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R Langwiński

Publications and source records attributed to R Langwiński.

At least 19 recordsLinked to original sources
PubMed1996

Effects of calcium channel antagonists on the reinforcing properties of morphine, ethanol and cocaine as measured by place conditioning.

Morphine, ethanol and cocaine were examined in place conditioning paradigm. After initial preferences were determined, animals were conditioned with morphine (5 mg/kg), ethanol (1 g/kg) and cocaine (5 mg/kg) alone or combinations of these drugs plus some calcium antagonists: nifedipine (5 and 10 mg/kg) and verapamil (5 and 10 mg/kg). Nifedipine prevented the ability of morphine and cocaine, but not of ethanol, to produce a place preference. Our results suggest that substances which can influence calcium distribution are involved in the rewarding actions of some drugs-morphine and cocaine. Dihydropyridine, a calcium channel antagonists might be clinically useful for the treatment of morphine and cocaine abuse.

Animals↗
PubMed1995

Influence of CGS 8216 on some acute effects of ethanol.

The central pharmacological effects of ethanol are well known and resemble those of the benzodiazepines (BZD). In addition BZD may interact with ethanol, resulting in enhanced cerebral depression. Ro 15-4513, BZD inverse agonist, potentially antagonizes a lot of effects of ethanol but not all. In our study, another BZD inverse agonist, CGS 8216, reverses the hypnotic effect of ethanol and hypoactivity in mice and rats. CGS 8216 increased also ethanol's locomotor stimulation in mice. This supports the hypothesis that some effects of ethanol are mediated by the GABA-BZD-chloride channel receptor complex. Our behavioural experiments described in this report suggest that CGS 8216, like Ro 15-4513, may act on the alpha-6 subunit of this receptor complex.

Animals↗
PubMed1987

Cross-tolerance between morphine and ethanol and their antinociceptive effects.

Morphinization of mice (37.5 mg morphine) and rats (75 mg) with subcutaneously implanted pellets has resulted in tolerance to the antinociceptive effect of morphine, measured in the tail-immersion test. All animals also developed cross-tolerance to the analgesic effects of ethanol (2.8 g/kg intraperitoneally for mice, per os for rats). These results suggest a commonality between morphine and ethanol antinociceptive action.

Analgesics↗
PubMed1987

Does the blockade of opioid receptors influence the development of ethanol dependence?

We have tested whether the opioid antagonists naloxone (2 mg/kg), naltrexone (2 mg/kg) and diprenorphine (0.2 mg/kg), and the agonist morphine (4-8 mg/kg) given subcutaneously (10 min before ethanol for 7 days) modify the ethanol withdrawal syndrome (audiogenic seizures) following chronic ethanol intoxication in rats. We found that naloxone, naltrexone and diprenorphine modified the ethanol withdrawal syndrome. These findings do not rule out the possibility of a biochemical link between the action of ethanol and opiates at the level of opioid receptors.

Alcoholism↗
PubMed1986

Audiogenic seizures during ethanol withdrawal can be blocked by a delta opioid agonist.

In rats the influence of the delta opioid agonists [Leu]enkephalin, [D-Ala2-D-Leu5]enkephalin, [D-Ala2]methionine enkephalinamide and synthetic analogue of [Met]enkephalin: Tyr-D-Ala-Gly-Phe-D-Leu-OMe on audiogenic seizures was tested during ethanol abstinence. All investigated drugs significantly inhibited this ethanol withdrawal symptom. The results are compatible with the hypothesis of opioid involvement in the ethanol abstinence syndrome.

Acoustic Stimulation↗
PubMed1983

The influence of pimozide, haloperidol, alpha-methyl-p-tyrosine and reserpine on the development of morphine dependence in rats.

It was found that pimozide, haloperidol and alpha-methyl-p-tyrosine (alpha-MT), drugs inhibiting central catecholaminergic (CA) transmission, increased the development of morphine dependence measured as wet dog shakes in rats. Reserpine inhibiting CA and serotoninergic (5-HT) transmission, decreased the development of morphine dependence in rats. The inhibitory effect of reserpine was reversed by 5-hydroxytryptophan (5-HTP), but not by L-dihydroxyphenylalanine (L-DOPA). These results suggest that wet dog shakes might develop as a result of regulatory adaptation in the 5-HT neurotransmitter system.

5-Hydroxytryptophan↗
PubMed1983

The role of central serotoninergic neurotransmission in the morphine abstinence syndrome in rats.

It was found that 200 mg/kg of DL-p-chlorophenylalanine (PCPA) and 2 mg/kg of methergoline drugs inhibiting central serotoninergic transmission-decreased naloxone precipitated abstinence wet dog shakes in morphine-dependent rats. The inhibitory effect of PCPA was reversed by 200 mg/kg of 5-hydroxy-L-tryptophan (5-HTP) but not by the same amount of L-tryptophan (TP). 5-HTP alone (200 mg/kg) increased wet dog shakes epissodes, whereas TP alone in the same dosage practically did not have any influence on the wet dog shakes in morphine-dependent rats. These findings suggest that brain serotonin may play some role in the expression of wet dog shakes in morphine-dependent rats.

5-Hydroxytryptophan↗
PubMed1983

The effect of antihistaminics on cataleptogenic action of analgesics and haloperidol.

