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Biomedical subjects

B Sung

Publications and source records attributed to B Sung.

11 recordsLinked to original sources
PubMed2001

Decrease in spinal CGRP and substance P is not related to neuropathic pain in a rat model.

We tested the hypothesis that the decrease in spinal levels of SP and CGRP after peripheral nerve injury is related to neuropathic pain. We compared two groups of rats, both of which were subjected to unilateral transection of the inferior and superior caudal trunks between the S1 and S2 spinal nerves. One group exhibited well-developed neuropathic signs after the nerve injury, whereas the other group showed poorly developed signs despite the same nerve injury. The decrease in immunoreactivity of CGRP and SP in the S1 dorsal horn (injured segment) was not significantly different between the two groups. These results suggest that the decrease in spinal levels of CGRP and SP after peripheral nerve injury is not related to neuropathic pain.

Animals↗
PubMed2000

Association of kappa opioid receptor mRNA upregulation in dorsal root ganglia with mechanical allodynia in mice following nerve injury.

This study examined the contribution of nerve injury alone or nerve injury with signs of neuropathic pain to alteration of kappa opioid receptor (KOR) mRNA expression. Two groups of mice, both of them were subjected to unilateral transection of the inferior and superior caudal trunks at the S1spinal nerve, were compared with respect to KOR mRNA expression by reverse transcriptase-polymerase chain reaction. One group showed exclusive pain behavior (PB+) as mechanical allodynia, and the other group exhibited no enhanced sensitivity to innocuous mechanical stimulation to the tail (PB-). Expression of total KOR and variants B and C mRNA increased ipsilaterally in dorsal root ganglia (DRG) of PB+ mice, whereas KOR variant A mRNA was not detected in DRG. These results show that KOR mRNA expression differs between PB+ and PB- groups of mice after nerve injury, and suggest an association of KOR expression with mechanical allodynia.

Animals↗
PubMed2000

Role of signals from the dorsal root ganglion in neuropathic pain in a rat model.

We examined whether signals from the neuroma or the dorsal root ganglion of the injured segment are critical for the generation of neuropathic pain. To this aim, we used a rat model of peripheral neuropathy made by transecting the inferior and superior caudal trunks at the level between the S1 and S2 spinal nerves under enflurane anesthesia. These animals displayed tail-withdrawal responses to normally innocuous mechanical stimulation applied to the tail with a von Frey hair (2 g). Also, these animals, compared to pre-surgical value, displayed shorter tail-withdrawal latencies following immersion of the tail to warm (40 degrees C) or cold (4 degrees C) water. Transection of the S1 spinal nerve between the dorsal root ganglion and neuroma did not change the behavioral signs of neuropathic pain. In contrast, S1 dorsal rhizotomy significantly reduced the behavioral signs. The data suggest that signals arising from the dorsal root ganglion cells of the injured segment, but not from the neuroma, are critical for the generation of neuropathic pain in this model.

Animals↗
PubMed1999

Is sympathetic sprouting in the dorsal root ganglia responsible for the production of neuropathic pain in a rat model?

Partial peripheral nerve injury often results in neuropathic pain that is aggravated by sympathetic excitation and induces sympathetic nerve sprouting in both the injured nerve and corresponding dorsal root ganglia (DRGs). Presently, the functional mechanisms of the interactions between the sprouting and injured somatic afferents remain uncertain. This study was performed to see whether the sprouting in the DRGs plays a key role in the development of neuropathic pain. To this aim, we compared two groups of rats, both of which were subjected to unilateral transection of the superior and inferior caudal trunks at the level between the S1 and S2 spinal nerves, with respect to sympathetic fiber sprouting; one group showed well-developed neuropathic pain behaviors (i.e. mechanical, cold and warm allodynia signs) and the other group showed poorly-developed ones. Immuno-histochemical staining with tyrosine hydroxylase (TH) antibody of the injured S1 DRG taken from both groups of rats after behavioral tests revealed that the magnitude of penetration of TH-positive fibers into the S1 DRG was not significantly different between the two groups. These results suggest that sympathetic nerve sprouting in the injured DRG is not a key factor in the development of neuropathic pain.

