Significant changes in mitochondrial distribution in different pain models of mice.

The development of pain after peripheral nerve and tissue injury involves not only neuronal pathways but also immune cells and glia. Central sensitization is thought to be a mechanism for such persistent pain, and ATP involves in the process. We examined the contribution of glia to neuronal excitation in the juvenile rat spinal dorsal horn which is subjected to neuropathic and inflammatory pain. In rats subjected to neuropathic pain, immunoreactivity for the microglial marker OX42 was markedly increased. In contrast, in rats subjected to inflammatory pain, immunoreactivity for the astrocyte marker glial fibrillary acidic protein was increased slightly. Optically-recorded neuronal excitation induced by single-pulse stimulation to the dorsal root was augmented in rats subjected to neuropathic and inflammatory pain compared to control rats. The bath application of a glial inhibitor minocycline and a p38 mitogen-activated protein kinase inhibitor SB203580 inhibited the neuronal excitation in rats subjected to neuropathic pain. A specific P2X1,2,3,4 antagonist TNP-ATP largely inhibited the neuronal excitation only in rats subjected to neuropathic pain rats. In contrast, an astroglial toxin L-alpha-aminoadipate, a gap junction blocker carbenoxolone and c-Jun N-terminal kinase inhibitor SP600125 inhibited the neuronal excitation only in rats subjected to inflammatory pain. A greater number of cells in spinal cord slices from rats subjected to neuropathic pain showed Ca2+ signaling in response to puff application of ATP. This Ca2+ signaling was inhibited by minocycline and TNP-ATP. These results directly support the notion that microglia is more involved in neuropathic pain and astrocyte in inflammatory pain.

/pdf/contribution-of-microglia-and-astrocytes-to-the-central-33fg1izme4.pdf

Contribution of microglia and astrocytes to the central sensitization, inflammatory and neuropathic pain in the juvenile rat

Background Peripheral inflammation leads to the development of persistent thermal hyperalgesia and mechanical allodynia associated with increased expression of interleukin-1β (IL-1β) in the spinal cord. The aim of the present study was to investigate the effects of thiazolidine derivatives, 1b ([2-(2-hydroxyphenyl)-1,3-thiazolidin-4-yl](morpholin-4-yl)methanone) and 1d (2-hydroxy-4-{[2-(2-hydroxyphenyl)-1,3-thiazolidine-4-carbonyl]amino}benzoic acid), on thermal hyperalgesia, mechanical allodynia and on IL-1β expression during carrageenan-induced inflammation in the spinal cord in mice. Inflammatory pain was induced by injecting 1% carrageenan into the right hind paw of the mice.
 Methods
 The animals were administered thiazolidine derivatives, 1b and 1d (1 mg/kg, 3 mg/kg, or 10 mg/kg), intraperitoneally 30 minutes before carrageenan administration. The animals’ behavior was evaluated by measuring thermal hyperalgesia, mechanical allodynia, and motor coordination. The IL-1β expression was measured by enzyme-linked immunosorbent assay. Acute and sub-acute toxicity studies were conducted to evaluate the toxicity profile of compounds.
 Results
 Treatment with the thiazolidine derivative, 1b and 1d, attenuated carrageenan-induced thermal hyperalgesia and mechanical allodynia at doses of 1 mg/kg, 3 mg/kg, and 10 mg/kg. No motor coordination deficits were observed in animals. The compounds also reduced IL-1β expression in the spinal cord of mice. Acute and sub-acute toxicity studies revealed that both compounds were safe.
 Conclusion
 The compounds exhibit promising activity against inflammatory pain due to their ability to produce anti-hyperalgesic and anti-allodynic effects and to inhibit IL-1β expression in the spinal cord.

/pdf/thiazolidine-derivatives-attenuate-carrageenan-induced-u8ffab8qbt.pdf

Thiazolidine Derivatives Attenuate Carrageenan-Induced Inflammatory Pain in Mice.

There is considerable interest in understanding long-term potentiation (LTP) of glutamatergic synaptic transmission because the molecular mechanisms involved in its induction and expression are thought to be essential for learning, memory and pain. The molecular mechanisms involved in induction and expression of LTP have been widely characterized, especially in the hippocampus and have been proposed to be cellular models of learning and memory. LTP in the spinal pain pathways has been considered as one of the cellular mechanisms of post-injury pain hypersensitivity (central sensitization). Extensive evidence has indicated that changes in both the presynaptic release of glutamate and postsynaptic response to glutamate are involved in expression of LTP. This chapter attempts a brief review of some of the postsynaptic mechanisms underlying induction, expression and modulation of the high frequency stimulation-induced LTP of excitatory synaptic transmission in the superficial dorsal horn of the spinal cord. It is becoming clear that the spinal LTP, which might contribute to hyperalgesia in animal models of pain, uses multiple mechanisms involving protein phosphorylation, similar to the processes associated with hippocampal LTP. Modulation of postsynaptic AMPA and NMDA receptor function caused by phosphorylation may play an important role in the induction and expression of synaptic plasticity at dorsal horn excitatory synapses.

Modulation of Long-Term Potentiation of Excitatory Synaptic Transmission in the Spinal Cord Dorsal Horn

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Modulation of Long-Term Potentiation of Excitatory Synaptic Transmission in the Spinal Cord Dorsal Horn