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M L Sotgiu

Publications and source records attributed to M L Sotgiu.

At least 37 records · Page 2Linked to original sources
PubMed1996

Injured nerve block alters adjacent nerves spinal interaction in neuropathic rats.

Baseline activity and responses to simultaneous saphenous stimulation of pairs of neurones recorded from sciatic (L5-6) and saphenous (L2) spinal cord segments, in rats with thermal hyperalgesia following sciatic constriction, were analysed before, during and after a sciatic nerve block with a local anaesthetic. In sciatic neurones, during the block, reductions of baseline activity (p < 0.001), increases in threshold of saphenous electrical stimulation (p < 0.01) and reductions of responses to electrical and to natural noxious saphenous stimuli (p < 0.001) were consistently found. The neuronal baseline and evoked activities remained unmodified in saphenous neurones. The contribution of input from injured periphery to central neurone circuitry mechanisms underlying the unmasking of improper afferents is discussed.

Afferent Pathways↗
PubMed1996

Peripheral mononeuropathy affects hypothalamic and splenocyte beta-endorphin levels but not immune function in the rat.

Beta-endorphin and substance P levels were measured in the hypothalamus of rats 14 days after chronic constriction injury of right sciatic nerve. Furthermore, beta-endorphin concentrations in splenocytes, phytoemoagglutinin-induced proliferation of splenocytes, and natural killer activity were assessed. We observed a significant increase of beta-endorphin and substance P hypothalamic levels, and a significant decrease of beta-endorphin concentrations in the immune cells. In contrast, the peripheral mononeuropathy did not affect the immune function. This study presents a picture of central and peripheral peptide changes consistent with a painful condition, but different from what previously observed in rats which underwent peripheral nerve deafferentation or stressful conditions.

Animals↗
PubMed1995

Spinal expansion of saphenous afferents after sciatic nerve constriction in rats.

In rats with chronic constriction of one sciatic nerve, neurone pair responses to saphenous electrical stimulation were simultaneously recorded in sciatic (L5-6) and in saphenous (L2) spinal areas. In 16 rats with thermal hyperalgesia, 43 pairs of neurons were recorded, 4 and 14 days after constriction, on both sides of the spinal cord. On the side ipsilateral to nerve constriction, stimulation of the saphenous evoked excitatory responses in 90% of neurones recorded in the L5-L6 sciatic area, regardless of the post-constriction time. No responses were evoked by saphenous stimulation of the L5-L6 contralateral spinal cord neurones. The possibility that pre-existing connections are unmasked after nerve injury and impinge on sensitized neurones, contributing to abnormal pain sensations such as, for instance, extraterritorial pain, is discussed.

Animals↗
PubMed1995

Poststimulus afterdischarges of spinal WDR and NS units in rats with chronic nerve constriction.

Forty pairs of wide dynamic range (WDR) and nociceptive specific (NS) neurones were simultaneously recorded in the dorsal horn of rats with chronic constriction injury (CCI) of the sciatic nerve. The responses to noxious mechanical stimulation were analysed and the afterdischarges were compared in the two neuronal populations. The number of neurones presenting an afterdischarge was higher in WDR than in NS population. Furthermore afterdischarges had significantly longer duration and greater magnitude with slower time course decays in WDR than in NS neurones. Given the role that afterdischarge may have in the prolonged transmission of nociceptive information, the possibility that WDR neurones could give a major contribute to the abnormal processing of noxious signals in CCI rats is proposed.

Animals↗
PubMed1995

Evidence that inhibitory mechanisms mask inappropriate somatotopic connections in the spinal cord of normal rat.

