PubMed Health⌕ Search

Biomedical subjects

I Jurna

Publications and source records attributed to I Jurna.

At least 19 recordsLinked to original sources
PubMed1992

Oral naloxone reduces constipation but not antinociception from oral morphine in the rat.

Oral administration of naloxone (10 mg/kg) antagonized the slowing of the intestinal transit caused by oral morphine (1, 2.5 and 5 mg/kg) in rats. Oral administration of naloxone (10 mg/kg) did not prevent the antinociceptive effect of orally administered morphine (2.5 mg/kg) in the tail-flick test carried out on rats. It is concluded that oral naloxone locally blocks the constipating effect of morphine, while it fails to reduce the central action of morphine due to extensive metabolization after oral administration.

Administration, Oral↗
PubMed1992

No psychological dependence after oral administration of morphine to rats.

Rats subjected to forced oral self-administration of morphine solutions without or in combination with two daily i.p. injections of morphine preferred drinking water when this was offered in addition to morphine solutions. The daily intake of morphine during the terminal phase of self-administration of morphine was 50-80 mg/kg (oral application alone) or 270 mg/kg (oral and i.p. application). Morphine treated animals showed withdrawal symptoms on administration of naloxone 1 mg/kg i.p. during the period of self-administration, but not when they had started drinking exclusively water. The tail-flick test revealed no tolerance during prolonged treatment with morphine. The results indicate that no psychological dependence developed when morphine was applied orally and regularly.

Administration, Oral↗
PubMed1991

Adenosine A1 and non-A1 receptors: intracellular analysis of the actions of adenosine agonists and antagonists in rat hippocampal neurons.

Adenosine and its agonists exert a depressant effect on neuronal activity by interacting with the adenosine A1 receptor. There is now also evidence for electrophysiological effects mediated by adenosine receptors other than the A1 type, possibly A2 receptors. A1 and A2 receptor-induced changes in the electrical properties of neuronal membranes were investigated by intracellularly recording from rat hippocampal CA1 neurons and using the adenosine agonists, 5'-N-ethylcarboxamidoadenosine (NECA) and R-phenylisopropyladenosine (PIA), and the unselective A1 and A2 receptor antagonist, theophylline and the selective A1 receptor antagonist, 8-cyclopenthyl-1,3-dipropylxanthine (DPCPX). PIA and NECA produced an inhibitory effect which was blocked by DPCPX and thus was mediated by A1 receptors. PIA produced inhibition at lower concentrations (0.1-1 mumol/l) than NECA (0.5-10 mumol/l), whereas at high concentrations (2.5 mumol/l) it exerted a dual effect, i.e. either an inhibitory or an excitatory one. During simultaneous perfusion with the A1 receptor antagonist DPCPX, PIA produced concentration-dependent excitatory effects at concentrations above 1 mumol/l. These excitatory effects were blocked by theophylline. DPCPX produced excitation that was enhanced by NECA. Forskolin caused no change in the membrane properties. It is concluded that (1) NECA and PIA affect the membrane properties not only by an action on the A1 but also on non-A1 receptors, because the excitatory effects of PIA and NECA were insensitive to DPCPX and abolished by theophylline; (2) PIA and NECA are more potent at A1 than at A2 receptors; (3) PIA is more potent than NECA at A1 and A2 receptors; (4) effects mediated by A2 receptors prevail over those mediated by A1 receptors when A2 receptors are activated; and (5) the non-A1 receptor-mediated effects are independent of an increased formation of cAMP.

Adenosine↗
PubMed1991

[Central analgesic effects of non-steroidal anti-rheumatic agents].

