The Experts below are selected from a list of 9 Experts worldwide ranked by ideXlab platform

Xi-cheng Li - One of the best experts on this subject based on the ideXlab platform.

  • Effect of 5-HT on pain modulation of substance P in spinal cord of rats.
    Acta Pharmacologica Sinica, 1995
    Co-Authors: Huai-zhen Ruan, Xi-cheng Li
    Abstract:

    AIM: To study the effect of serotonin (5-HT) on pain modulation of substance P (SP) in spinal cord of rats. METHODS: Using immunohisto-chemistry and measurement of pain threshold. RESULTS: The c-fos expression evoked by intrathecal injection (it) SP 10 micrograms and sc 5% formaldehyde (For) 150 microL in the hindpaw was densely distributed in the laminae I, II, V, and VI of spinal dorsal horn. The pain threshold in the SP group was decreased while the pain intensity rating measured by behavioral method in the For group was increased. The c-fos expression induced by it 5-HT 20 micrograms was mostly distributed in the spinal dorsal horn in laminae III-IV and the pain threshold was increased. SP and For induced c-fos expressions in the spinal cord and the pain responses were reduced by 5-HT and increased by 5-HT depletor Fenclonine 300 mg.kg-1. CONCLUSION: SP mainly played an algogenesia in the spinal cord. 5-HT inhibited the c-fos expression in the spinal cord evoked by SP and participated in pain modulation of SP.

F. Sicuteri - One of the best experts on this subject based on the ideXlab platform.

  • Eosinophilia Myalgia Syndrome
    Advances in Experimental Medicine and Biology, 1996
    Co-Authors: M. Nicolodi, F. Sicuteri
    Abstract:

    The serotonin theory of migraine (M) we proposed in the seventies indicated a pivotal role of serotonin in mechanism of M (Sicuteri et al., 1974). The analgesizing role of the indolamine was then stressed (Yaksh et al., 1977, Fields and Anderson, 1978). We began to study the serotonin mechanism in primary headache in the sixties. At that time we hypothesized that serotonin could have had a mainly excitatory effect on polymodal receptors. Their serotonin-mediated activation was supposed to evoke headache pain. This theory re-emerged in recent years, in spite of the fact that substantial data showing have been obtained indicating that M, as well as other related primary pains, are caused chiefly by a failure of serotonergic analgesizing systems in the CNS (Sicuteri et al., 1973, Sicuteri et al, 1978, Del Bianco et al., 1982, Rajiv et al., 1989, Lance, 1992). As a matter of fact, serotonin is a transmitter characterized by a double-faceted effect, in that it is a pain-sensitising agent at the periphery (by acting on polymodal receptors) (Sicuteri et al., 1965), whereas it displays an evident antinociceptive effect by activating serotonergic analgesizing systems in the CNS. The centrally mediated analgesizing effect seems to largely overcome the pain-sensitising peripheral effect of the amine (Kimball et al., 1960). Among the more convincing outcomes supporting this assumption we can cite the effect of Fenclonine, which we tested first in the late sixties (Sicuteri et al., 1973, Sicuteri et al., 1978). Fenclonine is a potent and irreversible inhibitor of tryptophan (Trp) hydroxylase, the rate-limiting enzyme in serotonin biosynthesis. When Fenclonine is administered, enzyme activity is reduced in both cell bodies and nerve terminals.

Huai-zhen Ruan - One of the best experts on this subject based on the ideXlab platform.

  • Effect of 5-HT on pain modulation of substance P in spinal cord of rats.
    Acta Pharmacologica Sinica, 1995
    Co-Authors: Huai-zhen Ruan, Xi-cheng Li
    Abstract:

    AIM: To study the effect of serotonin (5-HT) on pain modulation of substance P (SP) in spinal cord of rats. METHODS: Using immunohisto-chemistry and measurement of pain threshold. RESULTS: The c-fos expression evoked by intrathecal injection (it) SP 10 micrograms and sc 5% formaldehyde (For) 150 microL in the hindpaw was densely distributed in the laminae I, II, V, and VI of spinal dorsal horn. The pain threshold in the SP group was decreased while the pain intensity rating measured by behavioral method in the For group was increased. The c-fos expression induced by it 5-HT 20 micrograms was mostly distributed in the spinal dorsal horn in laminae III-IV and the pain threshold was increased. SP and For induced c-fos expressions in the spinal cord and the pain responses were reduced by 5-HT and increased by 5-HT depletor Fenclonine 300 mg.kg-1. CONCLUSION: SP mainly played an algogenesia in the spinal cord. 5-HT inhibited the c-fos expression in the spinal cord evoked by SP and participated in pain modulation of SP.

M. Nicolodi - One of the best experts on this subject based on the ideXlab platform.

  • Eosinophilia Myalgia Syndrome
    Advances in Experimental Medicine and Biology, 1996
    Co-Authors: M. Nicolodi, F. Sicuteri
    Abstract:

    The serotonin theory of migraine (M) we proposed in the seventies indicated a pivotal role of serotonin in mechanism of M (Sicuteri et al., 1974). The analgesizing role of the indolamine was then stressed (Yaksh et al., 1977, Fields and Anderson, 1978). We began to study the serotonin mechanism in primary headache in the sixties. At that time we hypothesized that serotonin could have had a mainly excitatory effect on polymodal receptors. Their serotonin-mediated activation was supposed to evoke headache pain. This theory re-emerged in recent years, in spite of the fact that substantial data showing have been obtained indicating that M, as well as other related primary pains, are caused chiefly by a failure of serotonergic analgesizing systems in the CNS (Sicuteri et al., 1973, Sicuteri et al, 1978, Del Bianco et al., 1982, Rajiv et al., 1989, Lance, 1992). As a matter of fact, serotonin is a transmitter characterized by a double-faceted effect, in that it is a pain-sensitising agent at the periphery (by acting on polymodal receptors) (Sicuteri et al., 1965), whereas it displays an evident antinociceptive effect by activating serotonergic analgesizing systems in the CNS. The centrally mediated analgesizing effect seems to largely overcome the pain-sensitising peripheral effect of the amine (Kimball et al., 1960). Among the more convincing outcomes supporting this assumption we can cite the effect of Fenclonine, which we tested first in the late sixties (Sicuteri et al., 1973, Sicuteri et al., 1978). Fenclonine is a potent and irreversible inhibitor of tryptophan (Trp) hydroxylase, the rate-limiting enzyme in serotonin biosynthesis. When Fenclonine is administered, enzyme activity is reduced in both cell bodies and nerve terminals.

Zhi-ming Xu - One of the best experts on this subject based on the ideXlab platform.

  • Anxiogenic effect of naltrexone in social interaction test in rats
    Acta Pharmacologica Sinica, 1996
    Co-Authors: Han-xia Zhang, Zhi-ming Xu
    Abstract:

    AIM: To study the anxiogenic effect of naltrexone (Nal) on the emotional state of rats. METHODS: The duration of active interaction was measured in the social interaction test in rats. RESULTS: Without influence on the locomotor activity, Nal (0.1-50 mg.kg-1) dose- and time-dependently decreased the duration of active interaction, which was antagonized by morphine (5 mg.kg-1) or Fenclonine (Fen, 150 mg.kg-1 x 3 d) and was enhanced by 5-hydroxytryptophan (5-HTP, 50 mg.kg-1). CONCLUSIONS: Nal produced anxiety via its blockade of opioid receptors; central opioidergic neurons were involved in the regulation of anxiety through their tonic inhibitions in serotonergic neurons.