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James L. Henry - One of the best experts on this subject based on the ideXlab platform.

  • an Inhibitory Postsynaptic Potential in spinal nociceptive neurones is mediated by adenosine through activation of atp sensitive k channels
    Drug Development Research, 1993
    Co-Authors: Michael W. Salter, Yves De Koninck, James L. Henry
    Abstract:

    Inhibitory processes within the dorsal horn participate in regulating the transmission of nociceptive information. Spinal nociceptive neurones are inhibited by cutaneously applied vibration and we have characterized this inhibition physiologically and pharmacologically [Salter et al., 1993]. This inhibition is evoked by activation of Pacinian corpuscle afferents and is mediated in the spinal cord by adenosine acting through P1-purinergic receptors. The adenosine-mediated inhibition of nociceptive neurones by vibration is the result of an Inhibitory Postsynaptic Potential (IPSP) produced by activating a K+ conductance. Adenosine is known to activate K+ currents in a number of different types of cell [Greene and Haas, 1985; Proctor and Dunwiddie, 1987; Segal, 1982; Trussell and Jackson, 1987; Gerber et al. 1989] and it has been reported that in cardiac muscle cells the + channels [Kirsch et al., 1990]. Therefore, we investigated the possibility that these channels might mediate the IPSP we have observed in nociceptive dorsal horn neurones upon vibratory stimulation applied to the skin. We found that the inhibition of nociceptive neurones by this stimulation is abolished by glibenclamide, a blocker of ATP-sensitive K+ Channels [Ashcroft, 1988; Schmid Antomarchi et al., 1987a,b]. In addition, the IPSP evoked by vibratory stimulation was blocked by direct intracellular injection of AYP. These results suggest that the adenosine-mediated IPSP in nociceptive spinal neurones results from activating ATP-sensitive K+ channels in these neurones. As this inhibition of nociceptive dorsal horn neurones may be the physiological basis for the analgesia produced by vibratory stimulation in humans [Bini et al., 1984; Lundeberg, 1984; Lundeberg et al., 1984; Ottoson et al., 1981], We suggest that activation of ATP-sensitive K+ channels ion nociceptive neurones may mediate this analgesia. A diversity of drugs exists which act on ATP-sensitive K+ channels and we further suggest that such drugs might be therapeutically useful in enhancing the analgesia produced by vibration or in producing analgesia on their own. © 1993 Wiley-Liss, Inc.

  • An Inhibitory Postsynaptic Potential in spinal nociceptive neurones is mediated by adenosine through activation of ATP‐sensitive K+ channels
    Drug Development Research, 1993
    Co-Authors: Michael W. Salter, Yves De Koninck, James L. Henry
    Abstract:

    Inhibitory processes within the dorsal horn participate in regulating the transmission of nociceptive information. Spinal nociceptive neurones are inhibited by cutaneously applied vibration and we have characterized this inhibition physiologically and pharmacologically [Salter et al., 1993]. This inhibition is evoked by activation of Pacinian corpuscle afferents and is mediated in the spinal cord by adenosine acting through P1-purinergic receptors. The adenosine-mediated inhibition of nociceptive neurones by vibration is the result of an Inhibitory Postsynaptic Potential (IPSP) produced by activating a K+ conductance. Adenosine is known to activate K+ currents in a number of different types of cell [Greene and Haas, 1985; Proctor and Dunwiddie, 1987; Segal, 1982; Trussell and Jackson, 1987; Gerber et al. 1989] and it has been reported that in cardiac muscle cells the + channels [Kirsch et al., 1990]. Therefore, we investigated the possibility that these channels might mediate the IPSP we have observed in nociceptive dorsal horn neurones upon vibratory stimulation applied to the skin. We found that the inhibition of nociceptive neurones by this stimulation is abolished by glibenclamide, a blocker of ATP-sensitive K+ Channels [Ashcroft, 1988; Schmid Antomarchi et al., 1987a,b]. In addition, the IPSP evoked by vibratory stimulation was blocked by direct intracellular injection of AYP. These results suggest that the adenosine-mediated IPSP in nociceptive spinal neurones results from activating ATP-sensitive K+ channels in these neurones. As this inhibition of nociceptive dorsal horn neurones may be the physiological basis for the analgesia produced by vibratory stimulation in humans [Bini et al., 1984; Lundeberg, 1984; Lundeberg et al., 1984; Ottoson et al., 1981], We suggest that activation of ATP-sensitive K+ channels ion nociceptive neurones may mediate this analgesia. A diversity of drugs exists which act on ATP-sensitive K+ channels and we further suggest that such drugs might be therapeutically useful in enhancing the analgesia produced by vibration or in producing analgesia on their own. © 1993 Wiley-Liss, Inc.

