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Preclinical research indicates that the spinal cord mediates antihyperalgesic effects of serotonin. Whether the’spinal serotonergic hypothesis’ is applicable to the mechanisms by which opioids induce hyperalgesia in chronic opioid users is unknown. This study evaluates the relationship between serotonergic function and pain and analgesia in a chronic opioid user population. Using microdialysis, the present study monitored the release of 5-hydroxyindoleacetic acid (5-HIAA), a metabolite of serotonin, in the dorsal horn of the spinal cord in a previously validated rat model of opioid-induced hyperalgesia. The role of spinal serotonergic function in opioid-induced analgesia was assessed by mechanical allodynia testing after intraplantar or intrathecal coadministration of the serotonin receptor agonist, 1,8-dipropyl-1-naphthalenylpiperazine (D-PHN), with fentanyl, morphine, or buprenorphine. Spinal 5-HIAA was elevated 5h after a 2 mg/kg intravenous dose of fentanyl. Intrathecal D-PHN (0.25-1.25 mM) dose-dependently inhibited the fentanyl-, buprenorphine-, and morphine-induced rise in spinal 5-HIAA. Intrathecal D-PHN did not alter spinal 5-HIAA in rats not previously exposed to opioids. Intrathecal coadministration of D-PHN significantly decreased mechanical allodynia in fentanyl- and morphine-exposed rats but not buprenorphine-exposed animals. These results show that serotonin release in the dorsal horn of the spinal cord contributes to opioid-induced hyperalgesia and that serotonin receptors may not be similarly involved in producing opioid analgesia. The results indicate that the’spinal serotonergic hypothesis’ may be specific to opioid-induced hyperalgesia.Q:

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* This file is part of the UCB release of Plan 9. It is subject to the license
* terms in the LICENSE file found in the top-level directory of this
* distribution and at No
* part of the UCB release of Plan 9, including this file, may be copied,
* modified, propagated, or distributed except according to the terms contained
* in the LICENSE file.
*/

#include
#include
#include “iobuf.h”

int
readline(char *s, int len)
{
int r, eof;
static char buf[256];

r = readn(Stdin, buf, sizeof(buf));
if (r > 0) {
if (r Loss of partially inactivated factor XII (Hageman factor) results in decreased levels of mouse natural antibodies