Administration of somatostatin analog octreotide in the ventrolateral orbital cortex produces sex-related antinociceptive effects on acute and formalin-induced nociceptive behavior in rats

Qu, Chenchen; Dang, Yonghui; Tang, Jing-Shi

doi:10.1016/j.neuint.2015.06.002

Cited by 5 publications

(4 citation statements)

References 57 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…There have been studies showing that apart from endocrinological effects, octreotide produces a number of beneficial effects in different disease states, including ischemia-reperfusion injury 27 , depression 28 , dementia 29 . Administration of octreotide in the ventrolateral orbital cortex has been shown to produce antinociceptive effects in formalin-induced nociceptive behavior in rats 12 . Moreover, it has been shown to attenuate manifestations of diabetic neuropathy 13 .…”

Section: Discussionmentioning

confidence: 98%

“…The role of somatostatin receptors, localized on the peripheral primary afferent terminals, in the development of pain sensitization has been reported 9 , 10 . It is also found to attenuate pain in formalin-induced pain model 11 , 12 and diabetic neuropathy model 13 . However, its role and molecular mechanisms in alcoholic neuropathy are not explored yet.…”

Section: Introductionmentioning

confidence: 91%

See 1 more Smart Citation

Beneficial effects of octreotide in alcohol-induced neuropathic pain. Role of H 2S, BDNF, TNF-α and Nrf2

Jiang

Wei

2021

Acta Cir. Bras.

View full text Add to dashboard Cite

Purpose To explore the role and molecular mechanisms of neuroprotective effects of octreotide in alcohol-induced neuropathic pain. Methods Male Wistar rats were employed and were administered a chronic ethanol diet containing 5% v/v alcohol for 28 days. The development of neuropathic pain was assessed using von Frey hair (mechanical allodynia), pinprick (mechanical hyperalgesia) and cold acetone drop tests (cold allodynia). The antinociceptive effects of octreotide (20 and 40 µg·kg –1 ) were assessed by its administration for 28 days in ethanol-treated rats. ANA-12 (0.25 and 0.50 mg·kg –1 ), brain-derived neurotrophic factor (BDNF) receptor blocker, was coadministered with octreotide. The sciatic nerve was isolated to assess the biochemical changes including hydrogen sulfide (H 2 S), cystathionine β synthase (CBS), cystathionine γ lyase (CSE), tumor necrosis factor-α (TNF-α), BDNF and nuclear factor erythroid 2-related factor 2 (Nrf2). Results Octreotide significantly attenuated chronic ethanol-induced neuropathic pain and it also restored the levels of H 2 S, CBS, CSE, BDNF, Nrf2 and decreased TNF-α levels. ANA-12 abolished the effects of octreotide on pain, TNF-α, BDNF, Nrf2 without any significant effects on H 2 S, CBS, CSE. Conclusions Octreotide may attenuate the behavioral manifestations of alcoholic neuropathic pain, which may be due to an increase in H 2 S, CBS, CSE, BDNF, Nrf2 and a decrease in neuroinflammation.

show abstract

Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 91%

Beneficial effects of octreotide in alcohol-induced neuropathic pain. Role of H 2S, BDNF, TNF-α and Nrf2

Jiang

Wei

2021

Acta Cir. Bras.

View full text Add to dashboard Cite

show abstract

“…The existing 5-HT 6 receptors in SNI rats are more sensitive and vulnerable to exogenous agonist treatment, so that agonist could induce anti-allodynia. The VLO received projections from spinal cord as well as contained output neurons that projected to the PAG (Tang et al, 2009;Qu et al, 2015). Therefore, it is reasonable to propose that the anti-allodynic effects elicited by 5-HT 6 receptor agonists are due to activation of the VLO neurons that project to the PAG, which further leads to activation of the PAG-brainstem descending inhibitory system and depresses the nociceptive transmission at the spinal cord level.…”

Section: Discussionmentioning

confidence: 99%

The 5-HT6 Receptors in the Ventrolateral Orbital Cortex Attenuate Allodynia in a Rodent Model of Neuropathic Pain

Zhang

Yang

et al. 2020

Front. Neurosci.

