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Biomedical subjects

G Guilbaud

Publications and source records attributed to G Guilbaud.

At least 109 records · Page 6Linked to original sources
PubMed1986

Analgesia produced by low doses of the opiate antagonist naloxone in arthritic rats is reduced in morphine-tolerant animals.

In a model of experimental chronic pain (adjuvant-induced arthritic rats), low doses of the opiate antagonist naloxone produced a profound analgesia. Maximum analgesia was seen with 3 micrograms/kg (i.v.). In contrast, hyperalgesia was obtained with much higher doses (1-3 mg/kg, i.v.). The hyperalgesic effects were not affected in arthritic animals rendered tolerant to morphine, but the paradoxical analgesic effects were significantly reduced. This decrease suggests that naloxone analgesia involves interaction with opiate receptors and that the operation of endorphinergic systems differs in normal animals and animals which experience persistent pain.

Animals↗
PubMed1986

[Role of the ventrobasal complex of the thalamus in nociception and pain: data obtained in the normal rat and in a model of clinical pain].

Recent anatomical, electrophysiological, neuropharmacological and behavioural studies have provided new elements for the understanding of the role of the thalamus in nociceptive and pain mechanism. Data presented here demonstrate that the thalamic ventrobasal complex (VB), which receives direct afferents from the spinothalamic tract in the rat and monkey, plays a role in the sensory-discriminatory component of pain in these two species. Apart from the electrophysiological aspect, we discuss the effects of analgesic compounds on neuronal responses observed at this level and modifications in a nociceptive reaction threshold after lesions of this structure in the non-anesthetized freely moving animal. Data obtained in the normal rat are compared with those obtained under the same experimental conditions in a clinical pain model: the arthritic rat. In these animals the capacity of the VB neurons to respond to somatic stimuli is profoundly modified, many of them being activated by moderate stimuli from inflamed joints (lateral pressure, movements). Spinal tracts transmitting messages from these joints appear to differ (at least in part) from those transmitting nociceptive messages in the normal rat. Finally, at similar doses, morphine is much more effective in these animals than in the normal rat. Results of these studies show that nociception and clinical pain are not always exactly dependent on the same systems.

Animals↗
PubMed1985

Electrophysiological evidence for a role of the anterolateral quadrant of the spinal cord in the transmission of noxious messages to the thalamic ventrobasal complex in the rat.

Responses to noxious mechanical and thermal stimulation applied to the hindpaws were recorded extracellularly from the same neurons of the ventrobasal complex of the rat thalamus (VB) before and after lesions of various areas of the cervical cord in order to determine the pathways carrying the afferent messages. It was demonstrated that lesions of the dorsal and dorsolateral portions of the cord failed to eliminate the VB neuronal responses to noxious stimulation. By contrast, lesion of one anterolateral quadrant eliminated the responses to a noxious stimulation applied to the hindpaw contralateral to the lesion. This occurred whether the lesion was ipsilateral or contralateral to the recording site. From the present study and the data in the literature, it is concluded that the fibers of the spino-thalamic tract which are completely crossed in the spinal cord, travel in the anterolateral quadrant and project directly onto the VB, are involved in the transmission of noxious messages from the cord to the VB neurons. This conclusion indicates that the VB neuronal responses to noxious stimulation of the hindpaw ipsilateral to the recording site depend on the spinothalamic projection to the opposite ventrobasal complex. This therefore suggests that some noxious messages which reach a particular VB neuron are conveyed via the opposite VB and the existence of a thalamo-cortico-thalamic loop is discussed.

Animals↗
PubMed1985

Electrophysiological properties of lemniscal afferents in rat after kainic acid lesions in the ventrobasal thalamus.

Kainic acid (KA) has been largely used as a neurotoxin, and its axon-sparing effect being repeatedly emphasized, on the basis of anatomical and biochemical data. The present study examines this 'axon-sparing' effect from an electrophysiological point of view and demonstrates that lemniscal fibers retain the capacity to convey somesthetic information 5-60 days after an injection of KA in the ventrobasal complex of the thalamus depriving these afferent fibers of their target cells.

