PubMed Health⌕ Search

Biomedical subjects

J M Benoist

Publications and source records attributed to J M Benoist.

At least 19 recordsLinked to original sources
PubMed1992

Primary somatosensory cortex in rats with pain-related behaviours due to a peripheral mononeuropathy after moderate ligation of one sciatic nerve: neuronal responsivity to somatic stimulation.

Single-unit recordings were made under moderate gaseous anaesthesia in the hindpaw representation area of the two primary somatosensory motor cortices (SmI) of rats (n = 58) rendered mononeuropathic by four loose ligatures placed around one common sciatic nerve 2-3 weeks beforehand. The rats exhibited clear hyperalgesia and allodynia from the paw with the ligated sciatic nerve, to both mechanical and thermal stimuli. From the tested neuronal population (n = 640), about the same proportion could be activated by somatic stimuli in each cortex: 165/362 (45%) in the cortex contralateral to the ligated sciatic nerve (Cc), 105/278 (37%) in the cortex ipsilateral to the ligated sciatic nerve (Ci). Neurones driven by light touch, exhibited RFs strictly contralateral to the recording sites. Their proportion and response characteristics were similar regardless of recording side. However, the number of neurones with RFs in the sciatic nerve territory was above 95% in the Ci, and was dramatically reduced to 43% in the Cc. By contrast, the number of neurones with RFs supplied by the saphenous nerve reached 57% on this side. Although the RF size of all the neurones appeared roughly normal, there were fewer Cc than Ci neurones with RFs located on the paw itself and with RFs of extremely small size in the sciatic nerve territory. The proportion of neurones responding to a joint stimulus was significantly higher in the Cc than in the Ci. The neuronal responses to joint stimuli of the paw with the ligated sciatic nerve were significantly more sustained than those recorded in the Ci and elicited from the normal paw. The proportion of neurones driven by mechanical stimulation which gave rise to nociceptive reactions in freely moving animals, i.e. "nociceptive" neurones, was comparable in each cortex. However, half of the Cc neurones exhibited paroxysmal discharges occurring without intentional stimulation and of long duration (1 min to several minutes). Only 66% of Cc but 93% of Ci "nociceptive" neurones were exclusively activated by pinch. The remaining Cc neurones were also activated by applying moderate pressure to the paw with the ligated nerve. Pinch responses from the paw with the ligated nerve were often more intense and of longer duration than responses elicited from the intact paw. The "nociceptive" Cc neurones were especially sensitive to thermal stimuli of 39-44 degrees C when the stimuli were applied to the paw with the ligated nerve. They also responded vigorously to a 10 degrees C stimulus applied to this paw.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1992

Further evidence for the involvement of SmI cortical neurons in nociception: modifications of their responsiveness over the early stage of a carrageenin-induced inflammation in the rat.

In this electrophysiological study, changes in the responsiveness of neurons in the primary somatosensory (SmI) cortex in rats were analyzed during the development of carrageenin (CRG)-induced inflammation, an animal model of acute inflammatory hyperalgesia. SmI neurons were characterized as responding to non-noxious light touch, non-noxious articular movement, or noxious pinch. A total of 23 neurons so characterized in three groups were recorded for 60 min (17 of these neurons were recorded for up to 150 min) after an intraplantar injection of CRG. The possible modifications in their background and evoked activities were analyzed over this period of time. After CRG administration, cells responding to noxious pinch stimuli (n = 8) showed a nonsignificant increase in spontaneous activity, but a significant increase in their evoked response to pinch. These results were quite similar to past observations in the ventrobasal nucleus of the thalamus (VB). Cells responding to non-noxious articular stimulation (n = 6) showed variable modifications and no significant increase in the mean evoked response for up to 60 min. These results for articular cells were also quite comparable to results seen for VB responses for similar cells. However, mean spontaneous activity, which showed a highly variable increase, was significantly increased after 60 min. The depressive effect of a local anesthetic, Xylocaine, was tested on the activities of four cells (one pinch, three light touch units) 60 min after CRG administration over a 20-min interval. Xylocaine was found to depress both spontaneous activity and responses to the effective somatic stimulus, thereby implying that the observed central modifications in neuronal discharge are linked to the peripheral inflammation. Modifications observed for each group of cells are compared with past observations in peripheral fibers, in spinal dorsal horn neurons, and especially in the VB under similar inflammatory conditions. These data confirm that the SmI cortex is involved in the nociceptive process. Furthermore, the contrast between some modifications observed at this level and past observations under similar inflammatory conditions suggests a unique role of some cortical neurons, which might partially account for mechanical allodynia.