A. Surprenant - One of the best experts on this subject based on the ideXlab platform.

  • Somatostatin‐mediated Inhibitory Postsynaptic Potential in sympathetically denervated guinea‐pig submucosal neurones.
    The Journal of physiology, 1993
    Co-Authors: K Z Shen, A. Surprenant
    Abstract:

    1. Intracellular recordings were made from submucosal neurones in guinea-pig ileum. In some animals, the extrinsic (sympathetic) nerves to the submucosal plexus were severed 5-7 days previously. The actions of somatostatin and somatostatin analogues on membrane Potential, membrane current and Inhibitory Postsynaptic Potentials (IPSPs) were examined. 2. Somatostatin, somatostatin(1-28), [D-Trp8]somatostatin and the somatostatin analogue CGP 23996 all produced equivalent maximum hyperpolarizations or outward currents; half-maximal concentrations (EC50 values) were 9-11 nM. The somatostatin analogue MK 678 had an EC50 of 0.9 nM. Extrinsic sympathectomy did not alter concentration-response relations for somatostatin or its analogues. 3. Somatostatin (> 100 nM) produced hyperpolarization or outward current that declined almost completely during superfusion for 2-4 min; decline of the somatostatin current was exponential with a time constant of 30 s in the presence of 2 microM somatostatin. Desensitization was not altered by extrinsic denervation. 4. Recovery from desensitization was rapid and followed the time course of agonist wash-out. Forskolin, phorbol esters, dithiothreitol, hydrogen peroxide, concanavalin A, or reducing temperature from 35 to 29 degrees C did not alter the time course, degree of, or recovery from desensitization. 5. The somatostatin-induced desensitization was of the homologous type; no cross-desensitization to opiate or alpha 2-adrenoceptor agonists (which activate the same potassium conductance) occurred. 6. Somatostatin desensitization did not alter the adrenergic IPSP seen in sympathetically innervated preparations but abolished the non-adrenergic IPSP recorded from normal preparations and from preparations in which the extrinsic sympathetic nerve supply had been surgically removed. 7. The selective blockade of the non-adrenergic IPSP by the homologous-type somatostatin desensitization characterized in the present study provides strong support for the hypothesis that somatostatin is the neurotransmitter underlying the non-adrenergic IPSP in both normal and extrinsically denervated submucosal neurones.

  • somatostatin mediated Inhibitory Postsynaptic Potential in sympathetically denervated guinea pig submucosal neurones
    The Journal of Physiology, 1993
    Co-Authors: K Z Shen, A. Surprenant
    Abstract:

    1. Intracellular recordings were made from submucosal neurones in guinea-pig ileum. In some animals, the extrinsic (sympathetic) nerves to the submucosal plexus were severed 5-7 days previously. The actions of somatostatin and somatostatin analogues on membrane Potential, membrane current and Inhibitory Postsynaptic Potentials (IPSPs) were examined. 2. Somatostatin, somatostatin(1-28), [D-Trp8]somatostatin and the somatostatin analogue CGP 23996 all produced equivalent maximum hyperpolarizations or outward currents; half-maximal concentrations (EC50 values) were 9-11 nM. The somatostatin analogue MK 678 had an EC50 of 0.9 nM. Extrinsic sympathectomy did not alter concentration-response relations for somatostatin or its analogues. 3. Somatostatin (> 100 nM) produced hyperpolarization or outward current that declined almost completely during superfusion for 2-4 min; decline of the somatostatin current was exponential with a time constant of 30 s in the presence of 2 microM somatostatin. Desensitization was not altered by extrinsic denervation. 4. Recovery from desensitization was rapid and followed the time course of agonist wash-out. Forskolin, phorbol esters, dithiothreitol, hydrogen peroxide, concanavalin A, or reducing temperature from 35 to 29 degrees C did not alter the time course, degree of, or recovery from desensitization. 5. The somatostatin-induced desensitization was of the homologous type; no cross-desensitization to opiate or alpha 2-adrenoceptor agonists (which activate the same potassium conductance) occurred. 6. Somatostatin desensitization did not alter the adrenergic IPSP seen in sympathetically innervated preparations but abolished the non-adrenergic IPSP recorded from normal preparations and from preparations in which the extrinsic sympathetic nerve supply had been surgically removed. 7. The selective blockade of the non-adrenergic IPSP by the homologous-type somatostatin desensitization characterized in the present study provides strong support for the hypothesis that somatostatin is the neurotransmitter underlying the non-adrenergic IPSP in both normal and extrinsically denervated submucosal neurones.

Michael W. Salter - One of the best experts on this subject based on the ideXlab platform.

  • an Inhibitory Postsynaptic Potential in spinal nociceptive neurones is mediated by adenosine through activation of atp sensitive k channels
    Drug Development Research, 1993
    Co-Authors: Michael W. Salter, Yves De Koninck, James L. Henry
    Abstract:

    Inhibitory processes within the dorsal horn participate in regulating the transmission of nociceptive information. Spinal nociceptive neurones are inhibited by cutaneously applied vibration and we have characterized this inhibition physiologically and pharmacologically [Salter et al., 1993]. This inhibition is evoked by activation of Pacinian corpuscle afferents and is mediated in the spinal cord by adenosine acting through P1-purinergic receptors. The adenosine-mediated inhibition of nociceptive neurones by vibration is the result of an Inhibitory Postsynaptic Potential (IPSP) produced by activating a K+ conductance. Adenosine is known to activate K+ currents in a number of different types of cell [Greene and Haas, 1985; Proctor and Dunwiddie, 1987; Segal, 1982; Trussell and Jackson, 1987; Gerber et al. 1989] and it has been reported that in cardiac muscle cells the + channels [Kirsch et al., 1990]. Therefore, we investigated the possibility that these channels might mediate the IPSP we have observed in nociceptive dorsal horn neurones upon vibratory stimulation applied to the skin. We found that the inhibition of nociceptive neurones by this stimulation is abolished by glibenclamide, a blocker of ATP-sensitive K+ Channels [Ashcroft, 1988; Schmid Antomarchi et al., 1987a,b]. In addition, the IPSP evoked by vibratory stimulation was blocked by direct intracellular injection of AYP. These results suggest that the adenosine-mediated IPSP in nociceptive spinal neurones results from activating ATP-sensitive K+ channels in these neurones. As this inhibition of nociceptive dorsal horn neurones may be the physiological basis for the analgesia produced by vibratory stimulation in humans [Bini et al., 1984; Lundeberg, 1984; Lundeberg et al., 1984; Ottoson et al., 1981], We suggest that activation of ATP-sensitive K+ channels ion nociceptive neurones may mediate this analgesia. A diversity of drugs exists which act on ATP-sensitive K+ channels and we further suggest that such drugs might be therapeutically useful in enhancing the analgesia produced by vibration or in producing analgesia on their own. © 1993 Wiley-Liss, Inc.

