OBJECTIVES: The purpose of this study was to investigate the effects of methysergide(serotonin receptor antagonist) on serum growth hormone response after electroconvulsive therapy(ECT). METHODS: We studied the changes of the serum growth hormone levels of the day before ECT(No ECT), ECT without methysergide pretreatment(ECT alone), and ECT with methysergide pretreatment(M+ECT) by radioimmunoassay method in 14 psychiatric patients. ECT was induced by the application of 110 volts for a period 0.3-1.0 second, using bitemporal electrodes. RESULTS: 1) Serum growth hormone levels at 15, 30, and 60 minutes after ECT were significantly increased in the ECT alone group than in the No ECT group(p<0.05). 2) Serum growth hormone levels at 15, 30, and 60 minites after ECT were significantly decreased in the M+ECT group than in the ECT alone group(p<0.05). CONCLUSION: These results suggest that the response of growth hormone after ECT seems to be mediated by the activation of serotonergic system.
Electroconvulsive Therapy* ; Electrodes ; Growth Hormone* ; Humans ; Methysergide* ; Radioimmunoassay

Melittin-induced tonic pain model is characterized by local inflammation, edema, spontaneous flinchings, and sustained mechanical hypersensitivity. These nociceptive responses are mediated through selective activation of capsaicin-sensitive primary afferent fibers by melittin. The present study was undertaken to elucidate the role of peripheral 5-hydroxytryptamine (5-HT) receptors in the melittin-induced nociceptive responses. Changes in mechanical threshold, flinching behaviors and paw thickness were measured in rat intraplantarly injected with melittin (40microgram/paw) alone or treated together with melittin and 5-HT receptor antagonists. WAY-100635 (100microgram & 200microgram/paw), isamoltane hemifumarate (100microgram & 200microgram/paw), methysergide maleate (60microgram, 120microgram & 200microgram/paw) and ICS-205,930 (100microgram & 200microgram/paw) were intraplantarly injected 20 min before melittin injection. All 5-HT receptor antagonists tested in this experiment significantly attenuated the ability of melittin to reduce mechanical threshold and to induce flinching behaviors. 5-HT receptor antagonists, except ICS-205,930, had mild inhibitory effect on melittin-induced edema. These experimental findings suggest that multiple peripheral 5-HT receptors are involved in the melittin-induced nociceptive responses.
Animals ; Edema ; Hypersensitivity ; Inflammation ; Melitten ; Methysergide ; Rats* ; Receptors, Serotonin ; Serotonin*

The mechanism of serotonin(5-HT) induced contraction and Ca++ mobilization was investigated in right cut from rat aorta. Since it is known that 5-HT can interact with alpha-adrenoceptors in addition to a specific action on 5-HT receptors, the effects alpha-adrenoceptors antagonists on these contractile responses to 5-HT were investigated. The results are as follows : 1) 5-HT produced a strong transient contraction and a concentration dependent contraction. 2) The contractile tension to 5-HT increased with extracellular Ca++ concentration (0.1-5mM). 3) The response produced by rings exposed to Ca++-free PSS was significantly weaker than that produced by rings exposed to calcium containing PSS. When rings of aorta that had been stimulated with 5-HT once for 30 min in Ca++-free TBT were washed 4 times for at least; 20 min in zero Ca++PSS to remove 5-HT, than reexposed to 5-HT in Ca++-free TBT, a phasic contraction was not seen during the second stimulation with 5-HT. 4) The contractile response of 5-HT was inhibited by alpha-adrenergic receptor blocker, phenoxybenzamine and phentolamine. Phentolamine(10(-8)M) antagonized response to high concentrations of 5-HT but responses to low concentrations of 5-HT were not antagonized. 5) The contraction induced by 5-HT in Ca++-free PSS was investigated with phentolamin, methysergide. It was blocked by methysergide but not blocked by phentolamine. 6) These results suggest that 5-HT -induced contraction is the effect of both transmembrane Ca++ influx and the mobilization of intracellular Ca++. Low concentration of 5-HT act on specific 5-HT receptors but high concentration of 5-HT also act on alpha-adreno-receptors.
Animals ; Aorta* ; Calcium ; Methysergide ; Phenoxybenzamine ; Phentolamine ; Rats* ; Receptors, Adrenergic ; Receptors, Serotonin ; Serotonin

Retroperitoneal fibrosis is a fibroproliferative process involving the retroperitoneum. It may be idiopathic or can be caused by methysergide ingestion, perianeurysmal inflammation, a leaking aneurysm, urinoma or irradiation. The symptoms and signs of retroperitoneal fibrosis are variable, and for diagnosis, imaging is therefore essential. The typical imaging finding is a fibrotic lesion in front of the lower vertebrae with ureteral obstruction. Atypical lesions, however, may occur in other parts of the retroperitoneum. The aim of this report is to describe the clinical features and various imaging findings of etroperitoneal fibrosis.
Aneurysm ; Diagnosis ; Eating ; Fibrosis ; Inflammation ; Methysergide ; Retroperitoneal Fibrosis* ; Spine ; Ureteral Obstruction ; Urinoma