Afferent Pathways↗
PubMed1991

Electrophysiological evidence that morphine can exert an antinociceptive effect in a neuropathic state: a study in the ventrobasal thalamus of rats after moderate ligation of one sciatic nerve.

This study was performed in rats with a mononeuropathy induced by loose ligatures around the common sciatic nerve 2 weeks before the recording session, and exhibiting clear alterations of several pain-related behaviours. Morphine injected intravenously (0.6 and 1 mg/kg) strongly depressed the ventrobasal thalamic neuronal responses to pinch applied to the lesioned or the non-lesioned hindpaw. The effect, comparable on the both sides, was dose-related and reversed by naloxone (0.1 mg/kg i.v.).

Analysis of Variance↗
PubMed1990

Neuronal responsiveness in the ventrobasal thalamic complex of rats with an experimental peripheral mononeuropathy.

1. Single-unit recordings were made, under moderate gaseous anesthesia (33% O2-66% N2O + 0.5/0.6% halothane), in the ventrobasal (VB) thalamic complex of rats (n = 42) with a mononeuropathy created 2-3 wk beforehand, by four loose ligatures around the common sciatic nerve. Before the recording session, three behavioral nociceptive tests to both mechanical and thermal stimuli revealed that these rats exhibited clear hyperalgesia (excessive reactions to noxious stimuli) and allodynia (nociceptive reactions to stimuli usually perceived as nonnoxious). 2. Neurons, characterized by their responses to manual mechanical stimuli, were classified into two groups: group 1 neurons exclusively driven by light tactile stimuli applied to the receptive field (RF), strictly contralateral to the recording site; and group 2 neurons, driven by sustained pinch applied to a large RF, often bilateral. 3. From the total population of neurons (n = 386), only those responding to stimuli applied to one posterior paw were studied; the proportion (35-40%) of these cells was comparable in each of the two VB: n = 93/262 and 44/124 in the VB contralateral (VBc) and ipsilateral (VBi) to the damaged nerve, respectively. The proportions of each functional group of neurons (group 1 or 2) were also similar on each side. 4. For all group 1 neurons the RFs size was comparable to that observed in normal rats. In the VBi the responses of these neurons presented the classical response pattern observed for VB neurons involved in touch transmission, as did the VBc group 1 neurons with RFs in the saphenous (Sa) territory. In sharp contrast, activities of VBc group 1 neurons with RFs in the sciatic (Sc) nerve territory exhibited several abnormalities: higher background activity, fading of the response with repetitive stimulation, and afterdischarges outlasting the applied stimulus. 5. As in normal rats, 52% of VB group 2 neurons exhibited bilateral symmetrical RFs. Their responses to mechanical stimuli were often greater for stimuli applied to the affected paw, and some of them could be activated by moderate pressure to this paw. Heat responses also illustrated the profound increased sensitivity of the lesioned side, and the activation threshold to thermal stimulation of these group 2 neurons was lowered by 4-6 degrees C compared to normal values. In addition, these neurons responded to immersion of the lesioned paw in a 10 degrees C water bath, a stimulus that was ineffective when applied to the opposite paw.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Evidence for peripheral serotonergic mechanisms in the early sensitization after carrageenin-induced inflammation: electrophysiological studies in the ventrobasal complex of the rat thalamus using a potent specific antagonist of peripheral 5-HT receptors.

