Catheterization of the thoracic spinal subarachnoid space in mice

Poon, Yan‐Yuen; Chang, Alice Y.W.; Ko, Sun; Chan, Samuel H.H.

doi:10.1016/j.jneumeth.2011.06.010

Cited by 7 publications

(7 citation statements)

References 15 publications

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“…This possibility is deemed unlikely because we have demonstrated that given intrathecally at a volume of 3 μL using our method, the highest levels of the spinal cord that the injected agents may reach are T1–T2. 28 …”

Section: Discussionmentioning

confidence: 99%

Activation of spinal nociceptin receptors induces cardiovascular depression and antinociception in an independent manner in mice

Tsai¹,

Poon²,

Huang³

et al. 2018

JPR

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PurposeThe nociceptin receptor (NOP) was discovered in 1994 and was designated opioid-like receptor; activation of NOP leads to reduced neuronal excitability. Although suggested by the anatomical localization of NOP in brain or spinal cord, the cardiovascular or nociceptive effects of its endogenous ligand, nociceptin, are equivocal. Taking advantage from intrathecal application of nociceptin to simultaneously activate NOP on sympathetic preganglionic neurons in the intermediolateral column (IML) and superficial laminae of dorsal horn, we investigated whether the nociceptin-induced cardiovascular effects engage the participation of baroreflex, and whether the concurrently elicited changes in blood pressure and pain responses are interrelated.MethodsNOPs in the thoracic spinal cord of ICR or C57BL/6 mice were identified with immunofluorescence staining and were activated through intrathecal administration of nocicetpin. The elicited changes in cardiovascular parameters and tail-flick nociceptive responses were measured.ResultsPositive immunoreactivity against NOP colocalized with neurons in the IML and superficial dorsal horn layers of thoracic spinal cord. Intrathecal administration of nociceptin (1, 2, or 5 nmol) elicited a significant and dose-dependent decrease in blood pressure or heart rate that was paralleled by reduced baroreflex-mediated sympathetic vasomotor tone and mirrored by augmented cardiac vagal baroreflex, alongside prolonged tail-flick latency with an efficacy of hypotension <<< antinociception. Coadministration of the specific NOP antagonist, UFP101 (10 nmol), blunted all nociceptin-elicited responses. However, restoring blood pressure to baseline level failed to affect the antinociceptive actions of nociceptin.ConclusionActivation of thoracic spinal NOP in ICR and C57BL/6 mice induces blood pressure and heart rate by decreasing the sympathetic outflow of both arms of the baroreflex arc to the blood vessels and the heart, and the antinociceptive responses to nociceptin are independent of and disproportional to its cardiovascular actions.

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Section: Discussionmentioning

confidence: 99%

Activation of spinal nociceptin receptors induces cardiovascular depression and antinociception in an independent manner in mice

Tsai¹,

Poon²,

Huang³

et al. 2018

JPR

Self Cite

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show abstract

“…The design and implantation of thoracic intrathecal catheters in mice followed our previously developed procedure. 28 Briefly, under pentobarbital sodium anesthesia (50 mg kg −1 , intraperitoneal), the left interspinous space between T12 and T13 was exposed after the supraspinous ligament and the left interspinous ligament between T12 and T13 was removed. A 0.5 cm long PU-10 catheter (Strategic Application Inc., Libertyville, IL, USA) was inserted tangentially into the subarachnoid space along the dorsal surface of the spinal cord through a dural opening.…”

Section: Subarachnoid Catheterizationmentioning

confidence: 99%

Activation of spinal nociceptin receptors induces cardiovascular depression and antinociception in an independent manner in mice

Huang

Poon

Tsai

2018

Proceedings for Annual Meeting of the Japanese Pharmacological Society

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The nociceptin receptor (NOP) was discovered in 1994 and was designated opioidlike receptor; activation of NOP leads to reduced neuronal excitability. Although suggested by the anatomical localization of NOP in brain or spinal cord, the cardiovascular or nociceptive effects of its endogenous ligand, nociceptin, are equivocal. Taking advantage from intrathecal application of nociceptin to simultaneously activate NOP on sympathetic preganglionic neurons in the intermediolateral column (IML) and superficial laminae of dorsal horn, we investigated whether the nociceptin-induced cardiovascular effects engage the participation of baroreflex, and whether the concurrently elicited changes in blood pressure and pain responses are interrelated. Methods: NOPs in the thoracic spinal cord of ICR or C57BL/6 mice were identified with immunofluorescence staining and were activated through intrathecal administration of nocicetpin. The elicited changes in cardiovascular parameters and tail-flick nociceptive responses were measured. Results: Positive immunoreactivity against NOP colocalized with neurons in the IML and superficial dorsal horn layers of thoracic spinal cord. Intrathecal administration of nociceptin (1, 2, or 5 nmol) elicited a significant and dose-dependent decrease in blood pressure or heart rate that was paralleled by reduced baroreflex-mediated sympathetic vasomotor tone and mirrored by augmented cardiac vagal baroreflex, alongside prolonged tail-flick latency with an efficacy of hypotension <<< antinociception. Coadministration of the specific NOP antagonist, UFP101 (10 nmol), blunted all nociceptin-elicited responses. However, restoring blood pressure to baseline level failed to affect the antinociceptive actions of nociceptin. Conclusion: Activation of thoracic spinal NOP in ICR and C57BL/6 mice induces blood pressure and heart rate by decreasing the sympathetic outflow of both arms of the baroreflex arc to the blood vessels and the heart, and the antinociceptive responses to nociceptin are independent of and disproportional to its cardiovascular actions.

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“…Subarachnoid catheter placement in both lumbar and thoracic spinal cord of mice requires a surgical approach, although the lumbar technique involves only the skin (Poon et al, 2011;Wu et al, 2004). The size of the catheter is important, as less postoperative motor dysfunction was observed with PU-10 (OD 0.25 mm) compared to PE-5 (OD 0.51 mm).…”

Section: B Spinal Cathetersmentioning

confidence: 99%

“…The size of the catheter is important, as less postoperative motor dysfunction was observed with PU-10 (OD 0.25 mm) compared to PE-5 (OD 0.51 mm). In the PU-10 group, all mice surviving anesthesia and the immediate postoperative period had no motor deficits (Poon et al, 2011). Surgical access in placement of the thoracic catheter required removal of the paravertebral musculature from T11 through L1, and removal of dorsal interspinous and interspinous ligaments between T12 and T13.…”

Section: B Spinal Cathetersmentioning

confidence: 99%