View full text Add to dashboard Cite

Mechanical allodynia, characterized by a painful sensation induced by innocuous stimuli, is thought to be caused by disruption in pain-related regions. Identification and reversal of this pathologic neuroadaptation are therefore beneficial for clinical treatment. Previous evidence suggests that 5-HT 6 receptors in the ventrolateral orbital cortex (VLO) are involved in neuropathic pain, but their function is poorly understood. The aim of the present study is to unveil the role of 5-HT 6 receptors in the VLO and the underlying mechanisms in pain modulation. Here, by using the spared nerve injury (SNI) pain model, first, we report that 5-HT 6 receptor protein decreased in the contralateral VLO compared with the ipsilateral VLO in rats with allodynia. Second, microinjection of the selective 5-HT 6 receptor agonists EMD-386088 and WAY-208466 into the contralateral VLO consistently and significantly depressed allodynia. Third, microinjection of the selective antagonist SB-258585 blocked the agonist-induced anti-allodynic effect, while the antagonist applied alone to the VLO had no effect. Furthermore, the anti-nociceptive effect of EMD-386088 on neuropathic pain was prevented by the adenylate cyclase (AC) inhibitor SQ-22536, and protein kinase A (PKA) inhibitor H89, suggesting that AC/PKA signaling might underlie the antinociception of agonists. Finally, the 5-HT 6 receptors were found to be colocalized with a glutamate transporter (EAAC1) by immunofluorescent staining, and the glutamate receptor antagonist kynurenic acid was found to completely block antinociception. These findings indicated that the antinociceptive effect of 5-HT 6 receptor agonists might occur via interaction with the glutamatergic system. Altogether, the agonists activated 5-HT 6 receptors present in the glutamatergic neurons in the VLO to facilitate the AC/PKA cascade, which subsequently might evoke glutamate release, thus depressing allodynia. These findings suggest a potential therapeutic role of 5-HT 6 receptor agonists in treating neuropathic pain.

show abstract

“…It is employed to manage acromegaly, diarrhoea in patients with vasoactive intestinal peptide-secreting tumours, acute haemorrhage from oesophageal varices in liver cirrhosis, fistula by reducing gastrointestinal fistula and refractory hypoglycemia 3 . Apart from that, it has been shown to produce beneficial effects in brain-related problems, including idiopathic intracranial hypertension 4 , nociception 5 and status epilepticus 6 , as well as to exert protection in ischemic stroke 7 and severe acute pancreatitis-induced brain damage 8 . Accordingly, it was hypothesized that octreotide may exert beneficial effects in traumatic brain injury-subjected rats.…”

Section: Introductionmentioning

confidence: 99%

Octreotide-mediated neurofunctional recovery in rats following traumatic brain injury. Role of H2S, Nrf2 and TNF-α

Zhou

Cao²,

Feng

et al. 2021

Acta Cir. Bras.

View full text Add to dashboard Cite

Purpose: To explore the role and mechanisms of octreotide in neurofunctional recovery in the traumatic brain injury (TBI) model. Methods: Rats were subjected to midline incision followed by TBI in the prefrontal cortex region. After 72 hours, the behavioural and neurological deficits tests were performed, which included memory testing on Morris water maze for 5 days. Octreotide (15 and 30 mg/kg i.p. ) was administered 30 minutes before subjecting to TBI, and its administration was continued for three days. Results: In TBI-subjected rats, administration of octreotide restored on day 4 escape latency time (ELT) and increased the time spent in the target quadrant (TSTQ) on day 5, suggesting the improvement in learning and memory. It also increased the expression of H 2 S, Nrf2, and cystathionine-γ-lyase (CSE) in the prefrontal cortex, without any significant effect on cystathionine-β-synthase. Octreotide also decreased the TNF-α levels and neurological severity score. However, co-administration of CSE inhibitor (D,L-propargylglycine) abolished octreotide-mediated neurofunctional recovery, decreased the levels of H 2 S and Nrf2 and increased the levels of TNF-α. Conclusions: Octreotide improved the neurological functions in TBI-subjected rats, which may be due to up-regulation of H 2 S biosynthetic enzyme (CSE), levels of H 2 S and Nrf2 and down-regulation of neuroinflammation.

show abstract

Administration of somatostatin analog octreotide in the ventrolateral orbital cortex produces sex-related antinociceptive effects on acute and formalin-induced nociceptive behavior in rats

Cited by 5 publications

References 57 publications

Beneficial effects of octreotide in alcohol-induced neuropathic pain. Role of H 2S, BDNF, TNF-α and Nrf2

Beneficial effects of octreotide in alcohol-induced neuropathic pain. Role of H 2S, BDNF, TNF-α and Nrf2

The 5-HT6 Receptors in the Ventrolateral Orbital Cortex Attenuate Allodynia in a Rodent Model of Neuropathic Pain

Octreotide-mediated neurofunctional recovery in rats following traumatic brain injury. Role of H2S, Nrf2 and TNF-α

Contact Info

Product

Resources

About