Biomedical subjects

J S Tang

Publications and source records attributed to J S Tang.

At least 19 recordsLinked to original sources

PubMed2006

Roles of different subtypes of opioid receptors in mediating the ventrolateral orbital cortex opioid-induced inhibition of mirror-neuropathic pain in the rat.

Previous studies have demonstrated that opioid receptors in the prefrontal ventrolateral orbital cortex (VLO) are involved in anti-nociception. The aim of this current study was to examine whether opioid receptors in the VLO have effects on the hypersensitivity induced by contralateral L5 and L6 spinal nerve ligation (SNL), termed as mirror neuropathic pain (MNP) in the male rat. Morphine (1.0, 2.5, 5.0 microg) microinjected into the VLO contralateral to the SNL depressed the mechanical paw withdrawal assessed by von Frey filaments and the cold plate (4 degrees C)-induced paw lifting in a dose-dependent manner on the side without SNL. These effects were antagonized by microinjection of the non-selective opioid receptor antagonist naloxone (1.0 mug) into the same VLO site. Microinjection of endomorphin-1 (5.0 microg), a highly selective mu-opioid receptor agonist, and [d-Ala(2), d-Leu(5)]-enkephalin (DADLE, 10 microg), a delta-/mu-receptor agonist, also depressed the MNP. The effects of both drugs were blocked by selective mu-receptor antagonist beta-funaltrexamine (beta-FNA, 3.75 microg), but the effect of the DADLE was not influenced by the selective delta-receptor antagonist naltrindole (5.0 microg). Microinjection of the kappa-opioid receptor agonist spiradoline mesylate salt (U-62066) (100 microg) had no effect on the MNP. These results suggest that the VLO is involved in opioid-induced inhibition of the MNP and the effect is mediated by mu- (but not delta- and kappa-) opioid receptors.

Afferent Pathways↗

PubMed2004

Mu but not delta and kappa opioid receptor involvement in ventrolateral orbital cortex opioid-evoked antinociception in formalin test rats.

The present study was designed to investigate the roles of different subtypes of opioid receptors in ventrolateral orbital cortex (VLO) opioid-evoked antinociception in formalin test by using an automatic detection system for recording the nociceptive behavior (agitation) and a manual method for detecting the duration of licking the injected paw in the conscious rat. Formalin (5%, 50 microl) s.c. injected into the hindpaw produced a biphasic agitation response or lengthening duration of licking. Morphine (5 microg) microinjected unilaterally into VLO significantly inhibited the agitation response and the licking time, and these effects were blocked by pre-administration of the non-selective opioid receptor antagonist naloxone (1.0 microg) into the same site. Microinjection of endomorphin-1 (5 microg), a selective micro-receptor agonist, and [D-Ala2, D-Leu5]-enkephalin (DADLE, 10 microg), a delta-/micro-receptor agonist also inhibited the nociceptive behaviors, and both the effects were blocked by selective mu-receptor antagonist beta-funaltrexamine hydrochloride (beta-FNA; 3.75 microg), but the DADLE-evoked inhibition was not influenced by the selective delta-receptor antagonist naltrindole (5 microg). Microinjection of selective kappa-receptor agonist (+/-)-trans-U-50488 methanesulfonate salt (1.5 microg) failed to alter the nociceptive behaviors induced by formalin injection. The beta-FNA and naloxone applied into VLO and morphine into the adjacent regions ventral and dorsal to VLO had no effect on the formalin-evoked nociceptive behaviors. These results suggest that mu- but not delta- or kappa-opioid receptor is involved in the VLO opioid-evoked antinociception in formalin test rat.

Animals↗

PubMed2001

Morphine applied to the ventrolateral orbital cortex produces a naloxone-reversible antinociception in the rat.

Our previous findings have indicated that the ventrolateral orbital cortex (VLO) may be involved in modulation of nociception and plays an important role as a higher center of an endogenous analgesic system (a feedback loop) consisting of spinal cord-nucleus submedius (Sm)-VLO-periaqueductal gray (PAG)-spinal cord. To further investigate the neurotransmitter mechanism involved in this nociceptive modulatory pathway, we tested the effects of microinjection of morphine (5 microg, 0.5 microl) into VLO on the tail flick (TF) reflex. The results show that a unilateral microinjection of morphine into VLO dose-dependently suppresses the TF reflex. Furthermore, 6 min after termination of morphine injection, microinjection of opioid receptor antagonist naloxone (1.5 microg, 0.5 microl) into the same VLO site reverses this morphine-evoked inhibition of TF reflex. These results suggest that morphine application to the VLO may directly or indirectly activate VLO neurons projecting to the PAG through the opioid receptor mediation leading to activation of the brainstem descending inhibitory system and depression of the nociceptive inputs at the spinal cord level.