  • An Inhibitory Postsynaptic Potential in spinal nociceptive neurones is mediated by adenosine through activation of ATP‐sensitive K+ channels
    Drug Development Research, 1993
    Co-Authors: Michael W. Salter, Yves De Koninck, James L. Henry
    Abstract:

    Inhibitory processes within the dorsal horn participate in regulating the transmission of nociceptive information. Spinal nociceptive neurones are inhibited by cutaneously applied vibration and we have characterized this inhibition physiologically and pharmacologically [Salter et al., 1993]. This inhibition is evoked by activation of Pacinian corpuscle afferents and is mediated in the spinal cord by adenosine acting through P1-purinergic receptors. The adenosine-mediated inhibition of nociceptive neurones by vibration is the result of an Inhibitory Postsynaptic Potential (IPSP) produced by activating a K+ conductance. Adenosine is known to activate K+ currents in a number of different types of cell [Greene and Haas, 1985; Proctor and Dunwiddie, 1987; Segal, 1982; Trussell and Jackson, 1987; Gerber et al. 1989] and it has been reported that in cardiac muscle cells the + channels [Kirsch et al., 1990]. Therefore, we investigated the possibility that these channels might mediate the IPSP we have observed in nociceptive dorsal horn neurones upon vibratory stimulation applied to the skin. We found that the inhibition of nociceptive neurones by this stimulation is abolished by glibenclamide, a blocker of ATP-sensitive K+ Channels [Ashcroft, 1988; Schmid Antomarchi et al., 1987a,b]. In addition, the IPSP evoked by vibratory stimulation was blocked by direct intracellular injection of AYP. These results suggest that the adenosine-mediated IPSP in nociceptive spinal neurones results from activating ATP-sensitive K+ channels in these neurones. As this inhibition of nociceptive dorsal horn neurones may be the physiological basis for the analgesia produced by vibratory stimulation in humans [Bini et al., 1984; Lundeberg, 1984; Lundeberg et al., 1984; Ottoson et al., 1981], We suggest that activation of ATP-sensitive K+ channels ion nociceptive neurones may mediate this analgesia. A diversity of drugs exists which act on ATP-sensitive K+ channels and we further suggest that such drugs might be therapeutically useful in enhancing the analgesia produced by vibration or in producing analgesia on their own. © 1993 Wiley-Liss, Inc.

K Z Shen - One of the best experts on this subject based on the ideXlab platform.

  • Somatostatin‐mediated Inhibitory Postsynaptic Potential in sympathetically denervated guinea‐pig submucosal neurones.
    The Journal of physiology, 1993
    Co-Authors: K Z Shen, A. Surprenant
    Abstract:

    1. Intracellular recordings were made from submucosal neurones in guinea-pig ileum. In some animals, the extrinsic (sympathetic) nerves to the submucosal plexus were severed 5-7 days previously. The actions of somatostatin and somatostatin analogues on membrane Potential, membrane current and Inhibitory Postsynaptic Potentials (IPSPs) were examined. 2. Somatostatin, somatostatin(1-28), [D-Trp8]somatostatin and the somatostatin analogue CGP 23996 all produced equivalent maximum hyperpolarizations or outward currents; half-maximal concentrations (EC50 values) were 9-11 nM. The somatostatin analogue MK 678 had an EC50 of 0.9 nM. Extrinsic sympathectomy did not alter concentration-response relations for somatostatin or its analogues. 3. Somatostatin (> 100 nM) produced hyperpolarization or outward current that declined almost completely during superfusion for 2-4 min; decline of the somatostatin current was exponential with a time constant of 30 s in the presence of 2 microM somatostatin. Desensitization was not altered by extrinsic denervation. 4. Recovery from desensitization was rapid and followed the time course of agonist wash-out. Forskolin, phorbol esters, dithiothreitol, hydrogen peroxide, concanavalin A, or reducing temperature from 35 to 29 degrees C did not alter the time course, degree of, or recovery from desensitization. 5. The somatostatin-induced desensitization was of the homologous type; no cross-desensitization to opiate or alpha 2-adrenoceptor agonists (which activate the same potassium conductance) occurred. 6. Somatostatin desensitization did not alter the adrenergic IPSP seen in sympathetically innervated preparations but abolished the non-adrenergic IPSP recorded from normal preparations and from preparations in which the extrinsic sympathetic nerve supply had been surgically removed. 7. The selective blockade of the non-adrenergic IPSP by the homologous-type somatostatin desensitization characterized in the present study provides strong support for the hypothesis that somatostatin is the neurotransmitter underlying the non-adrenergic IPSP in both normal and extrinsically denervated submucosal neurones.

