Neurochemical properties of BDNF-containing neurons projecting to rostral ventromedial medulla in the ventrolateral periaqueductal gray

Yin, Jun-Bin; Wu, Huang-Hui; Dong, Yu-Lin; Zhang, Ting; Wang, Jian; Zhang, Yong; Wei, Yanyan; Lu, Ya-Cheng; Wu, Shengxi; Wang, Wen; Li, Yunqing

doi:10.3389/fncir.2014.00137

Cited by 33 publications

(33 citation statements)

References 78 publications

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“…In previous studies, it has been shown that injecting formalin into a rodent's hind paw can induce both acute spontaneous pain and long-term hyperalgesia behaviors (1)(2)(3). Long-term peripheral inflammation or tissue injury and central sensitization in the spinal cord and brain nucleus are all involved in the mediation or modulation of formalin-induced pain (4)(5)(6). There are advantages for precise clarity as to anti-nociceptive properties mediated by different mechanisms, such as peripheral anti-inflammation, and/ or central desensitization.…”

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confidence: 99%

The Analgesic Effects of Celecoxib on the Formalin-induced Short- and Long-term Inflammatory Pain

et al. 2017

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The non-steroidal anti-inflammatory drug celecoxib has long been used for reducing pain, in spite of moderate gastrointestinal side effects. In previous studies, it has been shown that celecoxib can inhibit formalin-induced spontaneous pain and secondary hyperalgesia. Injecting formalin into a rodent’s hind paw not only induces acute pain behaviors, but also produces long-lasting hyperalgesia. Whether celecoxib can also have long-lasting effects is still unknown. Our results show that pretreatment with an intraperitoneal injection of celecoxib at one hour before formalin injection induced inhibition on the spontaneous flinch and licking behaviors in the second phase but not the first phase. Meanwhile, FOS expressions were also reduced with celecoxib pretreatment. Consecutive administration of celecoxib also protects the hind paw from hypoalgesia and relieves formalininduced, long-lasting hyperalgesia in the ipsilateral hind paw. These analgesic effects may be related to suppression of the activation of neurons and astrocytes indicated by FOS and GFAP expressions. Based on the above findings, celecoxib demonstrated analgesic effects not only on acute spontaneous pain behavior but also on long-lasting hyperalgesia induced by formalin injection. The inhibition of neurons and astrocytes by celecoxib may be possible reasons for its analgesia. Key words: Formalin test, celecoxib, FOS, GFAP, hyperalgesia

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confidence: 99%

The Analgesic Effects of Celecoxib on the Formalin-induced Short- and Long-term Inflammatory Pain

et al. 2017

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“…In addition, the baroreceptor reflex is suppressed in neuropathic rats (Gemes et al, 2009), thus indicating that the baroreflex is also altered in chronic pain conditions, which suggests a more profound modification in neuronal activity induced by pain. A possible explanation for these modifications is that projecting fibers originating in the vlPAG release brain-derived neurotrophic factor (BDNF) in the RVLM (Yin et al, 2014). The BDNF is involved in plastic processes, such as neuronal proliferation and differentiation, leading to activity-dependent modifications in synapse physiology and structure (Korte et al, 1996;Liu et al, 2004;Malenka & Bear, 2004).…”

Section: Discussionmentioning

confidence: 99%

Ventrolateral periaqueductal grey matter neurotransmission modulates cardiac baroreflex activity

Lagatta

Ferreira‐Junior

Deolindo

et al. 2016

Eur J of Neuroscience

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Baroreflex activity is a neural mechanism responsible for short-term adjustments in blood pressure (BP). Several supramedullary areas, which send projections to the medulla, are able to control this reflex. In this context, the ventrolateral part of the periaqueductal grey matter (vlPAG), which is a mesencephalic structure, has been suggested to regulate the cardiovascular system. However, its involvement in baroreflex control has never been addressed. Therefore, our hypothesis is that the vlPAG neurotransmission is involved in baroreflex cardiac activity. Male Wistar rats had stainless steel guide cannulae unilaterally or bilaterally implanted in the vlPAG. Afterward, a catheter was inserted into the femoral artery for BP and HR recording. A second catheter was implanted into the femoral vein for baroreflex activation. When the nonselective synaptic blocker cobalt chloride (CoCl ) was unilaterally injected into the vlPAG, in either the left or the right hemisphere, it increased the tachycardic response to baroreflex activation. However, when CoCl was bilaterally microinjected into the vlPAG it decreased the tachycardic response to baroreflex stimulation. This work shows that vlPAG neurotransmission is involved in modulation of the tachycardic response of the baroreflex. Moreover, we suggest that the interconnections between the vlPAG of both hemispheres are activated during baroreflex stimulation. In this way, our work helps to improve the understanding about brain-heart circuitry control, emphasizing the role of the autonomic nervous system in such modulation.