The effect of ICS 205-930 (ICS), a specific 5-HT3 receptor antagonist, was analyzed on the sensitization of ventrobasal (VB) thalamic neuronal responses produced by an intraplantar injection of carrageenin. ICS was injected locally in the plantar paw, simultaneously, or after carrageenin (at 20 min or later than 70 min). The progressive increase of the VB neuronal responses to pinch (total number of spikes in the discharge) due to carrageenin sensitization, was prevented, blocked, or reversed, by intraplantar ICS, at a dose as low as 3.2 ng/kg, when injected, simultaneously or in the first half-hour following the carrageenin injection itself. The carrageenin sensitization then reappeared, 50-90 min after the initiation of the inflammation. By contrast to these early injections of ICS, a later administration of ICS (70 min or more, after the carrageenin injection), did not influence the sensitization. The time course of the effects of this 5-HT3 antagonist receptor agrees well with the time course of 5-HT release into the inflammatory exudate. These data, and those previously reported on the action of aspirin and of a peripheral antihistamine on carrageenin sensitization, are compared. These results indicate the relative participation of the various inflammatory substances released in the exudate, and the importance of timing of administration for an effective antagonism of the hyperalgesia elicited by this inflammation.

Action Potentials↗
PubMed1989

Evidence for central phenomena participating in the changes of responses of ventrobasal thalamic neurons in arthritic rats.

In this study performed in the Freund's adjuvant-induced arthritic rat, a local injection of lidocaine in one hind paw strongly depressed the ventrobasal thalamic neuronal responses to mild stimulation of both ankles. In parallel, a behavioral study provided evidence for a bilateral hypoalgesia, tested by the vocalization threshold to paw pressure, after a unilateral anesthetic block. The involvement of central phenomena in the changes of neuronal responsivity described in this model of experimental pain is therefore suggested.

Action Potentials↗
PubMed1988

Behavioural and electrophysiological studies on the paradoxical antinociceptive effects of an extremely low dose of naloxone in an animal model of acute and localized inflammation.

We have previously described the paradoxical antinociceptive effect of low doses of an opiate antagonist, naloxone, in rats suffering from chronic arthritis induced by Freund's adjuvant. In the present work, the appearance of this naloxone sensitivity was studied, using a model of inflammatory hyperalgesia with a more rapid onset, namely carrageenin-induced rat paw edema. In these animals, an extremely low dose of naloxone (3 micrograms/kg i.v.), induced a clear antinociceptive effect (as gauged by the vocalisation threshold to paw pressure), which was observed for both the edematous and the contralateral hind-paw. Small and transient 1 h after carrageenin injection, this effect increased progressively 4 h and 24 h later, reaching a level comparable to that observed with morphine 1 mg/kg i.v. in normal rats, at 24 h. Electrophysiological studies performed in parallel, confirmed the behavioural data so that 24 h after the injection of carrageenin, naloxone (3 micrograms/kg i.v.) reduced the VB thalamic neuronal responses elicited by stimulation of the inflamed paw by 50%. Hypothesis concerning the mechanisms of the paradoxical action of naloxone in models of inflammatory hyperalgesia are discussed.

Action Potentials↗
PubMed1988

Behavioural and electrophysiological evidence for an analgesic effect of a non-steroidal anti-inflammatory agent, sodium diclofenac.

The effects of various i.v. doses of diclofenac sodium (Voltaren, 1.5, 3, 6 and 9 mg/kg) were evaluated by measuring the vocalization threshold in response to paw pressure in normal and in Freund's adjuvant-induced arthritic rats. An electrophysiological study performed in parallel in arthritic rats considered the effects of 6 mg/kg i.v. diclofenac on ventrobasal thalamic neuronal responses driven by mild stimulation of an inflamed joint. In normal rats, 6 and 9 mg/kg i.v. diclofenac raised vocalization thresholds significantly (maximum vocalization thresholds were respectively 135.67 +/- 3.30% and 157.41 +/- 4.62% of the preinjection control at 30 min, n = 9 in each group), while no effect was observed with 3 mg/kg. In arthritic rats, i.v. doses of 3, 6 and 9 mg/kg diclofenac induced a clear analgesic effect (maximum vocalization thresholds were respectively 172.22 +/- 4.26, 201.78 +/- 4.76, 222.33 +/- 5.10% of the control at 25 min, n = 9 in each group), whereas a dose of 1.5 mg/kg i.v. did not raise the threshold. In arthritic rats, the VB neuronal responses were depressed by about 50% 20 min after an injection of 6 mg/kg i.v. diclofenac. These results clearly establish that diclofenac produces a dose-dependent analgesic effect, which is more potent in arthritic than in normal rats.