  • somatostatin mediated Inhibitory Postsynaptic Potential in sympathetically denervated guinea pig submucosal neurones
    The Journal of Physiology, 1993
    Co-Authors: K Z Shen, A. Surprenant
    Abstract:

    1. Intracellular recordings were made from submucosal neurones in guinea-pig ileum. In some animals, the extrinsic (sympathetic) nerves to the submucosal plexus were severed 5-7 days previously. The actions of somatostatin and somatostatin analogues on membrane Potential, membrane current and Inhibitory Postsynaptic Potentials (IPSPs) were examined. 2. Somatostatin, somatostatin(1-28), [D-Trp8]somatostatin and the somatostatin analogue CGP 23996 all produced equivalent maximum hyperpolarizations or outward currents; half-maximal concentrations (EC50 values) were 9-11 nM. The somatostatin analogue MK 678 had an EC50 of 0.9 nM. Extrinsic sympathectomy did not alter concentration-response relations for somatostatin or its analogues. 3. Somatostatin (> 100 nM) produced hyperpolarization or outward current that declined almost completely during superfusion for 2-4 min; decline of the somatostatin current was exponential with a time constant of 30 s in the presence of 2 microM somatostatin. Desensitization was not altered by extrinsic denervation. 4. Recovery from desensitization was rapid and followed the time course of agonist wash-out. Forskolin, phorbol esters, dithiothreitol, hydrogen peroxide, concanavalin A, or reducing temperature from 35 to 29 degrees C did not alter the time course, degree of, or recovery from desensitization. 5. The somatostatin-induced desensitization was of the homologous type; no cross-desensitization to opiate or alpha 2-adrenoceptor agonists (which activate the same potassium conductance) occurred. 6. Somatostatin desensitization did not alter the adrenergic IPSP seen in sympathetically innervated preparations but abolished the non-adrenergic IPSP recorded from normal preparations and from preparations in which the extrinsic sympathetic nerve supply had been surgically removed. 7. The selective blockade of the non-adrenergic IPSP by the homologous-type somatostatin desensitization characterized in the present study provides strong support for the hypothesis that somatostatin is the neurotransmitter underlying the non-adrenergic IPSP in both normal and extrinsically denervated submucosal neurones.

Yves De Koninck - One of the best experts on this subject based on the ideXlab platform.

  • an Inhibitory Postsynaptic Potential in spinal nociceptive neurones is mediated by adenosine through activation of atp sensitive k channels
    Drug Development Research, 1993
    Co-Authors: Michael W. Salter, Yves De Koninck, James L. Henry
    Abstract:

