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F C Tulunay

Publications and source records attributed to F C Tulunay.

At least 37 records · Page 2Linked to original sources
PubMed1982

Possible physiological control of morphine analgesia in mice.

Several laboratories have reported that dynorphin and vasopressin may be present in the same neurons and released together in a fixed ratio. In this study, we report that vasopressin and dynorphin can regulate morphine-induced analgesia in the mouse tail-flick test. Its action is opposite that observed for dynorphin because, when administered simultaneously with morphine, vasopressin in a dose-related manner potentiated morphine-induced analgesia while dynorphin antagonized it. When vasopressin and dynorphin is administered together with morphine, morphine ED50 returned to control level.

Analgesia↗
PubMed1982

The effects of morphine and delta-9-tetrahydrocannabinol on motor activity in rats.

Acute treatment of rats either by high doses of morphine or delta 9-tetrahydrocannabinol (THC) decreased locomotor activity. Naloxone reversed morphine-induced depression completely and reversed THC-induced depression only partially. On day 3 of treatment, tolerance developed to the locomotor inhibitory action of THC or morphine and partial cross-tolerance was observed to the depressant action of THC. Naloxone slightly depressed locomotor activity in THC-tolerant rats, but increased motor activity in morphine-tolerant rats.

Animals↗
PubMed1981

Possible regulatory role of dynorphin-(1-13) on narcotic-induced changes in naloxone efficacy.

Pretreatment of mice with a single injection of morphine, beta-endorphin, Leu-enkephalin, FK33824 or [D-Ala2-D-Leu5]enkephalin, for 3 h increased the ability of naloxone to antagonize the analgesic effects of morphine. However, dynorphin-(1-13) can only antagonize morphine, beta-endorphin or Leu-enkephalin induced increased naloxone efficacy but not FK33824 or [D-Ala2-D-Leu2]enkephalin. Dynorphin itself can also increase naloxone efficacy when treated alone. However, this effect can be prevented when animals are pretreated with dynorphin and naloxone together.

Analgesia↗
PubMed1981

Antagonism by chlornaltrexamine of some effects of delta 9-tetrahydrocannabinol in rats.

Chlornaltrexamine (beta-CNA) a selective, long-acting irreversible opiate antagonist inhibited the analgesia, hypothermia, hypothermia tolerance and physical dependence produced by delta 9-tetrahydrocannabinol (THC) in rats. The results suggest that there are some common features between cannabis and opiates and some actions of THC may be mediated by opioid related mechanisms in the central nervous system.

Analgesia↗
PubMed1981

Possible regulatory role of dynorphin on morphine- and beta-endorphin-induced analgesia.

In previous studies, we observed that dynorphin- (1-13), but not dynorphin-(1-9), can significantly inhibit morphine- or beta-endorphin-induced analgesia despite not having any appreciable analgesic activity itself. Dynorphin-(1-13) showed no inhibitory effect on Sandoz FK33824-induced analgesia. In the present study, we examined the effect of dynorphin on morphine-, beta-endorphin-, D-ala2-D-leu5-enkephalin- or Sandoz FK33824-induced analgesia in both naive, morphine-tolerant and morphine-dependent mice. It was found that although dynorphin may inhibit morphine- or beta-endorphin-induced analgesia in naive animals, the peptide is not effective in inhibiting D-ala2-D-leu5-enkephalin- or Sandoz FK33824-induced analgesia. Dynorphin is also effective in blocking spontaneous withdrawal jumping in morphine-dependent animals. It is suggested that dynorphin-(1-13) may play a modulatory role in regulating analgesia due to morphine or beta-endorphin, but not that due to enkephalin. The action of peptides on morphine- or beta-endorphin-induced analgesia in the naive state is different from that of the tolerant state, suggesting that dynorphin may be involved in the development of morphine tolerance and physical dependence.

Analgesics↗
PubMed1980

Effect of delta 9-tetrahydrocannabinol on the morphine-induced hyperactivity of mice.

The effect of delta 9-tetrahydrocannabinol (THC) on the locomotor activity-stimulating action of morphine has been investigated in mice. THC (10 mg/kg) has been found to potentiate morphine-induced hyperactivity. On the other hand, the stimulating action of morphine on motor activity strongly diminished in mice rendered tolerant by the implantation of a morphine pellet. The pretreatment of morphine-tolerant mice with the same dose of THC did not change the effect of morphine on the motor activity. These results suggest that tolerance also developed to the potentiating action of THC on morphine-induced hyperactivity during the development of tolerance to this action of morphine.

