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R R Ji

Publications and source records attributed to R R Ji.

29 records · Page 2Linked to original sources
PubMed1995

Central and peripheral expression of galanin in response to inflammation.

Using in situ hybridization, immunohistochemistry and receptor binding methodology, the galanin messenger RNA levels, galanin binding and galanin-like immunoreactivity were examined in rats injected with carrageenan into the left hindpaw. Three days after injection, a distinct increase (63%) in galanin messenger RNA-positive neurons was observed in the medial laminae I and II of the ipsilateral dorsal horn (lumbar 4 and 5) as compared to the contralateral side. However, no alteration was found in galanin binding and galanin-like immunoreactivity in the dorsal horn. In dorsal root ganglia (lumbar 5), inflammation induced a significant decrease in galanin messenger RNA (39%) and galanin peptide (47%) on the ipsilateral side. Galanin binding was not detected in dorsal root ganglia, neither on the inflammatory nor on the control side. Increased levels of galanin-like immunoreactivity and galanin messenger RNA were seen in cells in the inflamed dermis and epidermis, especially in stratum granulosum. Most of the galanin-immunoreactive cells contained ED1-like immunoreactivity, a marker for macrophages. A strong galanin binding was seen in the inflamed dermis. Such binding sites may be targets for galanin released from local cells in inflamed dermis. Taken together, our results suggest that both neuronal and non-neuronal galanin or a galanin-like peptide is involved in the response to inflammation.

Animals↗
PubMed1995

Expression of mu-, delta-, and kappa-opioid receptor-like immunoreactivities in rat dorsal root ganglia after carrageenan-induced inflammation.

Recently, antisera that recognize unique epitopes of the cloned mu-, delta-, and kappa-opioid, receptors (MOR, DOR, KOR, respectively) have been developed. In the present study MOR-, DOR-, and KOR-like immunoreactivities (LIs) were examined in rat dorsal root ganglia (DRGs, L4-5) after injection of carrageenan (CAR) into the hindpaw. In normal control rats 20.9%, 13.5%, and 9% of the DRG neurons contained MOR-, DOR-, KOR-LI, respectively. A marked upregulation in MOR-LI was observed in DRG neurons 1 and 3 d after inflammation. In contrast, CAR induced a distinct downregulation in DOR- and KOR-LIs. MOR-, DOR-, and KOR-LIs were preferentially localized in small DRG neurons. MOR-LI was often located in patches in the cytoplasm, and in some cells close to the somatic plasmalemma. However, DOR- and KOR-LIs mainly showed a diffuse staining pattern within cytoplasm. Two or even all three receptors could sometimes be found to coexist in DRG neurons. In the spinal cord, these receptors were mainly confined to the superficial dorsal horn, with a somewhat diffuse staining which was strong for MOR-LI, and weak for KOR-LI. DOR-LI had distinctly punctate, varicose distribution. CAG induced-alterations in opioid receptor staining in spinal cord were much less pronounced than those in the DRGs with a small increase in MOR-LI and a slight decrease in DOR-LI ipsilaterally. There was an accumulation of all three types of receptors in the sciatic nerve both proximal and distal to the ligation site as early as 2 hr, indicating both antero- and retrograde transport of multiple opioid receptors. However, DOR-LI accumulation was stronger than that of MOR- and KOR-LIs. Taken together, these results suggest that all three opioid receptors are involved in the response to inflammation and that they may play different roles in this pathological state. The coexistence of MOR, DOR, and KOR in at least some primary sensory neurons provides a substrate for functional interactions between these receptors.

Animals↗
PubMed1994

Galanin antisense oligonucleotides reduce galanin levels in dorsal root ganglia and induce autotomy in rats after axotomy.

Antisense (AS) oligonucleotides (ONs) to galanin (GAL) were applied to the proximal end of a transected sciatic nerve, allowing their cellular uptake and transport into injured axons. GAL expression in dorsal root ganglia and self-mutilation behavior (autotomy) were then studied. AS-ONs with phosphorothioate or allyl modifications significantly suppressed the axotomy-induced increase in GAL levels, as demonstrated by immunohistochemistry and exaggerated autotomy behavior, whereas no significant effect on GAL mRNA levels could be demonstrated with in situ hybridization. Allyl-ONs were more effective than phosphorothioate-ONs. An AS-ON with three base mismatches did not induce any of the above effects. These results support the view that the inhibition of axotomy-induced GAL up-regulation is related to autotomy.

