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Biomedical subjects

I Jurna

Publications and source records attributed to I Jurna.

At least 55 records · Page 3Linked to original sources
PubMed1983

Effects of intrathecally administered pentobarbital and naloxone on the activity evoked in ascending axons of the rat spinal cord by stimulation of afferent A and C fibres. Further evidence for a tonic endorphinergic inhibition in nociception.

The effects of intrathecally administered pentobarbital and naloxone on activity in ascending axons were determined in decerebrate rats with the spinal cord transected at the lower thoracic level. Activity in ascending axons of the spinal cord was recorded below the site of transection and evoked by electrical stimulation of afferent A beta, A delta or C fibres in the sural nerve. Pentobarbital 250 micrograms depressed activity evoked by stimulation of non-nociceptive A beta and nociceptive C fibres; it did not change activity in response to stimulation of A delta fibres. A low dose (100 micrograms) had no effect of A beta and C fibre-evoked activity but depressed spontaneous activity in the ascending axons. Naloxone 5 micrograms enhanced the spontaneous and evoked activities only in those ascending axons which responded to C fibre stimulation. Pretreatment with pentobarbital 250 micrograms prevented the facilitation by naloxone of C fibre-evoked activity. Naloxone was ineffective even when it was administered in a dose of 100 micrograms simultaneously with pentobarbital. Intrathecal injections of magnesium chloride depressed spontaneous and C fibre-evoked activities and markedly reduced the facilitatory effect of naloxone. It is concluded that nociceptive C fibre-evoked activity is subject to the inhibitory control of endorphinergic neurones and that naloxone facilitates this activity by producing release from inhibition.

Afferent Pathways↗
PubMed1982

Intrathecal pentobarbital prevents naloxone-induced facilitation of the tail-flick response in the rat.

In rats with acute transection of the lower thoracic spinal cord, intrathecal administration of naloxone in doses of 1, 2, 5 and 50 microgram dose-dependently reduced the latency of the tail-flick response to radiant heat. An intrathecal injection of pentobarbital (100 microgram) prolonged the latency and prevented the facilitatory effect of naloxone. It is concluded that the antagonism between naloxone and pentobarbital is of the non-competitive or functional (physiological) type.

Animals↗
PubMed1982

Analgesic effect of intrathecal morphine demonstrated in ascending nociceptive activity in the rat spinal cord an in effectiveness of caerulein and cholecystokinin octapeptide.

The effect of intrathecal injections of morphine and the two peptides, caerulein and cholecystokinin octapeptide (CCK-8), on the activity in ascending axons of the spinal cord evoked by electrical stimulation of primary nociceptive afferents was studied in spinal rats with decerebration. Morphine (20 microgram) depressed the spontaneous activity and the activity evoked from either A delta-or C-fibres. The co-activation by A delta-fibre stimulation of ascending axons activated by stimulation of C-fibres and the activity in ascending axons activated by stimulation of afferent A beta-fibres were not influenced by morphine. C-Fibre-evoked ascending activity was also depressed by morphine (10 microgram and 5 microgram). Ascending nociceptive activity was not changed by caerulein (30 ng) and CCK-8 300 ng, but it was depressed by a subsequent injection of morphine (20 microgram). The depressant effects of morphine were abolished by an intravenous injection of concluded that: (i) an intrathecal injection of morphine selectively depressed the ascending nociceptive activity; (ii) the depression produced by morphine is an equivalent for spinal analgesia following intrathecal injection of morphine to man; and (iii) the two components of the spinal nociceptive system, the motor and the sensory path, can independently be influenced by drugs.

Afferent Pathways↗
PubMed1982

Intrathecal substance P depresses spinal motor and sensory responses to stimulation of nociceptive afferents--antagonism by naloxone.