Afferent Pathways↗
PubMed1985

Can tolerance to morphine be induced in arthritic rats?

The effects of acute injections of morphine (0.1-1 mg/kg i.v.) upon vocalization threshold elicited by pressure of the paw were analyzed in normal and arthritic rats, both groups being initially pretreated with calculated doses of morphine. The analgesic effects of morphine were greatly reduced in both groups of chronically morphine-treated rats. The lowest doses (0.1 mg/kg in normal rats; 0.1 and 0.3 mg/kg in arthritic animals) became totally ineffective, while the highest dose (1 mg/kg) elicited a threshold increase only equivalent to that induced by 0.3 mg/kg in non-tolerant chronically vehicle-treated rats. Tolerance to morphine can be induced in rats suffering from arthritis, and appeared to be more complete than in normal rats.

Animals↗
PubMed1985

Thalamic nociceptive systems.

A role for thalamic structures in the processing of signals of nociception and pain has been suggested on the basis of clinical data since the turn of the century. Searches for a 'pain centre' by lesion or stimulation were often disappointing and the electrophysiological data were rare and usually contradictory. However, recent electrophysiological anatomical and neuropharmacological studies, made in various species (mainly rat and monkey) appear now progressively to give some clues in the understanding of pain process at the thalamic level. These studies have been mainly concerned with the areas receiving projections from ascending spinal pathways conveying noxious inputs, either directly by the spinothalamic tract or indirectly by the spinoreticulothalamic pathway. The eventual respective roles of these thalamic structures are considered. Electrophysiological recordings from thalamic structures in a model of experimental pain, arthritic rats, are also presented.

Afferent Pathways↗
PubMed1985

The effect of lysine acetylsalicylate on joint capsule mechanoreceptors in rats with polyarthritis.

Joint capsule mechanoreceptors in arthritic rats are more sensitive to pressure than similar receptors in normal animals. This greater sensitivity was reversed by the intravenous or topical administration of lysine acetylsalicylate in anaesthetised rats in doses of 15 to 50 mgm ASA-equivalent/kg. The reduction in sensitivity began within 5-10 min and reached a minimum mean value of 35% of the control after 35 to 40 min. During this period there was a negative linear or exponential relation between the amplitude of response to a controlled mechanical stimulus and time after administration of lysine acetylsalicylate. Control values of sensitivity were reached about 65-70 min following treatment with lysine acetylsalicylate. The results are interpreted as indicating that the high sensitivity of the arthritic joint capsule receptors is due to locally produced prostaglandins, such as prostacyclin.

Administration, Topical↗
PubMed1985

Sensory receptors in ankle joint capsules of normal and arthritic rats.

The responses of afferent fibers innervating the capsule of the ankle joint have been investigated in 34 normal and 19 arthritic anaesthetised rats. Afferent fiber diameter and conduction velocity were in the same range in normal and arthritic rats. All receptors examined were excited by mechanical stimulation of the joint capsule and the majority adapted slowly. A resting discharge was absent in normal rats in contrast to the arthritic animals where it was present in about 25% of the sample. The mechanical thresholds of the responses, measured using either von Frey hairs or the force transducer, ranged from 4.6 mN to 65 mN for 11 units recorded in normal and exceeded 80 mN for 11 others. For 30 units recorded in arthritic animals the thresholds ranged from 0.4 to 46 mN. When tested, pressure on the ankle or small degrees of flexion or extension produced a high rate of discharge in receptors of arthritics while similar stimuli were ineffective in normals. Repeated indentation at short intervals caused a progressive reduction in response to 10 to 15% of control values in normal and almost to extinction in arthritic rats. Recovery occurred within minutes in normals but was delayed in arthritics. These results suggest that the changes in responsiveness of somatosensory neurons and in behaviour, previously described in arthritic rats, can be partly accounted for in terms of the altered properties of the joint capsule receptors.