NSAIDs, including acetylsalicylic acid, are frequently classified as peripherally-acting analgesics. This is based on the fact that these substances, among other effects, inhibit the biosynthesis of prostaglandines. A few solid arguments, however, stand against an exclusively peripheral mode of the analgesic action of NSAIDs in the sense of an inhibition of prostaglandin synthesis. It should be noted here that the analgesically-effective doses do not suffice to block prostaglandin synthesis. Furthermore, the inhibiting effects of paracetamol and metamizol are far weaker or are not at all present, although both substances are reliably-effective analgesics. The NSAIDs indometacin, ibuprofen, and diclofenac are capable of suppressing the sensory response of the nociceptive system via a central effect. In experimental studies with rats under urethane anesthesia, the nociceptive activity of individual neurons of the thalamus (the dorsomedial part of the ventral nucleus) was measured. The activity was triggered via an electric stimulation of afferent C-fibres in the ipsilateral or contralateral sural nerve. The NSAIDs named suppressed the evoked nociceptive activity in a dose-dependent manner. At the highest doses, the suppression resulted in a difference of approx. 60% of the control activity. The ED50 values were 5 mg/kg for indometacin, 10.9 mg/kg for diclofenac, and 15.6 mg/kg for ibuprofen. These results support the theory that the central effects of NSAIDs contribute to their analgesic efficacy. The possible mechanisms of these effects will be discussed. A practical significance of the central analgesic effects of NSAIDs could be that their therapeutic applicability is not limited only to the treatment of pain, which results from an activation of nociceptors.

Animals↗
PubMed1990

Acute effects of vitamin B6 and fixed combinations of vitamin B1, B6 and B12 on nociceptive activity evoked in the rat thalamus: dose-response relationship and combinations with morphine and paracetamol.

Nociceptive activity was elicited in neurones of the thalamus by supramaximal electrical stimulation of afferent C fibres in the sural nerve of rats under urethane anesthesia. The fixed combination of vitamin B1, B6, and B12 (Neurobion) as well as of vitamin B6 administered by i.p. injection dose-dependently reduced the evoked nociceptive activity. The ED50 of Neurobion is 4.6 ml/kg (at 100 min after injection) and that of vitamin B6 is 189 mg/kg (at 90 min after injection). The minimum effective doses of Neurobion and vitamin B6 are 0.5 ml/kg and 40 mg/kg, respectively. When Neurobion or vitamin B6 were given at their minimum effective doses, and the minimum effective doses of morphine (0.025 mg/kg) or paracetamol (5 mg/kg) were injected i.v. 80 min later, i.e., when the maximum effect of higher doses of Neurobion or vitamin B6 was about to develop, no supraadditive effect developed. It is concluded that the antinociceptive effect caused by a single injection of Neurobion is largely due to vitamin B6. Vitamin B12 may contribute to this effect, whereas vitamin B1 alone exhibited only a slight effect on nociception. Moreover, it appears that Neurobion produces its antinociceptive effect after a single injection and after repeated administration during several days by different mechanisms so that the effect of analgesic agents is not enhanced following a single injection of Neurobion but may be enhanced after repeated administration of the compound.

Acetaminophen↗
PubMed1990

Intrathecal somatostatin produces effects dependent on the interval between catheter implantation and drug injection.

Intrathecal (i.t.) injection of somatostatin has been reported to depress nociceptive reflexes as well as to cause severe disturbance of somatomotor performance. The present study was designed to assess the dependence of these effects on the dose and the interval between implantation of the catheter and i.t. injection of somatostatin in rats. The effects produced by i.t. injection of somatostatin consisted of an increase in the response latencies of nociceptive responses to noxious heat, impairment of motor performance and grooming behavior, convulsions, and death. Except for grooming behavior, these were related in incidence and degree to the dose and the interval, the potency of somatostatin being highest at short intervals. Sham operations also affected the effectiveness of somatostatin.

Animals↗
PubMed1979

Nociceptive threshold after neonatal capsaicin treatment.

The nociceptive threshold as determined by the reaction time in the hot-plate and tail-flick tests was measured 3 to 4 months after pretreatment of young rats with capsaicin (50 mg kg-1 s.c.). The reaction time in the tail-flick test was prolonged in rats pretreated with capsaicin on the 2nd day of life. Capsaicin pretreatment up to the 10th day of life also resulted in a prolonged reaction time in the hot-plate test whereas capsaicin pretreatment after the 10th day of life was without effect. The elevation of the nociceptive threshold after neonatal capsaicin pretreatment most likely follows from degeneration of afferent nerve fibres activated by noxious stimuli.

Animals↗
PubMed1979

The anti-nociceptive effect of reserpine and haloperidol mediated by the nigro-striatal system: antagonism by naloxone.