In the present study, the antinociceptive profiles of Campanula punctata extract were examined in ICR mice. The Campanula punctata contain a large dose of saponin. Campanula punctata extract administered orally (200 mg/kg) showed an antinociceptive effect as measured by the tail-flick and hot-plate tests. In addition, Campanula punctata extract attenuated the writhing numbers in the acetic acid-induced writhing test. Furthermore, the cumulative nociceptive response time for intrathecal (i.t.) injection of substance P (0.7 microgram) was diminished by Campanula punctata extract. Intraperitoneal (i.p.) pretreatment with yohimbine (alpha2-adrenergic receptor antagonist) attenuated antinociceptive effect induced by Campanula punctata extract in the writhing test. However, naloxone (opioid receptor antagonist) or methysergide (5-HT serotonergic receptor antagonist) did not affect antinociception induced by Campanula punctata extract in the writhing test. Our results suggest that Campanula punctata extract shows an antinociceptive property in various pain models. Furthermore, this antinociceptive effect of Campanula punctata extract may be mediated by alpha2-adrenergic receptor, but not opioidergic and serotonergic receptors.
Animals ; Campanulaceae ; Methysergide ; Mice ; Mice, Inbred ICR ; Naloxone ; Reaction Time ; Saponins ; Substance P ; Yohimbine

In the present study, the antinociceptive profiles of Agrimonia pilosa Ledeb extract were examined in ICR mice. Agrimonia pilosa Ledeb extract administered orally (200 mg/kg) showed an antinociceptive effect as measured by the tail-flick and hot-plate tests. In addition, Agrimonia pilosa Ledeb extract attenuated the writhing numbers in the acetic acid-induced writhing test. Furthermore, the cumulative nociceptive response time for intrathecal (i.t.) injection of substance P (0.7 microg) was diminished by Agrimonia pilosa Ledeb extract. Intraperitoneal (i.p.) pretreatment with yohimbine (alpha2-adrenergic receptor antagonist) attenuated antinociceptive effect induced by Agrimonia pilosa Ledeb extract in the writhing test. However, naloxone (opioid receptor antagonist) or methysergide (5-HT serotonergic receptor antagonist) did not affect antinociception induced by Agrimonia pilosa Ledeb extract in the writhing test. Our results suggest that Agrimonia pilosa Ledeb extract shows an antinociceptive property in various pain models. Furthermore, this antinociceptive effect of Agrimonia pilosa Ledeb extract may be mediated by alpha2-adrenergic receptor, but not opioidergic and serotonergic receptors.
Agrimonia ; Animals ; Methysergide ; Mice ; Mice, Inbred ICR ; Naloxone ; Reaction Time ; Substance P ; Yohimbine

Central tryptaminergic system has been shown to play an important role in the regulation of renal function: 5-HT-1 (5-hydroxytryptamine-1) receptors might seem to mediate the diuresis and natriuresis, whereas the 5-HT-2 and 5-HT-3 receptors mediate the antidiuretic and antinatriuretic effects. This study attempted to delineate the role of central 5-HT-1A subtype in the regulation of rabbit renal function by observing the renal effects of intracerebroventricularly(icv)-administered PAPP (p-aminophenylethyl-m-trifluoromethylphenyl piperazine, LY165163), a selective agonist of 5-HT-1A receptors. PAPP in doses ranging from 40 to 350 microgram/kg icv induced significantly diuresis, natriuresis, and kaliuresis, along with increased renal perfusion and glomerular filtration. Systemic blood pressure was also increased. Free water reabsorption (T-cH-2O), a measure of ADH (antidiuretic hormone) secretion, was increased also. Intravenous 350 microgram/kg of PAPP elicited antidiuresis and antinatriuresis together with decreased blood pressure, thus indicating that the effects of icv PAPP were brought about through the central mechanisms, not by direct peripheral effects of the drug on kidney. Ketanserin, a selective 5-HT-2 antagonist, 40 microgram/kg icv, did not affect the renal effects of the icv PAPP. Methysergide, a non-selective 5-HT-1 antagonist, also did not block the renal functional responses by the icv PAPP. NAN-190, a 5-HT-1A antagonist, also did not antagonized the renal action of the icv PAPP. However the increased free water reabsorption was abolished by both methysergide or ketanserin pretreatment. The increments of blood pressure by icv PAPP was blocked only by NAN-190 pretreatment. These observations suggest that the central 5-HT-1A receptor might be involved in the central regulation of rabbit renal function by exerting the diuretic and natriuretic influences.
Blood Pressure ; Diuresis ; Filtration ; Ketanserin ; Kidney ; Methysergide ; Natriuresis ; Perfusion ; Rabbits* ; Water