Analgesics, Opioid↗

PubMed2001

Novel reduced benzo[j]fluranthen-3-ones from Cladosporium cf. cladosporioides with cytokine production and tyrosine kinase inhibitory properties.

A series of reduced benzo[j]fluoranthen-3-ones (1-4) was isolated from fermentations of a fungal strain CBUK20700 (CBS 100220), classified as Cladosporium cf. cladosporioides, during a microbial extract screening programme to identify inhibitors of anti-CD28-induced interleukin-2 (IL-2) production by Jurkat E6-1 cells as potential immunosuppressive agents. These compounds were also found to be tyrosine kinase inhibitors. The structures of compounds 1-4 were elucidated by spectroscopic methods including the HMQC, HMBC and NOESY NMR experiments. The most potent compound in the series, (6bS,7R,8S)-7-methoxy-4,8,9-trihydroxy-1,6b,7,8-tetrahydro-2H-benzo[j]fluoranthen-3-one (1) inhibited anti-CD28-induced IL-2 production and Abl tyrosine kinase with IC50 values of 400 and 60 nM respectively. The 6b-stereoisomeric 2 was a moderate inhibitor of both IL-2 production and Abl tyrosine kinase while the 8-oxo derivative 3 was inactive in both assays. The 8-O-methyl ether 4 was a moderate inhibitor of IL-2 production but exhibited potent inhibition of Abl tyrosine kinase with an IC50 of 45 nM.

Antibodies↗

PubMed2000

Surgical treatment for recurrent hepatocellular carcinoma with tumor thrombi in right atrium: using cardiopulmonary bypass and deep hypothermic circulatory arrest.

Tumor in the right atrium creates a life-threatening condition and should be removed immediately. A cirrhotic patient who had recurrent hepatocellular carcinoma (HCC) over remnant liver with tumor thrombi extending to inferior vena cava (IVC) and right atrium presented with impending congestive heart failure. The recurrent tumor and its thrombi were successfully resected en-bloc using cardiopulmonary bypass and hypothermic circulatory arrest. Although the patient's disease-free and actual survival time were only 6 months and 14 months, respectively, he was rescued from heart failure. This aggressive surgical strategy creates further possibility to treat such advanced HCC cases. Further investigations regarding adjuvant therapies in these circumstances, however, are necessary.

Adult↗

PubMed2000

Pain relief after arthroscopic knee surgery: intravenous morphine, epidural morphine, and intra-articular morphine.

OBJECTIVE: The aim of this study was to compare the analgesic efficacy and side effects of intravenous (IV), epidural, and intra-articular (IA) morphine after arthroscopic knee surgery. DESIGN: Prospective, randomized, double-blind clinical investigation. SETTING: Medical center, university teaching hospital. PATIENTS: Inpatients with an American Society of Anesthesiologists physical status of I or II who were scheduled for elective arthroscopic knee surgery. INTERVENTIONS AND OUTCOME MEASURES: A total of 75 patients scheduled for arthroscopic knee surgery under epidural anesthesia were randomly divided into three groups (n = 25 in each group). At the end of surgery, patients in group 1 received 3 mg of IV morphine, patients in group 2 received 3 mg of epidural morphine, and patients in group 3 received 3 mg of IA morphine. Patients were then observed for 24 hours. During the observation period, the proportion of patients requiring rescue analgesia with intramuscular diclofenac in each group was calculated and the occurrence of morphine-related side effects was recorded. RESULTS: We found that patients who received IV morphine requested more rescue analgesia than those who received either epidural or IA morphine. The proportions of patients requiring rescue analgesia in the IV, epidural, and IA groups were 65%, 13%, and 9%, respectively (p < 0.01 in group 1 vs. group 2 and in group 1 vs. group 3). Epidural morphine was associated with higher incidences of nausea and vomiting, pruritus, and urinary retention than IA morphine (range, p < 0.05-0.01 in group 2 vs. group 3). CONCLUSIONS: Patients who received IA morphine consumed less rescue analgesia than those who received IV morphine. They also reported fewer side effects than those patients who received epidural morphine. Intra-articular morphine may be the method of choice for pain relief after arthroscopic knee surgery.