Adaptation, Physiological↗
PubMed1984

Further evidence for changes in the responsiveness of somatosensory neurons in arthritic rats: a study of the posterior intralaminar region of the thalamus.

In 21 arthritic rats, responses of 128 somatosensory neurons located in the intralaminar region of the thalamus were studied. This study reveals a profound change in the responses of intralaminar neurons in such rats, as compared with those observed in normal animals. Most of the activated neurons (98/120) were driven by moderate mechanical stimulation applied to the joints, while only few neurons (7/120) were exclusively driven by intense mechanical stimuli such as pinch. In addition numerous activated neurons were located in the ascending branch of the CL where in normal rat, few somatosensory 'noxious' neurons have been recorded.

Animals↗
PubMed1984

Further evidence for a bidirectional effect of naloxone on the pain threshold in tolerant and non-tolerant arthritic rats.

In arthritic rats, low doses of naloxone induced powerful analgesic effects (as gauged by the vocalization threshold elicited by pressure on the paw) which were marked for 3 and 6 micrograms/kg IV, whereas high doses (1000 and 3000 micrograms/kg IV) induced hyperalgesia. This bidirectional effect persisted in arthritic rats rendered tolerant to morphine, but whereas the analgesic effects were suppressed or reduced, the hyperalgesic effects induced by the higher doses were unchanged. These results suggest that the analgesic and hyperalgesic effects might be mediated by different systems.

Animals↗
PubMed1984

[Acute inflammation and hyperalgesia: their consequences on the responses of various neurons of the ventrobasal thalamic complex in rats].

Neuronal responses elicited in the ventrobasal thalamic complex by somatic noxious stimuli are facilitated early in the course of carrageenin-induced acute inflammation, (i) the responses evoked by noxious stimuli applied on the injected paw were enhanced (50-300%); (ii) similar increase was also observed for responses obtained from preexisting receptive fields distinct from the injection site; (iii) moreover, new responses could be elicited by noxious stimuli applied in initially unresponsive areas. These data suggest the involvement of central mechanisms underlying these changes.

Animals↗
PubMed1983

Altered properties and laminar distribution of neuronal responses to peripheral stimulation in the SmI cortex of the arthritic rat.

The properties of the neuronal responses to different types of mechanical peripheral stimulation were studied during electrode penetrations in the first somatosensory cortex of anaesthetized rats with polyarthritis. Very few neurons were driven by light cutaneous stimulation (such as brushing) or by intense mechanical stimulation. Most of the neurons were driven by joint movement and/or moderate pressure on the skin. These neurons could be found in all cortical layers, the majority being located in layer V. These results contrast sharply with the properties and laminar distribution of the different functional categories of cortical neurons, as observed in normal animals.

Animals↗
PubMed1983

Low dose of morphine microinjected in the ventral periaqueductal gray matter of the rat depresses responses of nociceptive ventrobasal thalamic neurons.

The effect of low doses of morphine (2 micrograms in 0.2 microliter) microinjected in the periaqueductal gray matter (PAG) was studied on responses of 11 nociceptive (N) and 3 non-nociceptive (Nn) ventrobasal (VB) thalamic neurons in lightly anesthetized rats. Responses of Nn neurons were unmodified but their receptive field was consistently enlarged during 50-60 min. Responses of N neurons to calibrated pinches were strongly depressed when the microinjection site was located in the PAG or in the dorsal raphe (NDR) (7 cases), and not significantly changed when morphine was applied in the dorsal PAG. For the 7 depressed neurons, the mean value of the responses expressed as a percentage of the control was 20.12 +/- 5.17, 15 min after morphine application. This depressive effect was variably reversed by naloxone (0.1-0.5 mg/kg).

Animals↗
PubMed1983

The analgesic effects of morphine, but not those of the enkephalinase inhibitor thiorphan, are enhanced in arthritic rats.

