Brain research bulletin
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Brain research bulletin · Feb 2012
Electroacupuncture inhibits phosphorylation of spinal phosphatidylinositol 3-kinase/Akt in a carrageenan-induced inflammatory rat model.
We investigated the changes of pain-related spinal signaling pathway after electroacupuncture (EA) stimulation in a carrageenan-induced rat model. EA stimulation (2Hz, 1mA) was needle-delivered for 30 min at acupoints corresponding to Zusanli and Sanyinjiao 3 h after carrageenan injection. Thermal and mechanical sensitivity of the hindpaw induced by carrageenan was strongly inhibited by EA stimulation. ⋯ Immunohistochemical analyses confirmed that phosphorylation of PI3K and Akt showed a similar pattern as Western blotting and were observed in most neurons and a few astrocytes. EA and PI3K inhibitor synergistically inhibited carrageenan-induced hyperalgesia. These results reveal that both neuronal PI3K and Akt may play an important role in EA-induced antinociception via inactivation in an inflammatory pain model.
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Brain research bulletin · Feb 2012
The central versus peripheral antinociceptive effects of μ-opioid receptor agonists in the new model of rat visceral pain.
This study describes the antinociceptive effects of μ-opioid agonists, d-Ala(2),N-Me-Phe(4),Gly(5)-ol-enkephalin (DAMGO) and morphine in a model of rat visceral pain in which nociceptive responses were triggered by 2% acetic acid intraperitoneal (i.p.) injections. DAMGO and morphine were administered i.p., to the same site where acetic acid was delivered or intracerebroventricularly (i.c.v.). The antinociceptive actions of i.p. versus i.c.v. administered DAMGO or morphine were evaluated in the late phase of permanent visceral nociceptive responses. ⋯ On the other hand, i.c.v. injections of NAL-M partially antagonized the antinociceptive effect of i.p. morphine and failed to affect the antinociceptive action of i.p. DAMGO indicating the partial and pure peripheral antinociceptive effects of morphine and DAMGO, respectively. These results suggest the role of either central or peripheral μ-opioid receptors (MOR) in mediating antinociceptive effects of i.p. μ-opioid agonists in the rat late permanent visceral pain model which closely resembles the clinical situation.
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Brain research bulletin · Feb 2012
Effects of anti-rVEGF on the expression of VEGF receptor-2 and P2X(2/3) receptors of the spinal dorsal horn in neuropathic pain rats.
Neuropathic pain is caused by the peripheral or central nervous system structure damage or dysfunction. VEGF is involved in nociception and inflammation. VEGF may target VEGF receptor-2 (VEGFR-2) on the surface of neurons. ⋯ Therefore, VEGF may activate VEGFR-2 to participate the process of neuropathic pain. Anti-rVEGF treatment in CCI rats reduced the expression of VEGFR-2 and inhibited the transmission of neuropathic pain in L4/5 SDH via decreasing the expression of P2X(2/3). There is a cross-potentiation between VEGFR-2 and P2X(2/3) receptors in neuropathic pain state.
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Brain research bulletin · Feb 2012
Anticonvulsant effect of unilateral anterior thalamic high frequency electrical stimulation on amygdala-kindled seizures in rat.
Deep brain stimulation (DBS) is an emerging treatment of epilepsy. Anterior nucleus of the thalamus (ANT) is considered to be an attractive target due to its close connection to the limbic structures and wide regions of neocortex. In this study, we examined the effect of unilateral high frequency stimulation (HFS) of the ANT on amygdala-kindled seizures in Wistar rats. ⋯ HFS of the ipsilateral ANT significantly decreased the incidence of generalized seizures and the mean behavioral seizure stage and afterdischarge duration (ADD), and shortened cumulative ADD and cumulative generalized seizure duration. Furthermore, HFS of the ipsilateral ANT significantly increased the afterdischarge threshold (ADT). Our data suggest that unilateral HFS of the ANT may be an effective method of inhibiting kindled seizures by suppressing the susceptibility to seizures and generating long lasting anti-epileptic effect preventing the recurrence of kindled seizures, providing an alternative to bilateral ANT DBS for refractory epilepsy.
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Brain research bulletin · Feb 2012
Creatine reduces oxidative stress markers but does not protect against seizure susceptibility after severe traumatic brain injury.
Achievements made over the last years have highlighted the important role of creatine in health and disease. However, its effects on hyperexcitable circuit and oxidative damage induced by traumatic brain injury (TBI) are not well understood. In the present study we revealed that severe TBI elicited by fluid percussion brain injury induced oxidative damage characterized by protein carbonylation, thiobarbituric acid reactive species (TBARS) increase and Na(+),K(+)-ATPase activity inhibition 4 and 8 days after neuronal injury. ⋯ In addition, creatine supplementation had no effect on convulsive parameters induced by a subconvulsant dose of PTZ. Current experiments provide evidence that lipid and protein oxidation represents a separate pathway in the early post-traumatic seizures susceptibility. Furthermore, the lack of consistent anticonvulsant effect exerted by creatine in this early phase suggests that its apparent antioxidant effect does not protect against excitatory input generation induced by TBI.