Arthroscopy↗

PubMed1999

Morphine applied to the thalamic nucleus submedius produces a naloxone reversible antinociceptive effect in the rat.

Our previous studies have indicated that the thalamic nucleus submedius (Sm) is involved in nociceptive modulation and plays an important role in an endogenous analgesic system (a feedback loop) consisting of spinal cord - Sm - ventrolateral orbital cortex (VLO) - periaqueductal gray (PAG) - spinal cord. To further investigate the neurotransmitter and receptor mechanisms in this nociceptive modulatory pathway, we tested the effects of microinjection of morphine and naloxone into the Sm on the rat tail flick (TF) reflex. A unilateral microinjection of morphine (8.0 mM, 0.5 microl) into the Sm significantly depressed the TF reflex, whereas a unilateral microinjection of naloxone (5.0 mM, 0.5 microl) into the Sm facilitated the TF reflex. Five minutes after morphine application into Sm, injection of naloxone in this nucleus markedly reversed the inhibition evoked by applying morphine in Sm. These findings suggest that the endogenous opioid peptides may be involved in the antinociceptive effects evoked by activation of the Sm-VLO-PAG pathway which depressed the nociceptive inputs at the spinal level via the brainstem descending inhibitory system, and exert a tonic descending influence.

Analgesia↗

PubMed1999

Inhibitory effects of 5-hydroxytryptamine microinjection into thalamic nucleus submedius on rat tail flick reflex are mediated by 5-HT2 receptors.

Our previous findings indicated that electrical or chemical activation of the thalamic nucleus submedius (Sm) produced significant antinociceptive effects and that these effect were blocked by lesion or depression of the ventrolateral orbital cortex (VLO) or the periaqueductal gray (PAG) suggesting a role of the Sm in modulation of nociception. To further investigate the neurotransmitter mechanism involved in this nociceptive modulatory pathway, we tested the effects of microinjection of 5-hydroxytryptamine (5-HT, 50 mM, 0.5 microl) into Sm on the tail flick (TF) reflex. The results show that a unilateral microinjection of 5-HT into Sm significantly depresses the TF reflex; and that this effect is repeatable and dose-dependent. Furthermore, microinjection of 5-HT2 receptor antagonist cyproheptadine (CPT, 0.3 mM, 0.5 microl) into the same Sm site reverses this 5-HT-evoked inhibition of TF reflex. These results suggest that 5-HT application to the Sm may activate Sm neurons through the 5-HT2 receptors leading to activation of the brainstem descending inhibitory system via the VLO and depression of the nociceptive information at the spinal level.

Animals↗

PubMed1999

Electrically-evoked inhibitory effects of the nucleus submedius on the jaw-opening reflex are mediated by ventrolateral orbital cortex and periaqueductal gray matter in the rat.

In previous studies we have shown that electrical stimulation of the nucleus submedius inhibits the rat radiant heat-induced tail flick reflex, and that this antinociceptive effect is mediated by the ventrolateral orbital cortex and periaqueductal gray. The aim of the present study was to examine whether electrical stimulation of the nucleus submedius could inhibit the rat jaw-opening reflex, and to determine whether electrolytic lesions of the ventrolateral orbital cortex or the periaqueductal gray could attenuate the nucleus submedius-evoked inhibition. Experiments were performed on pentobarbital-anesthetized rats. The jaw-opening reflex elicited by electrical stimulation of the tooth pulp or the facial skin was monitored by recording the evoked digastric electromyogram. Conditioning stimulation was delivered unilaterally to the nucleus submedius 90 ms prior to each test stimulus to the tooth pulp. After that, electrolytic lesions were made in ventrolateral orbital cortex or periaqueductal gray, and the effect of nucleus submedius stimulation on the jaw-opening reflex was re-examined. Unilateral electrical stimulation of nucleus submedius was found to significantly depress the jaw-opening reflex (mean threshold of 28.0+/-1.4 microA, n = 48), and the magnitude of inhibition increased linearly when the stimulus intensity was increased from 20 to 70 microA, resulting in depression of the digastric electromyogram amplitude from 18.4+/-5.4% to 74.0+/-4.9% of the control (P < 0.01, n = 37). The onset of inhibition occured 60 ms after the beginning of nucleus submedius stimulation and lasted about 100 ms, as determined by varying the conditioning-test time interval. Furthermore, ipsilateral lesions of the ventrolateral orbital cortex or bilateral lesions of the lateral or ventrolateral parts of periaqueductal gray eliminated the nucleus submedius-evoked inhibition of the jaw-opening reflex. These data suggest that the nucleus submedius plays an important role in modulation of orofacial nociception, and provide further support for a hypothesis that the antinociceptive effect of nucleus submedius stimulation is mediated by ventrolateral orbital cortex and activation of a descending inhibitory system in the periaqueductal gray.