The effect of an injection of substance P into the subarachnoid space was studied on a motor and a sensory response elicited by supramaximal stimulation of the sural nerve in spinal rats. Substance P 10 micrograms depressed the reflex activation in the electromyogram recorded from the ipsilateral tibialis anterior muscle; the depression was significant 5 and 10 min after the injection. Substance P 10 micrograms reduced the activity in ascending axons of the spinal cord evoked by stimulation of afferent C fibres; the effect developed slowly, lasted longer than 60 min and was abolished by an i.v. injection of nalaoxone 0.2 mg/kg. Only half the number of ascending axons tested showed a depression by substance P, and the administration of a higher dose (50 micrograms) did not produce an effect in a greater number of axons. Substance P did not influence the activity evoked in ascending axons by stimulation of afferent A beta and A delta fibres. The depression by substance P of ascending nocieceptive activity was antagonized by an i.v. injection of naloxone 0.2 mg/kg. When naloxone 0.2 mg/ng i.v. was administered alone, it increased the activity in ascending axons activated by afferent C fibre stimulation. It is concluded that (i) substance P depresses spinal nociceptive activity without the intermediation of endorphinergic neurons, and (ii) naloxone antagonizes tonic inhibition of the spinal nociceptive system mediated by endogenous opioid peptides and, by facilitating excitatory transmission through disinhibition, neutralizes the depression produced by substance P.

Afferent Pathways↗
PubMed1981

Aminophylline differentiates between the depressant effects of morphine on the spinal nociceptive reflex and on the spinal ascending activity evoked from afferent C fibres.

The action of aminophylline on anti-nociceptive effects of morphine in rats was tested on the tail-flick response to noxious heat and on the activity evoked in ascending axons of the spinal cord by stimulation of nociceptive afferents. The depression of the tail-flick response produced by an intraperitoneal (i.p.) injection of morphine 2 mg/kg in intact and spinal rats was abolished by an i.p. injection of aminophylline 25 mg/kg. The activity evoked in ascending axons of spinal rats by electrical stimulation of afferent C fibres of the sural nerve was depressed by an intravenous (i.v.) injection of morphine 2 mg/kg. Aminophylline 25 mg/kg injected i.v. after morphine produced a slight and transient increase in the ascending activity immediately after its administration but did not abolish the depressant effect of morphine. Naloxone 0.2 mg/kg administered after aminophylline antagonized the depressant effect of morphine on the ascending activity. It is suggested that morphine exerts its depressant effect on the two nociceptive responses (the motor and the sensory response) by different mechanisms, one being sensitive to aminophylline, the other being relatively resistant to the action of the purine derivative.

Afferent Pathways↗
PubMed1981

Intrathecal substance P depresses the tail-flick response - antagonism by naloxone.

Substance P injected into the lumbar subarachnoid space of rats depressed the tail-flick response to radiant heat in a dose-dependent way. The effective doses ranged from 0.1 microgram to 100 micrograms per rat (ED 50: 1.5 microgram/rat). The maximum of the effect was reached 20 min after intrathecal injection and the effect lasted for about 30 min. An antinociceptive effect was also observed after intrathecal injection of substance P 1 microgram to spinal rats. The depression of the tail-flick response produced by intrathecal administration of substance P was abolished by intrathecal (5 micrograms/rat) or i.p. (0.5 mg/kg) injections of naloxone.

Animals↗
PubMed1981

Changes in the activity of nigral neurones induced by morphine and other opiates in rats with an intact brain and after prenigral decerebration.

The effect of morphine and related opiates on the spontaneous activity of nigral neurones was studied in unanaesthetized rats with an intact brain or after prenigral decerebration. Less than 50% of the neurones were influenced by the opiates. In the intact brain, intravenous (i.v.) injection of morphine 2 mg/kg, dextrorphan 1 mg/kg and tilidine 5 mg/kg increased the discharge rate, whereas levorphanol 1 mg/kg, pethidine 20 mg/kg and codeine 10 mg/kg reduced it. Naloxone 0.2 mg/kg i.v. abolished the effects of morphine, levorphanol and codeine; it reduced the effect of pethidine and was ineffective against dextrorphan and tilidine. Intracaudate injections of morphine 10 microgram and pethidine 50 microgram increased the spontaneous activity of some neurones in the ipsilateral substantia nigra and reduced that of others; the increase in activity after morphine was more pronounced than the depression. The effects of intracaudate injections of morphine or pethidine were reduced by i.v. naloxone. After prenigral decerebration, i.v. injections of morphine depressed, and i.v. injections of levorphanol increased the activity of nigral neurones; pethidine i.v. either increased or reduced the spontaneous activity. These effects were reduced or abolished by naloxone. It is concluded that opiates including morphine affect the activity of nigral neurones not only by an action on opiate receptors in the striatum but also by an action on opiate receptors outside the striatum (e.g. in the substantia nigra and, perhaps, by an action unrelated to opiate receptors.

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↗