Animals↗
PubMed1994

Increased expression of galanin in the rat superior cervical ganglion after pre- and postganglionic nerve lesions.

Using immunohistochemistry the expression of galanin (GAL) and galanin message-associated peptide (GMAP) in the superior cervical ganglion (SCG) was investigated 2, 4, 7, and 14 days after unilateral transection of the cervical sympathetic trunk (decentralization) or after cutting the external and internal carotid nerves (axotomy), as well as 7 days after removal of parotid gland tissue. In control SCGs including the sympathetic trunk and the carotid nerves, very few neurons and fibers were GAL/GMAP-positive. Two and 7 days after decentralization, about 5% of all counted neuron profiles in the ipsilateral SCG were GAL/GMAP immunoreactive. Immunoreactive cell bodies were distributed throughout the SCG, with a greater number in the most caudal portion of the ganglion. Many GAL/GMAP-positive nerve fibers were observed in the whole SCG, with strongly fluorescent bundles of immunoreactive fibers accumulated at the caudal end of the SCG. Several GAL/GMAP-immunoreactive nerve fibers were seen ipsilaterally in the external carotid nerve, whereas only a few positive fibers could be observed in the internal carotid nerve. About 2% of all counted neuron profiles in SCGs ipsilateral to decentralization still contained GAL/GMAP-immunoreactivity 14 days after the operation. The number of GAL/GMAP-positive cell bodies was at least doubled in the contralateral SCGs after decentralization compared to controls. After axotomy, about 50% of all counted neuron profiles were GAL/GMAP-positive in the ipsilateral SCG and distributed throughout the SCG. A strong accumulation of immunoreactive nerve fibers was observed in both the internal and external carotid nerves. The number of GAL/GMAP-positive cell bodies was slightly increased in the contralateral SCGs. After unilateral removal of parotid gland tissue, many GAL/GMAP-positive cell bodies and some fibers were observed in the caudal half of the ipsilateral SCG. The number of immunoreactive nerve fibers was increased also in the external carotid nerve, but not in the internal carotid nerve. In situ hybridization revealed prepro GAL mRNA in about 5% of all SCG neuron profiles in decentralized SCGs, paralleling the increase seen in GAL/GMAP peptide content. There was also a small increase in prepro VIP mRNA-positive cells in the caudal part of the SCG. The present results indicate that both pre- and postganglionic lesions increase the content of GAL/GMAP in the SCG, with a much more pronounced increase after transection of the carotid nerves.

Animals↗
PubMed1994

Expression of neuropeptide Y and neuropeptide Y (Y1) receptor mRNA in rat spinal cord and dorsal root ganglia following peripheral tissue inflammation.

By using in situ hybridization histochemistry and immunohistochemistry, neuropeptide Y (NPY) and NPY (Y1) receptor mRNA as well as NPY-like immunoreactivity were examined in the lumbar spinal cord (L4-L5) and in dorsal root ganglia (DRG, L5) in rats injected with complete Freund's adjuvant (CFA) into the hindpaw. A rapid and marked increase in NPY mRNA expression was observed in ipsilateral dorsal horn neurons 6 hr after inoculation as compared to the contralateral side. This was mainly found in the medial part of spinal lamina II. The peak level (88% increase) was reached at 3 d. In adjacent sections of the spinal cord, 96% and 33% increases were found in the number of dynorphin and enkephalin mRNA-positive neurons, respectively. Unilateral inflammation also induced a moderate increase in NPY-like immunoreactivity and the number of NPY-immunoreactive neurons in the medial part of the ipsilateral spinal dorsal horn. In addition, a marked elevation in the expression of c-Fos-like protein was observed in ipsilateral spinal neurons in laminae I, II, and V. However, no NPY mRNA-positive or NPY-immunoreactive neurons were found in the ipsilateral and contralateral DRGs in rats receiving CFA injection. Furthermore, a marked upregulation of NPY (Y1) receptor mRNA expression was detected in the ipsilateral spinal dorsal horn 1 d and 3 d after inoculation. These Y1 receptor mRNA-positive cells were mainly distributed in the medial laminae II and III. Numerous Y1 mRNA-positive, small neuron profiles were found bilaterally in the DRGs in CFA-treated rats. CFA evoked a 34% increase in the number of Y1 mRNA-positive neurons in ipsilateral DRGs as compared to contralateral DRGs. The distinct upregulation of NPY and NPY (Y1) receptor in response to peripheral inflammation suggests an involvement of NPY in the response to inflammation and in nociception.