Animals↗

PubMed1999

Hepatitis viral status in patients undergoing liver resection for hepatocellular carcinoma.

BACKGROUND: Hepatitis B and C viruses are the main causative agents of hepatocellular carcinoma (HCC). The influence of hepatitis viral status on liver resection for HCC remains undetermined. METHODS: Patients who underwent curative resection for HCC were divided into four groups: group 1, seronegative for hepatitis B surface antigen (HBsAg) and antihepatitis C antibody (HCVAb); group 2, seropositive for HBsAg only; group 3, seropositive for HCVAb only; and group 4, seropositive for HBsAg and HCVAb. The clinicopathological characteristics and surgical results of the four groups were compared. Resection of HCC was determined according to liver functional reserve and tumour extent. RESULTS: There were 40, 131, 70 and 20 patients in groups 1, 2, 3 and 4 respectively. Due to patient selection bias, there were significant differences in some background features, resectional extent and pathological characteristics among the four groups. Postoperative morbidity and mortality, as well as the Union Internacional Contra la Cancrum tumour node metastasis stages, did not differ. Patients in group 1 had a higher disease-free survival rate than those in group 2 (P = 0. 02). The actuarial survival rates of patients in groups 2 and 4 were lower than those of groups 1 and 3. CONCLUSION: With careful patient selection, the hepatitis viral status does not influence the surgical risks of hepatectomy for HCC. After liver resection for HCC, the long-term survival rate of patients seronegative for HBsAg is greater than that of patients seropositive for HBsAg.

Aged↗

PubMed1999

Liver resection for hepatocellular carcinoma in octogenarians.

BACKGROUND: Liver resection is risky in patients aged > or = 80 years. Because of short life expectancies and improved nonoperative modalities, the role of liver resection in octogenarians with hepatocellular carcinoma (HCC) is unclear. METHODS: A retrospective review of the operative results of 260 patients with HCC between 1991 and 1997 was performed. According to the age at the time of operation, these patients were divided into 2 groups. Group 1 comprised 21 patients aged > or = 80 years, and group 2 comprised the other 239 younger patients. The backgrounds, pathologic features of the tumor, and operative results of the patients were compared. RESULTS: Octogenarians had a higher incidence of associated medical diseases, a higher incidence of negative serum hepatitis B surface antigen, a lower alpha-fetoprotein level, and a higher indocyanine green retention rate. Although octogenarians had a longer postoperative hospital stay, there were no significant differences between the 2 groups regarding operative morbidity and mortality. The 5-year disease-free and actuarial survival rates for octogenarians and younger patients were 50.6% and 35.3% (P = .15) and 40.9% and 59.3% (P = .46), respectively. CONCLUSION: Under meticulous preoperative assessments and postoperative care, liver resection for HCC is justified in selected octogenarians, with short- and long-term results comparable to those of younger patients.

Actuarial Analysis↗

PubMed1998

Inhibitory effects of electrical stimulation of ventrolateral orbital cortex on the rat jaw-opening reflex.