    Inhibitory processes within the dorsal horn participate in regulating the transmission of nociceptive information. Spinal nociceptive neurones are inhibited by cutaneously applied vibration and we have characterized this inhibition physiologically and pharmacologically [Salter et al., 1993]. This inhibition is evoked by activation of Pacinian corpuscle afferents and is mediated in the spinal cord by adenosine acting through P1-purinergic receptors. The adenosine-mediated inhibition of nociceptive neurones by vibration is the result of an Inhibitory Postsynaptic Potential (IPSP) produced by activating a K+ conductance. Adenosine is known to activate K+ currents in a number of different types of cell [Greene and Haas, 1985; Proctor and Dunwiddie, 1987; Segal, 1982; Trussell and Jackson, 1987; Gerber et al. 1989] and it has been reported that in cardiac muscle cells the + channels [Kirsch et al., 1990]. Therefore, we investigated the possibility that these channels might mediate the IPSP we have observed in nociceptive dorsal horn neurones upon vibratory stimulation applied to the skin. We found that the inhibition of nociceptive neurones by this stimulation is abolished by glibenclamide, a blocker of ATP-sensitive K+ Channels [Ashcroft, 1988; Schmid Antomarchi et al., 1987a,b]. In addition, the IPSP evoked by vibratory stimulation was blocked by direct intracellular injection of AYP. These results suggest that the adenosine-mediated IPSP in nociceptive spinal neurones results from activating ATP-sensitive K+ channels in these neurones. As this inhibition of nociceptive dorsal horn neurones may be the physiological basis for the analgesia produced by vibratory stimulation in humans [Bini et al., 1984; Lundeberg, 1984; Lundeberg et al., 1984; Ottoson et al., 1981], We suggest that activation of ATP-sensitive K+ channels ion nociceptive neurones may mediate this analgesia. A diversity of drugs exists which act on ATP-sensitive K+ channels and we further suggest that such drugs might be therapeutically useful in enhancing the analgesia produced by vibration or in producing analgesia on their own. © 1993 Wiley-Liss, Inc.

  • An Inhibitory Postsynaptic Potential in spinal nociceptive neurones is mediated by adenosine through activation of ATP‐sensitive K+ channels
    Drug Development Research, 1993
    Co-Authors: Michael W. Salter, Yves De Koninck, James L. Henry
    Abstract:

    Inhibitory processes within the dorsal horn participate in regulating the transmission of nociceptive information. Spinal nociceptive neurones are inhibited by cutaneously applied vibration and we have characterized this inhibition physiologically and pharmacologically [Salter et al., 1993]. This inhibition is evoked by activation of Pacinian corpuscle afferents and is mediated in the spinal cord by adenosine acting through P1-purinergic receptors. The adenosine-mediated inhibition of nociceptive neurones by vibration is the result of an Inhibitory Postsynaptic Potential (IPSP) produced by activating a K+ conductance. Adenosine is known to activate K+ currents in a number of different types of cell [Greene and Haas, 1985; Proctor and Dunwiddie, 1987; Segal, 1982; Trussell and Jackson, 1987; Gerber et al. 1989] and it has been reported that in cardiac muscle cells the + channels [Kirsch et al., 1990]. Therefore, we investigated the possibility that these channels might mediate the IPSP we have observed in nociceptive dorsal horn neurones upon vibratory stimulation applied to the skin. We found that the inhibition of nociceptive neurones by this stimulation is abolished by glibenclamide, a blocker of ATP-sensitive K+ Channels [Ashcroft, 1988; Schmid Antomarchi et al., 1987a,b]. In addition, the IPSP evoked by vibratory stimulation was blocked by direct intracellular injection of AYP. These results suggest that the adenosine-mediated IPSP in nociceptive spinal neurones results from activating ATP-sensitive K+ channels in these neurones. As this inhibition of nociceptive dorsal horn neurones may be the physiological basis for the analgesia produced by vibratory stimulation in humans [Bini et al., 1984; Lundeberg, 1984; Lundeberg et al., 1984; Ottoson et al., 1981], We suggest that activation of ATP-sensitive K+ channels ion nociceptive neurones may mediate this analgesia. A diversity of drugs exists which act on ATP-sensitive K+ channels and we further suggest that such drugs might be therapeutically useful in enhancing the analgesia produced by vibration or in producing analgesia on their own. © 1993 Wiley-Liss, Inc.