Animals↗
PubMed1999

Some membrane property changes following axotomy in A delta-type DRG cells are related to cold allodynia in rat.

Numerous studies have suggested that changes in electrophysiological properties of primary sensory neurons after axonal injury contribute to the generation of neuropathic pain. Presently, however, it is unclear which of the changes is important. To address this issue, we performed behavioral and electrophysiological experiments in a double-blind fashion; we made intracellular recordings in the S1 dorsal root ganglia excised from rats exhibiting cold allodynia behavior after chronic S1 spinal nerve transaction (allodynia-positive group) and from rats lacking such behavior after the same nerve injury (allodynia-negative group) or sham injury (sham group). In this study, we sought which of the membrane property changes produced by the spinal nerve injury in each of C-, Adelta- and Aalpha/beta-cell populations was unique to the allodynia-positive group. Analyses of our data revealed that only some changes in Adelta-cells (e.g. the decrease in resting membrane potential and in the threshold of central process) were more pronounced in or unique to the allodynia-positive group. We concluded that certain membrane property changes in the somata and dorsal root axons of Adelta-cells might be important in the generation of cold allodynia.

Action Potentials↗
PubMed1998

Supraspinal involvement in the production of mechanical allodynia by spinal nerve injury in rats.

This study examined whether or not the production of mechanical allodynia in a rat model of neuropathic pain required an involvement of supraspinal site(s). To this aim, we assessed the effect of spinal cord section at the L1 segment level on the mechanical allodynia sign (i.e. tail flick/twitch response), which was elicited by innocuous von Frey hair stimulation of the tail after unilateral transection of the tail-innervating nerve superior caudal trunk (SCT) at the level between the S3 and S4 spinal nerves. Cord transection or hemisection of the cord ipsilateral to the injured SCT drastically (though not completely) blocked the behavioral sign of mechanical allodynia (leaving noxious pinprick-elicited tail withdrawal reflex intact), whereas sham section or contralateral hemisection of the cord was without effect. These results suggest that the generation of mechanical allodynia following partial peripheral nerve injury involves transmission of the triggering sensory signal to a site(s) rostral to the L1 segment via an ipsilateral pathway(s).

Animals↗
PubMed1998

Amount of sympathetic sprouting in the dorsal root ganglia is not correlated to the level of sympathetic dependence of neuropathic pain in a rat model.

Incomplete peripheral nerve injury often leads to neuropathic pains, some of which are relieved by sympathectomy, and results in sympathetic postganglionic nerve fiber sprouting in the dorsal root ganglion (DRG). This study was performed to see whether the sprouting in the DRG plays a key role in the sympathetic dependence of neuropathic pain. To this aim, we compared two groups of rats, both of which were subjected to unilateral transection of the inferior and superior caudal trunks at the levels between the S1 and S2, S2 and S3, and S3 and S4 spinal nerves, with respect to sympathetic fiber sprouting; one group showed neuropathic pain behaviours (i.e. mechanical and cold allodynia signs) which were very sensitive to phentolamine, alpha adrenergic blocker, and the other group exhibited no sensitivity. Immuno-histochemical staining with tyrosine hydroxylase antibody of the S1-S3 DRGs was not correlated with the sensitivity to phentolamine. These results suggest that the degree of sympathetic dependence of neuropathic pain is not a function of the extent of the sympathetic postganglionic nerve fiber sprouting in the DRG.

Adrenergic alpha-Antagonists↗
PubMed1998

Nitric oxide mediates behavioral signs of neuropathic pain in an experimental rat model.