The aim of the present study was to evaluate the central antinociceptive effects of eugenol after intraperitoneal administration. Experiments were carried out using male Sprague-Dawley rats. Subcutaneous injection of 5% formalin-induced nociceptive behavioral responses was used as the pain model. Subcutaneous injection of 5% formalin significantly produced nociceptive responses by increasing the licking time during nociceptive behavior. Subsequent intraperitoneal injection of 100 mg/kg of eugenol led to a significant decrease in the licking time. However, low dose of eugenol (50 mg/kg) did not affect the nociceptive behavioral responses produced by subcutaneous injection of formalin. Intrathecal injection of 30 µg of naloxone, an opioid receptor antagonist, significantly blocked antinociceptive effects produced by intraperitoneal injection of eugenol. Neither intrathecal injection of methysergide (30 µg), a serotonin receptor antagonist nor phentolamine (30 µg), an α-adrenergic receptor antagonist influenced antinociceptive effects of eugenol, as compared to the vehicle treatment. These results suggest that central opioid pathway participates in mediating the antinociceptive effects of eugenol.
Eugenol ; Formaldehyde ; Humans ; Injections, Intraperitoneal ; Injections, Spinal ; Injections, Subcutaneous ; Male ; Methysergide ; Naloxone ; Negotiating ; Phentolamine ; Rats, Sprague-Dawley ; Receptors, Opioid ; Serotonin

BACKGROUND: Although the efficacy of morphine in a neuropathic pain state is somewhat controversial, spinally administered morphine reversed the tactile allodynia in a previous animal study. Using a behaviorial test, we examined the involvement of serotonergic and adenosine receptors in the mechanism of the antiallodynic action of the intrathecal morphine by injection of serotonergic and adenosine antagonist in a rat model of neuropathic pain induced by a spinal nerve ligation. METHODS: Male Sprague-Dawley rats were prepared with a tight ligation of the left lumbar 5th and 6th spinal nerve and a chronic lumbar intrathecal catheter implantation. Morphine 1 microgram was administered intrathecally to attenuate the tactile allodynia. Methysergide 10 microgram and 30 microgram, theophylline 20 microgram was administered intrathecally before and after the injection of morphine in order to investigate the reversal of an increased allodynic threshold by morphine. The allodynic thresholds for the left hindpaw withdrawl to von Frey hairs were assessed and converted to %MPE. RESULTS: The tactile allodynic threshold was significantly increased by 1 microgram of intrathecal morphine (P < 0.05). Methysergide 10 microgram and 30 microgram, but not theophylline 20 microgram, reversed significantly the antiallodynic effect of intrathecal morphine in pre- and post-treatment (P < 0.05). CONCLUSIONS: The results suggested that the mechanism of tactile antiallodynia induced by intrathecal morphine appears to be mediated by serotonin receptor system at the spinal level in the rat model of spinal nerve ligation.
Adenosine ; Animals ; Catheters ; Hair ; Humans ; Hyperalgesia ; Ligation* ; Male ; Methysergide* ; Models, Animal ; Morphine* ; Neuralgia* ; Rats, Sprague-Dawley ; Receptors, Purinergic P1 ; Serotonin ; Spinal Nerves* ; Theophylline*

BACKGROUND: Nerve injury may produce a tactile allodynia. However, there are few reports regarding the interaction of morphine and selective serotonin reuptake inhibitors (SSRIs) during a neuropathic pain state. Therefore, we investigated the antiallodynic interaction between morphine and SSRIs in a rat model of neuropathic pain. METHODS: Rats were prepared with a tight ligation of the left fifth and sixth lumbar spinal nerves and chronic intrathecal catheter implantation. Mechanical allodynia was then measured by application of von Frey filaments. Morphine, citalopram and paroxetine were administered intrathecally to obtain the dose-response curves. The 50% effective dose of morphine and citalopram or paroxetine were then coadministered to evaluate the drug interaction. In addition, naloxone and methysergide were administered to examine the reversal of the antiallodynic effect. RESULTS: Intrathecal morphine produced a dose-dependent antagonism of the tactile allodynia, but intrathecal citalopram or paroxetine showed no antiallodynic effects. In addition, a morphine-citalopram or paroxetine combination produced an increase in the withdrawal threshold, but naloxone and methysergide reversed the antiallodynic effect. In addition, no interactions were observed between naloxone and citalopram or paroxetine, or morphine and methysergide. CONCLUSIONS: These results suggest that activation of both micron-opioid and serotonin receptors is required for the increased interaction to occur between morphine and SSRIs administered to reduce tactile allodynia. Thus, serotonin receptors take part in the antiallodynic action of morphine at the spinal level.
Animals ; Catheters ; Citalopram ; Drug Interactions ; Hyperalgesia ; Ligation ; Methysergide ; Morphine ; Naloxone ; Neuralgia ; Paroxetine ; Rats ; Receptors, Serotonin ; Serotonin ; Serotonin Uptake Inhibitors ; Spinal Nerves