Action Potentials↗
PubMed1987

Initial nociceptive sensitization in carrageenin-induced rat paw inflammation is dependent on amine autacoid mechanisms: electrophysiological and behavioural evidence obtained with a quaternary antihistamine, thiazinamium.

We have studied the ability of a quaternary antihistamine, thiazinamium, to inhibit the nociceptive sensitization that occurs early, during the first hour, following intraplantar injection of the polysaccharide carrageenin in the rat. Parallel studies were performed with an electrophysiological model (changes in responsiveness of ventro-basal thalamic cells driven by noxious stimulation of the paws), and a behavioural test (changes in threshold stimulus necessary to elicit vocalization by gradually increased pressure to the paws). When thiazinamium was given intravenously 10 min before carrageenin, no sensitization due to inflammation was found in either test. By contrast, when thiazinamium was administered 20 min after carrageenin, there was a clear sensitization in both tests that did not differ from that found in animals not treated with the antagonist. Paw oedema was also slightly decreased by pretreatment with thiazinamium. These results suggests that early inflammatory sensitization of peripheral nociceptors is mainly dependent on an initial release of histamine (and/or serotonin, since thiazinamium could also have some antiserotoninergic activity).

Animals↗
PubMed1987

Neuronal response thresholds to and encoding of thermal stimuli during carrageenin-hyperalgesic-inflammation in the ventro-basal thalamus of the rat.

This study analyzed neuronal encoding and response thresholds to thermal stimuli at the ventro-basal (V.B.) thalamus level during a hyperalgesic inflammation induced by intra-plantar injection of carrageenin in the rat. The threshold and the encoding capacity of the cells were studied during two phases of the inflammatory process, namely the "acute" phase (the first two hours following the injection), and "sub-acute" phase 24 h after). In this second phase the hyperalgesia was verified using a behavioral nociceptive test, just prior to the recording session. Only VB neurones with a receptive field that included the injected paw were considered. In the acute phase, neurones exclusively driven by noxious stimuli were studied before and during the first two hours following the induction of the inflammatory oedema. In the sub-acute phase two groups of neurones which, on the basis of our previous studies, were presumably involved in the transmission of messages giving rise to the hyperalgesia could be separated: a group of neurones which were driven by intense mechanical stimuli and another group driven by moderate mechanical stimulation applied to the inflamed joints and/or the surrounding cutaneous areas. In the "acute" phase there was a dramatic lowering (by about 4 degrees C) of the response threshold of the neurones when the thermal stimulus was applied to the injected paw, although their threshold to the mechanical stimulus was still high. A linear encoding of the bath temperature used as a stimulus was observed for both the injected and the non-injected paws. For a few neurones, a leftward shift of the stimulus-response curve was found for the inflamed limb. In the "sub-acute" phase, neurones with high thresholds to the mechanical indentations still exhibited a low response threshold to the thermal stimulation, not only from the injected but also from the non-injected paw. The other group of neurones responded with relatively low thresholds to the both stimulus modalities. By contrast to the acute phase, the two groups of neurones exhibited only a weak ability to encode the stimulus intensity especially when the stimulus was applied to the inflamed paw. Both peripheral and central mechanisms are likely to be involved in the modifications of response threshold and encoding capacity at the VB thalamus level seen in these conditions of hyperalgesic inflammation. The differential time course of the responses to a liminal or to a supra-liminal temperature during the inflammation, are discussed in reference to some of the mismatches occurring in clinical situations of hyperalgesia.

Action Potentials↗
PubMed1987

Thresholds and encoding of neuronal responses to mechanical stimuli in the ventro-basal thalamus during carrageenin-induced hyperalgesic inflammation in the rat.