Animals↗
PubMed1980

Correlation between the dose and development of acute tolerance to the hypothermic effect of THC.

The administration of 0.3-40 mg/kg delta 9-tetrahydrocannabinol (THC) produced a dose-dependent hypothermia in rats. The maximal hypothermic effect was obtained with the dose of 2.5 mg/kg of THC. When the same doses of THC were repeated on days 2 and 3, tolerance to the hypothermic effect of THC was apparent. Doses of THC higher than 2.5 mg/kg induced a significant and dose-dependent tolerance after the first administration whereas with the lower doses, tolerance was only apparent after the second injection. The possible mechanism of these effects of THC is discussed.

Animals↗
PubMed1979

Interaction between delta 9-tetrahydrocannabinol and morphine on the motor activity of mice.

The present experiments dealt the effects of delta 9-tetrahydrocannabinol (THC) on the locomotor activity stimulating action of morphine in mice. In the first series of experiments, the pretreatments of mice by THC in doses up to 20 mg/kg have been found to potentiate the morphine-induced hyperactivity in dose-dependent manner, but higher doses of THC did not produce such an action. In the second series of experiments the dose-response curve of morphine for the motor activity has been found to shift to the left by the pretreatment of mice with 10 mg/kg of THC. These results show a synergism between morphine and THC and suggest that both drugs may share some common site of action.

Animals↗
PubMed1979

Enhanced naloxone potency and the development of narcotic tolerance.

When various biogenic amine modifying drugs were administered to mice which were pretreated with morphine, none of the drugs except atropine and haloperidol altered the usual doubling of the naloxone efficacy which is observed in morphine-pretreated mice. Atropine appeared to decrease the potency of naloxone. Haloperidol, which did not alter naloxone potency in normal mice, further increased the naloxone potency in morphine-pretreated mice. When the biogenic amine modifiers were injected chronically to mice during the development of morphine tolerance, again none of the drugs, except haloperidol and atropine altered the development of tolerance. Haloperidol appeared to enhance and atropine to inhibit the degree of tolerance. These results indicate that it is the alteration in the narcotic-induced enhancement of naloxone potency and not the mere alteration of noloxone potency by various drugs, which can be used as an indicator of the alterations in the development of tolerance.

Animals↗
PubMed1976

The effect of biogenic amine modifiers on morphine analgesia and its antagonism by naloxone.

The stimulation of dopaminergic receptors, inhibition of serotonin synthesis or blockade of muscarinic receptors by various modifiers led to inhibition of morphine analgesia in mice. Blockade of dopaminergic receptors or the increase in serotonergic or cholinergic activity resulted in the enhancement of morphine analgesia. Serotonergic and cholinergic systems are proposed as positive and the dopaminergic system as negative modulators of morphine analgesia. The modulation of naloxone antagonism was much more complicated than that of morphine analgesia and often the effect of biogenic amine modifiers on antagonism differed from that on analgesia. The fact than biogenic amine modifiers do not affect morphine analgesia and naloxone antagonism by a similar pattern suggests that interaction of narcotics and narcotic antagonists with analgesic receptors may not be exactly the same.

Analgesia↗
PubMed1976

The effect of lithium chloride on morphine- and pyrogen-induced hyperthermia in rats.

In rats, doses of morphine between 2.5 and 20 mg/kg produced hyperthermia, 50-400 mg/kg lithium chloride induced dose-dependent hypothermia. These doses of lithium chloride inhibited morphine- and pyrogen-induced hyperthermia. The hypothermic effect of lithium may be due to the replacement of sodium ions by lithium ions in the hypothalamus. The antagonism between morphine and lithium is nonspecific.

Animals↗
PubMed1975

The effect of dopaminergic stimulation and blockade on the nociceptive and antinociceptive responses of mice.

Agents which stimulate dopaminergic receptors directly or indirectly such as apomorphine and L-dopa, increased the reactivity of mice to a nociceptive stimulus. The increased reactivity was pharmacologically quantitated by estimating the hyperalgesic ED50 to be 4.4 and 115 mg/kg for apomorphine and L-dopa, respectively. This hyperalgesia was blocked by the dopamine receptor blocking agents, haloperidol and pimozide, but not by the narcotic antagonist, naloxone. Apomorphine antagonizes morphine analgesia. However the induced hyperalgesia only accounts for part of the antagonistic activity of apomorphine. The majority of the antagonistic activity of apomorphine appears to be by means other than action on dopaminergic receptors.

Analgesics↗