Reserpine (10 mg/kg) and haloperidol (2 mg/kg) injected intraperitoneally increased the reaction time of the tail-flick response in intact but not in pre-nigrally decerebrate or spinal rats. The antinociceptive effect of both drugs was antagonized by intraperitoneal injections of dopa (100 mg/kg), apomorphine (2 mg/kg) or naloxone (1 mg/kg) as well as by bilateral micro-injections into the caudate nuclei of apomorphine (100 microgram and 20 microgram) and naloxone (10 microgram). It is concluded that the nigrostriatal feedback system is involved in the anti-nociceptive effect of reserpine and haloperidol.

Analgesics↗
PubMed1978

The effect of substantia negra stimulation and morphine on alpha-motoneurones and the tail-flick response.

Rats were used to study the effect of unilateral stimulation of the substantia nigra on the reflex discharge of alpha-motoneurones and on the reaction time of the tail-flick response. In preparations with prenigral decerebration, nigral stimulation facilitated monosynaptic alpha-reflex activity, whilst gamma-reflex activity remained unchanged. The facilitation of monosynaptic alpha-reflex activity was reduced by naloxone (1 mg/kg); morphine (2 mg/kg) did not change the number of alpha-reflex discharges, but it reduced the alpha-reflex latency, enhanced the effect of nigral stimulation on the latency and abolished the effect of naloxone on nigral facilitation. Nigral stimulation prolonged the reaction time of the tail-flick response in rats with an intact brain and after prenigral decerbration. Naloxone did not influence the anti-nociceptive effect of nigral stimulation, whilst morphine enhanced it in rats with an intact brain. The anti-nociceptive effect exerted by morphine in animals with an intact brain was abolished by prenigral decerbration, and an additional spinalization restored it. Inactivating the nigral neurones by unilateral microinjections of procaine or GABA into the substantia nigra depressed the nociceptive reflex. It is concluded that (1) activation of nigral neurones influenced mono- and polysynaptic reflexes in a reciprocal fashion by a pathway descending via brain stem relays to the spinal cord, (2) inactivation of nigral neurones produced similar changes in reflex activity by altering the function of the nigro-striatal feedback system, the outlet from the system to the spinal cord not being the substantia nigra, (3) morphine influenced the nociceptive reflex by an action at different levels of the central nervous system.

Animals↗
PubMed1977

Ipsilateral diminution of CRF-granules after unilateral hypothalamic lesions.

Axons terminating in the outer layer of the median eminence of rats contain light microscopically visible granules. The granules are assumed to represent a corticotropin-releasing factor and, therefore, are called CRF-granules. To find out whether neurons containing CRF-granules originate and run together with the neurons of the hypothalamus-neural lobe system (HNS), the effect of unilateral lesions in the HNS on the amount and distribution of CRF-granules was studied in bilaterally adrenalectomized rats. HNS lesions prevented the adrenalectomy-induced increase in CRF-granules on the side of the lesion. Lesions outside the HNS or sham lesions did not influence the amount and distribution of the granules. The findings suggest that CRF-granules are located in terminals of neurons whose perikarya are situated in magnocellular hypothalamic nuclei. It can also be concluded that the axons of these neurons run within the HNS and do not decussate.

Adrenalectomy↗
PubMed1977

[The effect of memantine (dimethylamino-adamantane) on membranes of sensory nerve fibres (author's transl)].

The effect of memantine (dimethylaminoadamantane), a new amantadinederivate with antiparknison-properties was investigated by the help of the sucrose gap method on sensory nerve fibres of the rat In normal Locke-solution memantine 10(-4) M reduced the amplitude of the compound action potential without change of the resting potential, increased the membrane resistance and depressed the repetitive activity elicited by depolarizing rectangular currents. The results of the experiments with changed concentrations of sodium, potassium and chloride ions in the suspensionmedium indicate that the membrane conductance of all three ions was reduced by memantine. Beside the antiparkinson properties these effects as well as those reported by others might be interpreted as a central muscle relaxing action of memantine. The possible implication of the demonstrated membrane effects of the drug is discussed in relation to its action on the dopaminergic transmission in the nigro-striatal system.

Action Potentials↗