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“…According to our previous research, a secondary and long-lasting mechanical allodynic and hyperalgesic response can be observed not only on the ipsilateral but also on the contralateral hind paw. Since sensory receptors in the bilateral area of secondary mechanical allodynia and hyperalgesia are unaffected, these sensory changes might be caused by central sensitization in the spinal cord and brain nucleus of the initial intense nociceptive discharge that follows the formalin injection (4)(5)(6). Various studies suggest that the release of immune substances and proinflammatory cytokines from spinal glia (7,8), and the bilateral signaling via commissural interneurons (9), might, in part, induce the mirror-image pain.…”

Section: Experimental Designmentioning

confidence: 99%

Contribution of Spinal PKCγ Expression to Short- and Long-lasting Pain Behaviors in Formalin-induced Inflamed Mice

Zhao

Yin

et al. 2018

Pain Phys

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Background: Over-expression of spinal protein kinase C γ (PKCγ) contributes to the induction of persistent bilateral hyperalgesia following inflammatory injury, yet the role of spinal PKCγ in short- and long-lasting pain behavior is poorly understood. Objective: This study aimed to characterize the contribution of spinal PKCγ to spontaneous pain and long-lasting bilateral hyperalgesia in formalin-induced inflamed mice using pharmacological inhibition. Study Design: Laboratory animal study. Setting: The study was performed in the Department of Human Anatomy and K.K. Leung Brain Research Centre, Preclinical School of Medicine, the Fourth Military Medical University (Xi’an, China) and the Department of Anesthesiology, Fuzhou General Hospital (Fuzhou, China). Methods: Male mice were unilaterally intraplantarly injected with formalin to induce inflammatory pain. Spontaneous pain behaviors, including flinches and lickings, were recorded by off-line video during the first hour post-injection and counted. Using von Frey tests, longlasting bilateral mechanical paw withdrawal thresholds were determined before injection and at indicated time points thereafter. Temporal expression of spinal PKCγ was observed by immunohistochemical staining. For pharmacological inhibition, mice were treated daily with intrathecal Tat carrier or selective PKCγ inhibitor KIG31-1, from 1 hour prior to 10 days after formalin injection. Spontaneous pain behaviors and long-lasting bilateral mechanical hyperalgesia were assessed. Spinal PKCγ expression was also observed by using immunohistochemical staining and western blot. Results: The number of PKCγ-immunoreactive (ir) spinal neurons was significantly higher at 10 days, but not 2 hours, after formalin intraplantar injection, and accompanied by long-lasting bilateral hyperalgesia. Furthermore, long-lasting bilateral hyperalgesia could be reversed by pharmacological inhibition of over-expressed spinal PKCγ; however, pretreating with intrathecal KIG31-1 showed no antinociceptive effects on short-term spontaneous pain behaviors. Limitations: All results were obtained from the mice and no PKCγ inhibitors were available through clinical practice. Therefore, it remains difficult to draw definitive connections between animal research and human application. Conclusion: Our findings suggest that spinal PKCγ plays a predominant role in long-lasting bilateral hyperalgesia, but not in the spontaneous pain behaviors induced by formalin. Key words: Formalin, spontaneous pain, mechanical hyperalgesia, protein kinase C gamma, KIG31-1, mice

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Neurochemical properties of BDNF-containing neurons projecting to rostral ventromedial medulla in the ventrolateral periaqueductal gray

Cited by 33 publications

References 78 publications

The Analgesic Effects of Celecoxib on the Formalin-induced Short- and Long-term Inflammatory Pain

The Analgesic Effects of Celecoxib on the Formalin-induced Short- and Long-term Inflammatory Pain

Ventrolateral periaqueductal grey matter neurotransmission modulates cardiac baroreflex activity

Contribution of Spinal PKCγ Expression to Short- and Long-lasting Pain Behaviors in Formalin-induced Inflamed Mice

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