We investigated the effect of benzhydramine, thenalidine, mepyramine (H1 receptor antagonists) and cimetidine (H2 receptor antagonist) on cataleptogenic action of morphine, codeine, fentanyl, and haloperidol. Benzhydramine antagonized the catalepsy induced by analgesics (particularly by codeine). The antagonistic effect of thenalidine was weaker (but also very prominent for codeine catalepsy). Mepyramine did not affect the catalepsy induced by analgesics. All three H1 receptor antagonists attenuated the catalepsy induced by haloperidol. Cimetidine, injected intraventricularly, did not affect the catalepsy induced either by analgesics or by haloperidol. It is suggested that the antagonistic action of benzhydramine and thenalidine against analgesic catalepsy is related rather to their antiserotonin properties, while the anticataleptic activity of all three H1 receptor antagonists against haloperidol catalepsy is caused by their anticholinergic and antiserotonin properties.

Analgesics↗
PubMed1982

Effect of benzodiazepines on the central action of narcotic analgesics.

The effects of benzodiazepine (mainly diazepam) on the following central action of narcotic analgesics were tested: antinociceptive action (Randall-Selitto and hot plate tests), hypermotility, inhibition of methylphenidate stereotypy, catalepsy. Diazepam, in doses not affecting the pain threshold markedly potentiated morphine, codeine, etorphine, pentazocine and fentanyl antinociception. Hypermotility produced by morphine and fentanyl was inhibited by pretreatment with chlordiazepoxide, diazepam and clonazepam. Diazepam potentiated the inhibitory effect of opiates on methylphenidate-induced stereotyped gnawing in mice and increased the catalepsy induced by morphine and fentanyl in rats. In all experiments the effects of diazepam were suppressed by the substances which impair GABA-ergic neurotransmission: bicuculline and picrotoxin. Obtained results indicate that benzodiazepine potentiate the antinociceptive and cataleptogenic effects of opiates and their inhibitory influence on methylphenidate stereotypy. However, these drugs antagonize locomotor hyperactivity in mice. All these actions seem to be related to facilitation of GABA-ergic neurotransmission by benzodiazepines.

Analgesics, Opioid↗
PubMed1982

Cholinergic influences on opioids activity in rats.

The influence of cholinergic and anticholinergic agents on the catalepsy and antinociceptive action of morphine, codeine, fentanyl and pentazocine was studied in rats. Anticholinergic drugs scopolamine (3 and 6 mg/kg) and slightly atropine (1 mg/kg) enhanced morphine-induced catalepsy. Benztropine did not change this action of morphine. Cholinergic physostigmine (0.2 and 0.4 mg/kg) showed marked and dose-dependent antagonism toward morphine catalepsy, but pilocarpine, in doses of 2 and 4 mg/kg, failed to influence it. Catalepsy induced by codeine and fentanyl was nearly not influenced by cholinergic and anticholinergic agents. In the hot plate test, cholinergic influences on antinociceptive activity of analgesics are slight, but sometimes it may be observed the similar interaction as in morphine catalepsy: anticholinergic agents enhance, and cholinergic agents antagonize these effects. Present results indicate that some cholinergic and anticholinergic agents influence morphine catalepsy, and this influence is opposite to that observed in neuroleptic-induced catalepsy. Failure of the cholinergic influences on fentanyl- and codeine-induced catalepsy suggests that the mechanisms of cataleptogenic activity of morphine and other analgesics are not the same.

Analgesia↗
PubMed1981

Central action of narcotic analgesics. VIII. The effect of dopaminergic stimulants on the action of analgesics in rats.

We investigated the influence of apomorphine, amphetamine, amantadine, dimethylaminoadamantane, nomifensine, ergometrine and beta-phenylethylamine on cataleptogenic and antinociceptive action of analgesics in rats. Nomifensine, apomorphine, beta-phenylethylamine, amantadine and ergometrine antagonized the catalepsy induced by morphine and codeine. Catalepsy induced by fentanyl was depressed only by nomifensine and apomorphine. Amphetamine only slightly antagonized the analgesic-induced catalepsy and the effects were not dose-dependent. Dimethylaminoadamantane did not antagonize catalepsy at all. Antinociceptive action of morphine and codeine was antagonized by apomorphine and amphetamine. Ergometrine counteracted the action of morphine, and beta-phenylethylamine decreased the action of pentazocine. The results suggest that: 1. There are differences in the mechanism of cataleptogenic action of the opiates (morphine and codeine) and fentanyl; 2. Catalepsy after analgesia differs from the catalepsy produced by neuroleptics in respect of interaction with such drugs as amphetamine, apomorphine or dimethylaminoadamantane. Analgesic-induced catalepsy seems to depend on the presynaptic inhibition of dopaminergic neurotransmission; 3. Stimulation of the central dopaminergic system in rat brain either does not change or weakly antagonizes the action of analgesics in the hot plate test.

Amphetamine↗
PubMed1981

Central action of narcotic analgesics. IX. Participation of serotonin in the development of tolerance to cataleptogenic effects of morphine in rats.

Subcutaneous implantation of morphine-base (75 mg) pellets over a period of 72 h caused the development of tolerance ot cataleptogenic action of morphine in rats. The development of morphine tolerance was inhibited by p-chlorophenylalanine (pCPA) or reserpine, drugs which decrease the content of brain serotonin (5-HT). Administration of 5-hydroxytryptophan (5-HTP(, which protected 5-HT stores against depleting action of reserpine, prevented the above of reserpine on the development of morphine tolerance in rats. Blockade of 5-HT neurotransmission by pizotifen or cyproheptadine inhibited the development of morphine tolerance, while the increase of it by imipramine did not alter the development of this tolerance . The Obtained results have shown that serotonergic system plays an important role in the development of tolerance to cataleptogenic effects of morphine.

5-Hydroxytryptophan↗