scholarly journals Systemic pregabalin attenuates facial hypersensitivity and noxious stimulus-evoked release of glutamate in medullary dorsal horn in a rodent model of trigeminal neuropathic pain

2013 ◽  
Vol 62 (6) ◽  
pp. 831-835 ◽  
Author(s):  
Naresh Kumar ◽  
Pavel S. Cherkas ◽  
Vidya Varathan ◽  
Makiko Miyamoto ◽  
Chen Yu Chiang ◽  
...  
2009 ◽  
Vol 29 (36) ◽  
pp. 11161-11171 ◽  
Author(s):  
A. Okada-Ogawa ◽  
I. Suzuki ◽  
B. J. Sessle ◽  
C.-Y. Chiang ◽  
M. W. Salter ◽  
...  

2000 ◽  
Vol 83 (6) ◽  
pp. 3570-3574 ◽  
Author(s):  
Xiao-Min Wang ◽  
Kai-Ming Zhang ◽  
Layron O. Long ◽  
Carmina A. Flores ◽  
Sukhbir S. Mokha

The present study investigated the modulation of N-methyl-d-aspartate (NMDA)-evoked and peripheral cutaneous stimulus-evoked responses of trigeminal neurons by endomorphins, endogenous ligands for the μ-opioid receptor. Effects of endomorphins, administered microiontophoretically, were tested on the responses of nociceptive neurons recorded in the superficial and deeper dorsal horn of the medulla (trigeminal nucleus caudalis) in anesthetized rats. Endomorphin-1 and endomorphin-2 predominantly reduced the NMDA-evoked responses, producing an inhibitory effect of 54.1 ± 2.96% (mean ± SE; n = 34, P < 0.001) in 92% (34/37) of neurons and 63.6 ± 3.61% ( n = 32, P< 0.001) in 91% (32/35) of neurons, respectively. The inhibitory effect of endomorphins was modality specific; noxious stimulus-evoked responses were reduced more than nonnoxious stimulus-evoked responses. Naloxone applied at iontophoretic current that blocked the inhibitory effect of [d-Ala2, N-Me-Phe4, Gly5-ol]-enkephalin, reduced the peak inhibitory effect of endomorphins on the NMDA- and natural stimulus-evoked responses. We suggest that endomorphins by acting at μ-opioid receptor selectively modulate noxious stimulus-evoked responses in the medullary dorsal horn.


Author(s):  
Nuria García-Magro ◽  
Yasmina B. Martin ◽  
Pilar Negredo ◽  
Francisco Zafra ◽  
Carlos Avendaño

Craniofacial neuropathic pain affects millions of people worldwide and is often difficult to treat. Two key mechanisms underlying this condition are a loss of the negative control exerted by inhibitory interneurons and an early microglial reaction. Basic features of these mechanisms, however, are still poorly understood. Using the chronic constriction injury of the infraorbital nerve (CCI-IoN) model of neuropathic pain in mice, we have examined the changes in the expression of GAD, the synthetic enzyme of GABA, and GlyT2, the membrane transporter of glycine, as well as the microgliosis that occur at early (5 days) and late (21 days) stages post-CCI in the medullary and upper spinal dorsal horn. Our results show that CCI-IoN induces a down-regulation of GAD at both postinjury survival times, uniformly across the superficial laminae. The expression of GlyT2 showed a more discrete and heterogeneous reduction due to the basal presence in lamina III of &lsquo;patches&rsquo; of higher expression, interspersed within a less immunoreactive &lsquo;matrix&rsquo;, which showed a more substantial reduction in the expression of GlyT2. These patches coincided with foci lacking any perceptible microglial reaction, which stood out against a more diffuse areas of strong microgliosis. These findings may provide clues to better understand the neural mechanisms underlying allodynia in neuropathic pain syndromes.


2012 ◽  
Vol 61 (8) ◽  
pp. 1276-1279 ◽  
Author(s):  
Naresh Kumar ◽  
Pavel S. Cherkas ◽  
C.Y. Chiang ◽  
Jonathan O. Dostrovsky ◽  
Barry J. Sessle ◽  
...  

2017 ◽  
Vol 18 (8) ◽  
pp. 899-907 ◽  
Author(s):  
Weihua Ding ◽  
Zerong You ◽  
Shiqian Shen ◽  
Jinsheng Yang ◽  
Grewo Lim ◽  
...  

2021 ◽  
Vol 22 (9) ◽  
pp. 4564
Author(s):  
Nuria García-Magro ◽  
Yasmina B. Martin ◽  
Pilar Negredo ◽  
Francisco Zafra ◽  
Carlos Avendaño

Craniofacial neuropathic pain affects millions of people worldwide and is often difficult to treat. Two key mechanisms underlying this condition are a loss of the negative control exerted by inhibitory interneurons and an early microglial reaction. Basic features of these mechanisms, however, are still poorly understood. Using the chronic constriction injury of the infraorbital nerve (CCI-IoN) model of neuropathic pain in mice, we have examined the changes in the expression of GAD, the synthetic enzyme of GABA, and GlyT2, the membrane transporter of glycine, as well as the microgliosis that occur at early (5 days) and late (21 days) stages post-CCI in the medullary and upper spinal dorsal horn. Our results show that CCI-IoN induces a down-regulation of GAD at both postinjury survival times, uniformly across the superficial laminae. The expression of GlyT2 showed a more discrete and heterogeneous reduction due to the basal presence in lamina III of ‘patches’ of higher expression, interspersed within a less immunoreactive ‘matrix’, which showed a more substantial reduction in the expression of GlyT2. These patches coincided with foci lacking any perceptible microglial reaction, which stood out against a more diffuse area of strong microgliosis. These findings may provide clues to better understand the neural mechanisms underlying allodynia in neuropathic pain syndromes.


2017 ◽  
Vol 2 ◽  
pp. 13-17 ◽  
Author(s):  
Titilola Akintola ◽  
Charles Raver ◽  
Paige Studlack ◽  
Olivia Uddin ◽  
Radi Masri ◽  
...  

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