In previous studies, we have shown that electrically or chemically evoked activation of the ventrolateral orbital cortex (VLO) depresses the rat tail-flick (TF) reflex, and this antinociceptive effect is mediated by the periaqueductal gray (PAG). The aim of the present study was to examine whether electrical stimulation of the VLO could inhibit the rat jaw-opening reflex (JOR), and to determine whether electrolytic lesions of the PAG could attenuate this VLO-evoked inhibition. Unilateral electrical stimulation of the VLO significantly depressed the JOR elicited by tooth pulp or facial skin stimuli, with a mean threshold of 30.5+/-2.3 microA (n=22). Increasing stimulation intensities from 30 to 80 microA resulted in greater reduction of the dEMG amplitude from 22.9+/-5.0% to 69.7+/-3.7% of the baseline value (P<0.01, n=22). The inhibitory effect appeared 50 ms after the beginning of VLO stimulation and lasted about 150 ms, as determined by varying the conditioning-test (C-T) time interval. Unilateral lateral or ventrolateral lesions of the PAG produced only a small attenuation of the VLO-evoked inhibition of the JOR, but bilateral lesions eliminated this inhibition. These findings suggest that the VLO plays an important role in modulation of orofacial nociceptive inputs, and provide further support for the hypothesis that the antinociceptive effect of VLO is mediated by PAG leading to activation of a brainstem descending inhibitory system and depression of nociceptive inputs at the trigeminal level. The role played by VLO in pain modulation is discussed in association with the proposed endogenous analgesic system consisting of medullary cord-Sm-VLO-PAG-medullary cord.

Animals↗

PubMed1998

Prediction and limitation of hepatic tumor resection without blood transfusion in cirrhotic patients.

BACKGROUND: The need for blood transfusion in cirrhotic liver resection is difficult to determine because of inaccurate estimation of operative blood loss. Moreover, blood transfusion is detrimental to cirrhotic patients. OBJECTIVE: To investigate the predictors and limitations of hepatectomy without blood transfusion for cirrhotic patients. DESIGN: Retrospective study. SETTING: University hospital, a tertiary referral center. PATIENTS: A consecutive 163 cirrhotic patients underwent resection for liver tumor(s) under a policy of restrictive blood transfusion. INTERVENTIONS: Estimated blood losses and clinicopathological features of patients who received and those who did not receive a blood transfusion were compared. MAIN OUTCOME MEASURES: Estimated operative blood losses, preoperative assessments, and operative procedures. RESULTS: There were 48 patients in the group who received a blood transfusion, with 1275 +/- 650 mL (mean +/- SE) of blood transfused, and 115 patients in the group who did not receive a blood transfusion. From discriminant analysis, the cutoff value of estimated blood loss for blood transfusion was 1685 mL. Tumor size and site of hepatectomy were found to be independent variables influencing blood transfusion under logistic regression analysis. CONCLUSIONS: Most cirrhotic patients tolerate hepatectomy without blood transfusion when the estimated operative blood loss is less than 1600 mL. Hepatectomy can be performed in cirrhotic patients without blood transfusion if the tumor is small (<5 cm), and/or the resection area is confined to Couinaud segments II, III, and VI. In this study, the largest amount of estimated blood loss in cirrhotic liver resection without blood transfusion was 2350 mL, but the uppermost limit remains to be determined.

Adult↗

PubMed1997

Involvement of the frontal ventrolateral orbital cortex in descending inhibition of nociception mediated by the periaqueductal gray in rats.

Our previous findings which indicated that electrical stimulation of ventrolateral orbital cortex (VLO) can depress the rat tail flick (TF) reflex and that the VLO-evoked inhibitory effect is blocked by electrolytic lesions of periaqueductal gray (PAG) suggest a role of the VLO in the modulation of nociception. To further investigate the involvement of VLO in this nociceptive modulatory pathway, we tested the effects of microinjections of glutamate (200 mM, 0.7 microliter) into the VLO on the TF reflex. An unilateral microinjection of glutamate into the VLO significantly depressed the TF reflex; and this effect was repeatable. Furthermore, bilateral microinjections of gamma-aminobutyric acid (GABA: 100 mM, 0.5 microliter on each side) into the ventrolateral parts of PAG could eliminate this VLO-evoked inhibition of the TF reflex. These results, along with our previous findings provide further support for a hypothesis that VLO, as a higher center in the frontal cortex, plays an important role in modulation of nociception, and this role is mediated by PAG leading to activation of the brainstem descending inhibitory system which depresses the nociceptive information at the spinal level.

Animals↗

PubMed1997

Inhibitory effects of electrically evoked activation of ventrolateral orbital cortex on the tail-flick reflex are mediated by periaqueductal gray in rats.

