Biomedical subjects

Jin Mo Chung

Publications and source records attributed to Jin Mo Chung.

23 records · Page 2Linked to original sources

PubMed1999

Adrenergic sensitivity of the sensory receptors modulating mechanical allodynia in a rat neuropathic pain model.

This study focuses on changes in adrenergic sensitivity in untransected sensory axons that innervate an area of skin made neuropathic by transection of neighboring nerves. The segmental nerve injury model is favorable for this since all axons in the L5 and L6 nerves are transected whereas the L4 axons are intact. Earlier findings are that pain behaviors develop after this injury and that these behaviors are ameliorated by sympathectomy. The present study shows that behavior indicating mechanical allodynia can be rekindled after sympathectomy by intradermal norepinephrine and alpha-2 but not alpha-1 adrenergic ligands and the rekindling can be blocked by alpha-2 but not alpha-1 adrenergic antagonists. By contrast neither intradermal norepinephrine nor other adrenergic agonists or antagonists have any demonstrable effects in the normal or after either neuropathic surgery or sympathectomy alone. These data suggest that the combination of neuropathic surgery and sympathectomy results in an upregulation of active alpha-2 adrenergic receptors on the undamaged sensory axons that provide the remaining sensory innervation to a neuropathic area partially denervated by segmental nerve lesions. These changes on undamaged axons presumably compliment similar changes on the transected axons and, thus play a role in the development of neuropathic pain.

Adrenergic alpha-Agonists↗

PubMed1996

Contributions of injured and intact afferents to neuropathic pain in an experimental rat model.

This study was conducted to determine the contribution of peripheral inputs from injured and intact afferent fibers to behavioral signs of neuropathic pain, using a previously developed neuropathic rat model. Neuropathic injury was produced by tightly ligating the left L5 and L6 spinal nerves; this procedure induced rats to display neuropathic pain behaviors in the ipsilateral hindlimb. The behaviors included signs of mechanical and cold allodynia, as well as ongoing pain. Five days after neuropathic injury, peripheral inputs from injured segments (L5 and L6) or intact segments (L3 and L4) were blocked by either transection of the dorsal roots or application of a local anesthetic (bupivacaine) to the roots. Dorsal rhizotomy of the injured segments reduced all components of neuropathic pain behaviors. In contrast, dorsal rhizotomy of the uninjured segments abolished behavioral signs of mechanical and cold allodynia, but signs of ongoing pain were preserved. Blocking afferent inputs by application of bupivacaine mimicked the results of dorsal rhizotomy, in a reversible manner. These results suggest that afferent signals from injured and intact fibers play distinctively different roles in neuropathic pain: inputs from injured afferents maintain all components of neuropathic pain, while those from intact afferents mediate evoked pain such as mechanical and cold allodynia. An hypothesis is proposed to explain the results of the present as well as other published studies.

Animals↗

PubMed1996

Both motor and sensory abnormalities contribute to changes in foot posture in an experimental rat neuropathic model.

This study was undertaken to find out whether pain contributes to abnormal posture of the foot in rats displaying neuropathic pain behaviors, and if so, whether there is a specific abnormality which reflects the level of pain. We used a rat model of neuropathic pain which is produced by tightly ligating the L5 and L6 spinal nerves just distal to the dorsal root ganglion (DRG). The operation produced neuropathic pain behaviors along with abnormal foot posture as has been shown previously. On the other hand, injury to the same somatic sensory and motor fibers at a more proximal site by sectioning dorsal and ventral roots of the same segments did not produce neuropathic pain behaviors. Rats with dorsal and ventral rhizotomies showed an abnormality of foot posture despite the absence of neuropathic pain behaviors. However, the abnormality in these rats was less severe and lasted for a shorter period of time as compared to rats with spinal nerve ligation. This suggests that peripheral nerve injury in our rat neuropathic pain model produces a foot postural abnormality partially due to motor deficit. However, there is an additional component of the abnormality that is related to sensory function, possibly pain. Close examination of the data indicate that there is no single obvious abnormal foot posture which exclusively represents motor deficit or sensory abnormality. Rather, neuropathic rats are likely to display abnormal foot posture as a result of a complex mixture of motor and sensory abnormalities.

Animals↗

PubMed1994

Behavioral manifestations of an experimental model for peripheral neuropathy produced by spinal nerve ligation in the primate.

A goal of the present study was to document the behavioral changes observed in a model of painful neuropathy in the primate (Macaca fascicularis). A neuropathic state was induced by tight ligation of the L7 spinal nerve, just distal to the L7 dorsal root ganglion. Sensory testing was done on the ventral surface of the foot, a region that includes the L7 dermatome. Within 1 week following surgery, all monkeys (n = 3) developed a marked sensitivity to mechanical stimulation (with a camel hair brush and von Frey hairs), indicating the presence of mechanical allodynia. In 2 animals, the increased sensitivity to mechanical stimulation was also observed on the contralateral side. The threshold for withdrawal to a heat stimulus decreased, indicating the presence of heat hyperalgesia. Presentation of various cooling stimuli, such as acetone and cold water baths, suggested that cold allodynia had also developed. These behavioral phenomena are similar to those seen in humans diagnosed with peripheral neuropathic pain. The behavioral abnormalities are discussed in relation to the responses of spinothalamic tract cells recorded from primates with the same peripheral nerve injury (Palecek et al. 1992).

Animals↗

PubMed1992

An experimental model for peripheral neuropathy produced by segmental spinal nerve ligation in the rat.

We attempted to develop an experimental animal model for peripheral neuropathic pain. Under sodium pentobarbital anesthesia, both the L5 and L6 spinal nerves (group 1) or the L5 spinal nerve alone (group 2) of one side of the rat were tightly ligated. For comparison, a parallel study was conducted with another group of rats (group 3) which received a partial tight sciatic nerve ligation, a paradigm developed previously as a neuropathy model. Withdrawal latencies to application of radiant heat to the foot were tested for the next 16 weeks in all 3 groups. Sensitivity of the hind paw to mechanical stimulation was tested with von Frey filaments. The general behavior of each rat was noted during the entire test period. Results suggested that the surgical procedure in all 3 groups produced a long-lasting hyperalgesia to noxious heat (at least 5 weeks) and mechanical allodynia (at least 10 weeks) of the affected foot. In addition, there were behavioral signs of the presence of spontaneous pain in the affected foot. Therefore, we believe we have developed an experimental animal model for peripheral neuropathy using tight ligations of spinal nerves. The model manifests the symptoms of human patients with causalgia and is compatible with a previously developed neuropathy model. The present model has two unique features. First, the surgical procedure is stereotyped. Second, the levels of injured and intact spinal segments are completely separated, allowing independent experimental manipulations of the injured and intact spinal segments in future experiments to answer questions regarding mechanisms underlying causalgia.

Animals↗