the peripheral. Caffeine is a non-selective antagonist of A1, A2a, receptors of adenosine, which has a protective effect on neuropathic pain in some doses by inhibiting A2a, A2b receptors. Considering that the nitric oxide (NO) levels are apparently effective in the parts of caffeine central effects, thus, the purpose of this study was to investigate the effect of chronic caffeine administration on the hyperalgesia in neuropathic rats and levels of nitric oxide metabolites (NOx).
Materials and Methods: The present study was conducted on 40 adult male rats weighing 220-250 gr. Neuropathic pain was induced by chronic constriction injury (CCI) of sciatic nerve. Animals were randomly divided into 5 groups (n=8). The control group, which did not intervene on the sciatic nerve, the sham group, which the animals were surgically implanted but the sciatic nerve was not tied, the CCI group and test groups received oral doses of  caffeine orally (100 and 300 mg/L) for 28 days. Hyperalgesia was measured in all groups with Plantar test on days 4, 7, 14, 21, and 28 after surgery. The levels of NOx were measured by the Griess method in lumbar spinal cord tissue on day 28.
Results: Neuropathic rats showed decreased pain thresholds in hyperalgesia. Chronic caffeine at the doses of 100 and 300 mg/L in drinking water for 28 days significantly alleviated hyperalgesia (P<0.01, P<0.001).
Conclusion: According to the results of this study, chronic intake of caffeine can reduce hyperalgesia in neuropathic rat. It seems that the NO pathway is not involved in the central effect of caffeine on pain threshold in the CCI model of neuropathic pain.
 

Azam Mesdaghinia, Hamidreza Banafshe, Alireza Moravveji, Ghazal Hajiagajani, Narges Esmaeilian, Alireza Abed,
Volume 26, Issue 1 (3-2022)
Abstract

Background: Neuropathic pain due to chemotherapy is one of the most important types of chronic pain that despite the increasing advances in medical sciences, its treatment is associated with many problems. In this study, the effects of atomoxetine on paclitaxel-induced neuropathic pain and the effect of alpha-2 adrenergic receptor antagonist (yohimbine) on the analgesic effect of atomoxetine were researched.
Materials and Methods: Male mice received paclitaxel (2 mg/kg i.p.) from the first to the fifth day and atomoxetine (5, 10, and 15 mg/kg p.o.) was administered from the day 6 to 10. Mice were divided into different groups (n=8) and each group received a unique dose of the drug. On days 9, 10 and 11, Von Frey and acetone tests were performed. Also, the effect of alpha-2 adrenergic receptor antagonist (yohimbine) on the analgesic effect of atomoxetine was investigated. For this purpose, after pain induction, mice received atomoxetine (15 mg/kg p.o) with yohimbine (5 mg/kg i.p. 5) from day 6 to 10.
Results: Daily administration of atomoxetine (15 mg/kg p.o) effectively increased pain threshold in the cold and mechanical allodynia tests (P<0.01). Administration a single dose of atomoxetine on the 11th day did not alter behavioral tests.
Conclusion: According to these findings, it can be concluded that atomoxetine is able to reduce the severity of paclitaxel-induced neuropathic pain.


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