scholarly journals Stereological Study of Changes of GABA-Immunoreactive Neurons in Spinal Dorsal Horn of SNI Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Hong Liu ◽  
Weidong Li ◽  
Binbing Xu ◽  
Jiduan Jiang ◽  
Yuanyuan Zhang ◽  
...  

Objective. To observe the changes in the mechanical withdrawal threshold (MWT) and the proportion of GABA-immunoreactive neurons in spinal dorsal horn (SDH) of the spared nerve injury (SNI) rat model. Methods. Thirty-six healthy male SD rats were randomly divided into a sham-operated group (group D, n = 18 ) and an SNI group (group S, n = 18 ). The left sciatic nerve trunk and three branches were exposed, two of which, known as tibial and the peroneal nerve, were ligated and cut off. The sural nerve was preserved to build the SNI model in group S. The left sciatic nerve trunk and three branches were only exposed in group D. MWT tests were performed on the medial and lateral sides of the rats’ left hindpaw 1 day before surgery and at 7th, 14th, and 28th day after surgery. Results. In group S, compared with the baseline measured 1 day before surgery, MWT on the medial and lateral sides of the rats’ left hindpaw decreased significantly on the 7th, 14th, and 28th days after surgery ( P < 0.05 ), while in group D, there was no statistically significant difference ( P > 0.05 ). Compared with right SDH, there were not statistically significant reductions in the proportions of GABAergic neurons of left SDH on 7th and 28th day after SNI ( P > 0.05 ); however, the proportion of GABAergic neurons in left SDH significantly decreased, compared with that in right side on 14th day after SNI ( P < 0.05 ). On the same way, the proportions of GABAergic neurons on 7th, 14th, and 28th day after surgery were not statistically different ( P > 0.05 ) in group D. Conclusion. The SNI model could reduce the proportion of GABA-immunoreactive neurons in the rat’s spinal dorsal horn on the nerve-injured side, and this change was lasting, which might be related to the transformation of the GABA-immunoreactive neurons.

2008 ◽  
Vol 291 (10) ◽  
pp. 1334-1341 ◽  
Author(s):  
Jing Huang ◽  
Yayun Wang ◽  
Wei Wang ◽  
Yanyan Wei ◽  
Yunqing Li ◽  
...  

2011 ◽  
Vol 105 (6) ◽  
pp. 3010-3021 ◽  
Author(s):  
Hui-Juan Hu ◽  
Robert W. Gereau

Metabotropic glutamate (mGlu) receptors play important roles in the modulation of nociception. Previous studies demonstrated that mGlu5 modulates nociceptive plasticity via activation of ERK signaling. We have reported recently that the Kv4.2 K+ channel subunit underlies A-type currents in spinal cord dorsal horn neurons and that this channel is modulated by mGlu5-ERK signaling. In the present study, we tested the hypothesis that modulation of Kv4.2 by mGlu5 occurs in excitatory spinal dorsal horn neurons. With the use of a transgenic mouse strain expressing enhanced green fluorescent protein (GFP) under control of the promoter for the γ-amino butyric acid (GABA)-synthesizing enzyme, glutamic acid decarboxylase 67 (GAD67), we found that these GABAergic neurons express less Kv4.2-mediated A-type current than non-GAD67-GFP neurons. Furthermore, the mGlu1/5 agonist, (R,S)-3,5-dihydroxyphenylglycine, had no modulatory effects on A-type currents or neuronal excitability in this subgroup of GABAergic neurons but robustly modulated A-type currents and neuronal excitability in non-GFP-expressing neurons. Immunofluorescence studies revealed that Kv4.2 was highly colocalized with markers of excitatory neurons, such as vesicular glutamate transporter 1/2, PKCγ, and neurokinin 1, in cultured dorsal horn neurons. These results indicate that mGlu5-Kv4.2 signaling is associated with excitatory dorsal horn neurons and suggest that the pronociceptive effects of mGlu5 activation in the spinal cord likely involve enhanced excitability of excitatory neurons.


2009 ◽  
Vol 109 (6) ◽  
pp. 2000-2007 ◽  
Author(s):  
Gordana Miletic ◽  
Ashley M. Driver ◽  
Takako Miyabe-Nishiwaki ◽  
Vjekoslav Miletic

Pain ◽  
2010 ◽  
Vol 149 (1) ◽  
pp. 152-159 ◽  
Author(s):  
Gordana Miletic ◽  
Catalina I. Dumitrascu ◽  
Christopher E. Honstad ◽  
Daniela Micic ◽  
Vjekoslav Miletic

2020 ◽  
Author(s):  
Yuchao Fan ◽  
Xiao Liang ◽  
Bixin Zheng ◽  
Li Song

Abstract Background: Morphine is commonly used for treating acute and chronic pain. However, its using is complicated with tolerance and hyperalgesia. Endogenous melatoninergic system is involved in development of tolerance and hyperalgesia induced by chronic morphine administration, but the precise mechanism remains unknown. Methods: 18 male SD rats were randomly divided into Saline(Sal), Morphine(Mor) and Morphine+Chelerythrine (Mor+Che) group (n = 6, respectively). Each group were received twice-daily intrathecal injections of saline (10μl), morphine (15μg/10μl) or morphine (15μg/5μl)+ chelerythrine (5μg/5μl) for consecutive 9 days, respectively. MWT and TWL of all animals were recorded on day 1, 3, 5, 7, 9. The morphine tolerance was depicted as MPAE on day 1, 3, 5, 7, 9 and on day 10 which can be used to calculate for ED50 of each group. Then we determined the serum level of melatonin by ELISA and expression of MOR , MT1, MT2 and PKCγ by RT-qPCR and WB in spinal dorsal horn of three group rats.Results: Comparing with Sal group, the Mor group exhibited a significant lower serum melatonin level and up-regulation of expression of the MT1, MT2 and PKCγ in the spinal dorsal horn. Co-administration of chelerythrine with morphine not only attenuates morphine-induced hyperalgesia and tolerance, but also increases the down-regulation of serum melatonin level) and reduces the up-regulation of expression of MT1 and PKCγ in spinal dorsal horn compared with Mor group. Conclusion:Melatonin can reduce morphine-induced hyperalgesia and tolerance of rats via melatonin-MT1-PKCγ pathway.


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