Neuronal response thresholds and the encoding of mechanical stimulus intensity in the ventro-basal (VB) thalamus was analyzed in anaesthetized rats before and during the first two hours following induction of hyperalgesic inflammation. This inflammation was induced by the intra-plantar injection of carrageenin in the hindpaw contralateral to the recorded neurones. Only neurones exclusively driven by noxious stimuli and with a receptive field on or including the injected paw were considered. In this early phase of the inflammatory process, there was no significant modification of the response threshold to the mechanical stimulus (indentation of about 300 micron). This suggests the involvement of additional neuronal population(s) to account for the decrease in the vocalisation threshold to pressure observed in the freely moving animal at this time of the inflammation. A liner encoding of the indentation depth was observed before and after the carrageenin injection although the slope of the stimulus response-curve was steeper after the injection. The data emphasize that the carrageenin-sensitization acts differentially on the liminal and supra-liminal responses of the same neurone to a skin indentation, since in the first hour following the initiation of the inflammation the sensitization is essentially observed for responses obtained with stimulus intensity largely above the threshold value. With regard to previous observations using thermal stimulation, the results also illustrate that the carrageenin induced sensitization of responses differs depending on the stimulus intensity and modality used.

Animals↗
PubMed1986

Differential depressive action of two mu and delta opioid ligands on neuronal responses to noxious stimuli in the thalamic ventrobasal complex of rat.

In the present investigation the effects of selective agonists for mu (Tyr-D-Ala-Me-Phe-Gly-ol (DAGO)) and delta (Tyr-D-Thr-Gly-Phe-Leu-Thr (DTLET)) opioid receptors on neuronal activities induced by noxious cutaneous stimuli in the rat ventrobasal (VB) thalamus were analyzed. The two agonists produced a clear depressive action on thermal as well as mechanical noxious stimuli. The depressive action of DTLET (3 mg/kg i.v.) was lower and of shorter duration than that of DAGO (2 mg/kg i.v.). However, this effect is unambiguously related to the selective stimulation of opioid receptors since a consistent effect was also observed for a dose as low as 1.5 mg/kg i.v. of DTLET. Moreover, DTLET effect needs a high concentration of naloxone (0.5 mg/kg i.v.) to be reversed, while DAGO effect is totally reversed with 0.1 mg/kg i.v.

Action Potentials↗
PubMed1986

Modifications in the responsiveness of rat ventrobasal thalamic neurons at different stages of carrageenin-produced inflammation.

The present study was aimed at analyzing the responsiveness of the ventrobasal (VB) thalamic neurons in rats presenting with a hyperalgic carrageenin-produced inflammation. The following were studied: the responses of the same VB neuron, before and 15-145 min after the plantar injection of carrageenin in a part of its receptive field (RF) (acute phase); the responses of VB neurons located in the thalamus contralateral to the hyperalgesic inflamed paw, 24-96 h after the injection (subacute phase); and the effect of a local anesthetic injected in the inflamed paw, and that of an intravenous injection of Aspirin, on neuronal response modifications. Responses of VB neurons initially activated by light tactile stimuli (group 1; n = 4) and by moderate joint stimulation (group 3; n = 4) were not modified in the early period following the carrageenin injection. By contrast, in the first few minutes following the injection. VB neurons exclusively driven by noxious mechanical and thermal stimuli (group 2; n = 23), exhibited a clear enhancement of their responses, which persisted during the observation period. These modifications were also observed for responses obtained from part of the RF remote from the injection site; moreover there was an extension of the RF to areas distant from the injured paw. The local injection of an anesthetic (Xylocaine) in this paw, suppressed the modifications of responses of group 2 neurons, elicited not only from the injected paw, but also from the remote parts of the RF. At this time Aspirin was almost inefficient (even at the dose of 100 mg/kg) on responses of these group 2 neurons. In the subacute phase responses of 72 somatosensory neurons were analyzed. Twenty-five of 72 responded to rapid repetitive light tactile stimulation applied on a small contralateral RF (group 1); their responses were similar to those encountered in a normal situation. Thirty-three of 72 neurons responded to intense mechanical stimuli such as pinches (group 2). For half of them the response characteristics were similar to those described in the normal rat; for the other half responses appeared 'faded': short duration; absence of after-discharge; poor reproducibility. Fourteen of 72 neurons responded to moderate stimulation of the joints, deep tissues and/or surrounding cutaneous areas of the inflamed paw (group 3). Their RF was mostly unilateral, i.e. contralateral to the recording site; the responses were sustained during the stimulation but rarely exhibited after-discharge.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