The effects of various i.v. doses of morphine (0.1, 0.3 and 1 mg/kg) and of thiorphan, an inhibitor of enkephalinase (0.7, 2.5, 5, 10 and 15 mg/kg), were studied upon the vocalization threshold to foot pressure in normal rats and rats with Freund's adjuvant-induced arthritis. The vocalization threshold in arthritic rats was, before any injections, significantly lower than in normal rats (mean pressure threshold for vocalization: 115.2 g +/- 14.7 (n = 152) for arthritic rats vs 182.5 g +/- 21.3 for normal rats (n = 152). The various doses of morphine in raising the vocalization threshold were more efficient in arthritic than in normal rats (maximum vocalization threshold (% of control) following 1 mg/kg morphine = 225.70 +/- 10.21 in arthritic rats vs 140.75 +/- 6.87 in normal rats, n = 9 in each case). This effect was dose-dependent, and in every case, naloxone-reversible. Injected at doses of 5-15 mg/kg, thiorphan increased the vocalization threshold (maximum = 223.91% +/- 11.96 in arthritic rats vs 223.30% +/- 5.93 in normal rats for 15 mg/kg i.v., n = 9 for each group). This effect was not greater in arthritic than in normal rats. The dose of 2.5 mg/kg of thiorphan was insufficient. Administered at 0.7 mg/kg, thiorphan significantly decreased the vocalization threshold in the arthritic rats only. These effects of thiorphan were all naloxone-reversible using doses of naloxone which were one-hundredth of those of thiorphan.

Amino Acids, Sulfur↗
PubMed1983

Further evidence for a strong depressive effect of low doses of morphine on VB thalamic neuronal responses (a study on arthritic rats).

The effects of various i.v. morphine doses (30, 100 and 1000 micrograms/kg) were studied upon unitary ventral basal (VB) neuronal responses elicited by joint stimulation in 24 Freund's adjuvant induced arthritic rats. The depressive effect of morphine was significantly dose-related and generally naloxone-reversible; however there were sometimes some difficulties to reverse morphine effect with the lowest dose of naloxone (10 micrograms/kg). The effect of morphine was not significantly different from that obtained in normal rats upon responses of specific nociceptive VB neurons. Although these results do not explain enhancement of morphine analgesia in arthritic rats by comparison with normal rats, they do confirm efficiency of low doses of morphine upon VB neuronal responses elicited by stimuli which induce nociceptive reaction in freely moving animals.

Animals↗
PubMed1983

Rat somatosensory (SmI) cortex: I. Characteristics of neuronal responses to noxious stimulation and comparison with responses to non-noxious stimulation.

Single unit responses to noxious and non-noxious somatic stimulation were investigated in the somatosensory (SmI) cortex of rats under halothane-nitrous oxide anaesthesia. Four categories of neurons were observed: (1) neurons driven by non-noxious cutaneous stimulation, (2) neurons driven by non-noxious deep stimulation, (3) neurons driven by noxious stimulation only (nociceptive specific neurons), (4) neurons driven by noxious as well as non-noxious stimulation (convergent or nociceptive non-specific neurons). The receptive fields of the neurons driven by contralateral cutaneous non-noxious stimulation were small. These neurons responded phasically to cutaneous stimulation in the majority of cases. Neurons driven by stimulation of deep receptors (e.g. joint movement) could also be recorded in the same part of SmI cortex. Neurons driven by noxious stimulation had large receptive fields and were often tonically driven by noxious stimulation. Convergent (or nociceptive non-specific) neurons could often be inhibited from body parts not included in their excitatory receptive field. Some neurons driven by noxious stimulation were able to encode stimulus parameters such as temperature of a hot water bath or surface of the skin area stimulated. The different categories of neurons defined above could be successively recorded during a given electrode penetration. Evidence for the somatotopic organization of the different categories of inputs was obtained. These results strongly suggest that the first somatosensory (SmI) neocortex is involved in nociception.

Afferent Pathways↗