The present study found in lightly anesthetized rats that the radiant heat-evoked tail flick (TF) reflex was markedly inhibited by a unilateral electrical stimulation (a 20 ms train of 0.2 ms, 100 Hz, 30-100 microA pulses) of the ventrolateral orbital cortex (VLO), with the tail flick latency (TFL) being increased. The mean threshold of VLO stimulation for producing inhibition of the TF reflex was 39.2 +/- 8.7 microA (n = 26), and this inhibitory effect increased following increasing stimulation intensity from 40 to 70 microA. The inhibition developed and remained during the stimulation and disappeared rapidly after termination of the stimulation. When the VLO was stimulated at an intensity of 100 microA in addition to the inhibition an after-facilitation of the TF reflex (a decrease in TFL) was observed at 5-10 s after termination of the stimulation. Bilateral electrolytic lesions of the lateral or ventrolateral parts of the periaqueductal gray matter (PAG) dramatically reduced or eliminated the VLO-evoked inhibition, and the after-facilitation as well. The difference was significant between the TFL changes produced by VLO stimulation before and after PAG lesion (P < 0.01). The results suggest that the antinociception elicited by VLO stimulation is mediated by PAG, leading to activation of the brainstem descending inhibitory system which depresses the nociceptive transmission at the spinal level. The role played by VLO in pain modulation was discussed in association with the proposed endogenous analgesic system consisting of spinal cord-Sm-VLO-PAG-spinal cord.

Animals↗

PubMed1996

Inhibitory effects of electrical stimulation of thalamic nucleus submedius on the nociceptive responses of spinal dorsal horn neurons in the rat.

The aim of the present study is to examine whether stimulation of the thalamic nucleus submedius (Sm) exerts an inhibitory influence on the long latency responses (C-responses) of the spinal cord dorsal horn neurons evoked by noxious cutaneous electrical stimulation, in an attempt to provide electrophysiological evidence for involvement of the Sm in modulation of nociception. Single unit extracellular recordings from the dorsal horn neurons were obtained with glass micropipettes in pentobarbital-anesthetized rats. A total of 71 nociceptive neurons, including 61 wide dynamic range (WDR) and 10 nociceptive specific (NS) neurons, were studied in 29 rats. Electrical stimulation of either ipsilateral or contralateral Sm markedly suppressed the C-responses in most (75%, 53/71) of these neurons, and facilitated the responses in only a few neurons. In general, the inhibitory effect was dependent on both the stimulus intensity and the length of stimulus train, and the stimulus threshold for the inhibition to be elicited was about 50 microA when a 300-ms train of 0.2-ms pulses at 200 Hz was used. The inhibitory effect outlasted the Sm stimulation about 500 ms. Inhibition of C-responses could also be produced by stimulation of the dorsal hypothalamic area (DA). On the other hand, stimulation of the structures in the medial thalamus surrounding Sm had no obvious influences on the C-responses of the dorsal horn neurons. The findings of this study provided further support for the hypothesis that Sm may be implicated in the descending modulation of nociception.

Animals↗

PubMed1995

Inhibitory effects of electrical stimulation of thalamic nucleus submedius area on the rat tail flick reflex.

This study in lightly anesthetized rats found that unilateral electrical stimulation delivered to the ventral part of the thalamic nucleus submedius (Sm), the thalamic reuniens nucleus (Re) and the hypothalamic dorsal area (DA) markedly depressed the TF reflex, and this inhibitory effect increased following increasing stimulation intensity. Stimulation in the dorsal part of Sm did not produce any or only slight depression of the TF reflex. Furthermore, an ipsilateral electrolytic lesion of the ventrolateral orbital cortex (VLO) eliminated the unilateral Sm-evoked inhibition, but not the inhibition elicited by Re and DA and contralateral Sm stimulation. Finally, after bilateral electrolytic lesions of the ventrolateral periaqueductal gray (PAG) the DA and Re and contralateral Sm-evoked inhibitions were also eliminated. The results suggest that the Sm plays an important role in modulation of nociceptive inputs, and this role of Sm is mediated by the VLO and leads to activation of the PAG descending inhibitory system and depression of the nociceptive inputs at the spinal cord level.

Animals↗

PubMed1995

Effects of thalamic nucleus submedius lesions on the tail flick reflex inhibition evoked by hindlimb electrical stimulation in the rat.

Bilateral electrolytic lesions of the thalamic nucleus submedius (Sm) facilitated the TF reflex and attenuated the antinociception evoked by hindlimb electrical stimulation with high intensities in lightly anaesthetized rats. However, the antinociception produced by low intensity hindlimb stimulation was unchanged, except that the after-effect was reduced. The results show that the Sm is probably involved in pain modulation and plays an important role in mediation of the antinociception elicited by high intensity peripheral stimulation.

Animals↗