Animals↗
PubMed1994

Topical capsaicin treatment suppresses formalin-induced fos expression in rat spinal cord.

Capsaicin (Cap) is a pharmacological tool to inactivate nociceptive afferents. The present study was undertaken to investigate the effects of topical application of Cap to sciatic nerve on the formalin-induced expression of proto-oncogene proteins c-fos in the rat spinal cord using immunohistochemical display of fos-like protein. In rats subjected to formalin injection into the hind paw, numerous fos-like immunoreactivity (FLI) neurons were found in the spinal dorsal horn, with heavy labeling in laminae I-II and V-VI. Following pretreatment of Cap, formalin-induced FLI expression was significantly abolished. It was suggested that activation of Cap-sensitive unmyelinated nociceptive afferents following formalin injection was primarily responsible for the activation of c-fos gene. Our data also provided further evidence supporting that topical application was an effective way to block the transmission of noxious primary afferents.

Animals↗
PubMed1993

Induction of c-fos expression in the rostral medulla of rats following electroacupuncture stimulation.

The present study was designed to examine the induction of c-fos mRNA and Fos-like protein in the rostral medulla of awake rats following electroacupuncture (EA) stimulation, using in situ hybridization and immunohistochemical method. Rats were subjected to EA stimulation (100 Hz, 1-2-3 mA) for 30 min by inserting two needles into acupoints Zusanli (S36) and Sanyingjiao (Sp6) of each hind leg. Animals were sacrificed 1h and 2h after EA for in situ hybridization and immunohistochemical study, respectively. c-fos mRNA or Fos-like-immunoreactivity (FLI) neurons were densely distributed in the rostral ventromedial medulla (RVM), including raphe magnus nucleus, gigantocellular reticular nucleus, gigantocellular reticular nucleus alpha, as well as intermediate reticular nucleus. Neurons in the solitary tract nucleus also showed c-fos expression. The results suggest that the RVM may be an important region for mediating EA effect.

Afferent Pathways↗
PubMed1993

[Electroacupuncture enhances enkephalin mRNA expression in the spinal cord and medulla, an in situ hybridization study].

Previous studies in this laboratory have shown that electroacupuncture (EA) accelerated the release of enkephalin in the spinal cord. The present study was undertaken to investigate the effect of EA stimulation on the expression of preproenkephalin (PPE) mRNA in the rat spinal cord and medulla by in situ hybridization histochemical technique. Animals were administrated with 2 Hz EA stimulation (1-2-3 mA, 30 min) applied at acupoints sanyingjiao and zusanli of one hind leg. The rats were perfused 24 h after EA, and quantitative changes of PPE-mRNA expression were determined by emulsion autoradiography. EA stimulation was found to increase the number of neurons expressing PPE-mRNA in spinal cord and medulla. Increased expression of PPE-mRNA was more marked in ipsilateral dorsal horn of spinal cord (especially in laminae III-IV and contralateral ventromedial medulla (especially in the lateral paragigantocellular reticular nucleus). The results provide evidence in support of the enkephalinergic hypothesis of acupuncture analgesia. It is suggested that increased biosynthesis of enkephalin precursor would help to compensate for the loss of tissue storage of enkephalin during the period of EA stimulation.

Animals↗
PubMed1992

[Induction of Fos-like protein in the rat spinal cord following electroacupuncture stimulation].

The expression of the c-fos proto-oncogene has been regarded as a marker for noxious stimulation. We now report that electroacupuncture (EA) stimulation (100 Hz, 0.3 ms, 1-2-3 mA, 30 min) delivered into the acupoint Sanyinjiao (SP6) could also induce the c-fos expression in the rat spinal cord as demonstrated by immunohistochemical technique using antibody against the c-fos protein product Fos. In rats receiving EA stimulation, numerous cells with Fos-like immunoreactivity (FLI) were observed in both dorsal and ventral horn of the spinal cord with dense labelling in laminae III and IV of the ipsilateral side. Only scattered FLI cells were found in laminae I and II. In contrast, FLI evoked by noxious stimulation (5% formalin injected at the hindfoot subcutaneously) was shown mainly in laminae I and II, rather than in III and IV. The c-fos expression was very low in control animals receiving neither formalin nor EA administration. The present study indicates that the site specificity of the c-fos expression induced by EA is different from that evoked by noxious stimulation. The possibility that EA-induced Fos protein might participate in acupuncture analgesia is currently under investigation.

Animals↗