This study was conducted to determine whether nitric oxide (NO) is involved in the maintenance of behavioral signs of neuropathic pain induced by tightly ligating the left L5 and L6 spinal nerves. Neuropathic rats showed behavioral signs representing mechanical allodynia, cold allodynia and cold-stress exacerbated ongoing pain. Mechanical allodynia was suppressed by Nomega-nitro-L-arginine methyl ester (L-NAME; 200, 100, 50, 10 microM/kg, i.p.), a nitric oxide synthase inhibitor, in a dose-dependent manner. Cold allodynia and cold-stress exacerbated ongoing pain was also attenuated by L-NAME. Neither Nomega-nitro-D-arginine methyl ester (D-NAME; 200 microM/kg) nor saline changed any of the neuropathic pain behaviors. These results suggested that NO plays an important role in the maintenance of the behavioral signs of neuropathic pain and is involved in common steps in the maintenance of the different modalities of pain such as mechanical allodynia and cold allodynia.

Animals↗
PubMed1998

Cell type-specific changes of the membrane properties of peripherally-axotomized dorsal root ganglion neurons in a rat model of neuropathic pain.

Recent evidence indicates that neuropathic pain from partial peripheral nerve injury is maintained by electrophysiologically abnormal signals from injured sensory neurons. To gain an insight into the mechanisms underlying this electrophysiological abnormality, we examined the effects of S1 spinal nerve transection on the membrane properties of S1 dorsal root ganglion neurons one to two weeks after injury. This injury produced significant action potential broadening [40% (1 ms) in C-, 149% (1.5 ms) in A delta- and 84% (0.5 ms) in A alpha/beta-cells], which was primarily due to the enhancement of the "shoulder" appearing on the falling phase of the action potential in C- and A delta-cells and the emergence of a shoulder in A alpha/beta-cells, and significant cell-type specific changes in the time-course of the rising phase of the action potential; i.e. an increase in rise time (A delta: 35%, 0.15 ms; A alpha/beta: 13%, 0.04 ms) and a decrease in the maximal rate of rise (A delta: 17%, 77 V/s; A alpha/beta: 13%, 79 V/s). In addition, the nerve injury led to a significant reduction of the rheobase, an index of neuronal excitability, in all types of cells (by 41% in C-, 71% in A delta- and 59% in A alpha/beta-cells). The reduction of rheobase in A-cells was associated with a concomitant increase in apparent input resistance (by 269% in A delta- and 192% in A alpha/beta-cells), which was measured near the resting membrane potential. By contrast, the rheobase reduction in C-cells was associated with a concurrent depolarizing shift (approximately 4 mV) of the resting membrane potential. The nerve injury-induced reduction of rheobase was not accompanied by related change in input resistance or threshold potential in any of the cell populations. The present results indicate that chronic peripheral axotomy of dorsal root ganglion neurons, which gives rise to neuropathic pain, produces profound changes in the action potential waveform of dorsal root ganglion neurons in a cell type-specific fashion. Furthermore, the results suggest that the axotomy increases the excitability of dorsal root ganglion neurons not by altering input resistance (i.e. leak conductance) or threshold potential, but by increasing apparent input resistance near the resting membrane potential in A-cells and decreasing the resting membrane potential in C-cells.

Action Potentials↗
PubMed1989

Recurrent hypertonic dehydration due to selective defect in the osmoregulation of thirst.

A 6-year-old girl with recurrent episodes of hypertonic dehydration was studied. She denied thirst even with a plasma osmolality as high as 421 mosmol/kg. The hypernatremia was associated with an ability to concentrate urine (854 mosmol/kg). Volume expansion with water corrected hypernatremia (162 to 148 mEq/l) and resulted in an increased urine flow and urinary dilution (137 mosmol/kg) because of suppression of endogenous vasopressin (AVP) release (5.1 pg/ml). Hypertonic saline infusion raised the plasma AVP level (25.6 pg/ml) in response to changes in plasma osmolality (305 to 330 mosmol/kg) and led to a maximal urine osmolality of 818 mosmol/kg. With chronic forced fluid intake, the patient maintained a normal serum sodium concentration (range, 135-145 mEq/l) with a urine osmolality as low as 65 mosmol/kg. These findings are consistent with an isolated defect in the osmoregulation of thirst as the cause of the chronic hypertonic dehydration without deficiency in AVP secretion.

Arginine Vasopressin↗