1. The responses to stimulation of the sciatic and saphenous nerves have been studied in 65 pairs of spinal dorsal horn neurons simultaneously recorded at the L2 and L5-L6 lumbar segments of the rat's spinal cord. The neurons were recorded in anesthetized and paralyzed animals. 2. Five- or seven-barreled micropipettes were utilized for recording and for the application of drugs with iontophoresis or micropressure techniques. The drugs used were: strychnine, as a selective antagonist at glycine receptors; sodium glutamate and N-methyl-D-aspartate (NMDA), as agonists at excitatory glutamatergic receptors; glycine, as an agonist at the inhibitory glycine receptor; and the local anesthetic lidocaine, as a reversible local conduction blocker both in the periphery and in the spinal cord. 3. All neurons had cutaneous receptive fields in the ipsilateral hindpaw. Neurons responding exclusively to saphenous stimulation in L2 and to sciatic stimulation in L5-L6 were selected for this study. The responses consisted of bursts of > or = 5 spikes, often partially inserted in a field potential, with latencies of 5.0 +/- 1.1 (SD) and 5.2 +/- 1.2 ms, respectively. The thresholds of stimulation and the response latencies were controlled to be stable throughout the experiments. 4. Eighty-five percent (29 of 35) of the neurons tested in L5-L6 exhibited responses to saphenous stimulation during strychnine microejection in the recorded neurons. The neurons became again unresponsive to saphenous stimulation shortly after the end of strychnine ejection. 5. All the neurons tested in L5-L6 (n = 14) showed a significant increase in background activity and remained unresponsive to saphenous stimulation during glutamate microejection on the recorded neurons. 6. All the neurons tested in L5-L6 (n = 17) showed responses to saphenous stimulation after sciatic nerve block with local anesthetic. The responses to saphenous stimulation disappeared after the effect of local anesthetic ceased. 7. All the neurons tested in L5-L6 (n = 6), in rats with a local block of the sciatic nerve, showed a reversible increase in the background activity during NMDA microejection in the spinal saphenous area at L2. 8. In rats with a local block of the sciatic nerve, the responses evoked in L5-L6 neurons (n = 12) by saphenous stimulation were reduced both in field potential amplitude and in number of spikes during microejection of glycine, and were suppressed during microejection of lidocaine in the spinal saphenous area in L2.(ABSTRACT TRUNCATED AT 400 WORDS)

Afferent Pathways↗
PubMed1994

A study of early ongoing activity in dorsal horn units following sciatic nerve constriction.

An analysis was made of the background activity of spinal neurones involved in nociceptive processes during, and in the first hour after, sciatic nerve constriction in normal rats and in rats in which sciatic nerve conduction had been previously blocked with local anaesthetic. In both pure noxious and WDR neurones the results showed high frequency discharges at the time of ligation, followed by a slight but persistent increase in activity that reached, after 1 h, values 6-8 times those preligature. The increased post-injury discharge could be reduced by secondarily applying lidocaine on the peripheral site of constriction. There were no neuronal activity changes after the ligatures in rats with sciatic nerve pretreated with local anaesthetic. The likelihood that the early persistent increase in activity may have a role in the excitability change of spinal neurones observed in neuropathic pain is discussed.

Animals↗
PubMed1994

Different time-courses of i.v. lidocaine effect on ganglionic and spinal units in neuropathic rats.

The effect of intravenous lidocaine (4 mg kg-1) on ganglionic and spinal neuronal hyperactivity following sciatic chronic constriction injury (CCI) was studied in anaesthetized and curarized rats. A significant difference in the time course and magnitude of the lidocaine effect on the two neuronal populations was found. Longer lasting and more potent inhibitory effects on the dorsal horn neurones in comparison with ganglionic neurones were observed. By contrast the magnitude and time course of the inhibitory effects were highly comparable in dorsal horn neurones before and after acute rhizotomy. The results indicate that peripheral and central effects of lidocaine are not sequentially related. The likelihood that lidocaine inhibition at central sites may have a role in its analgesic effect, at least in the neuropathic model, is discussed.

Animals↗
PubMed1993

Diverse modulation by systemic lidocaine of iontophoretic NMDA and quisqualic acid induced excitations on rat dorsal horn neurons.

The effects of systemic lidocaine (3-4 mg/kg) on the responses of 60 wide dynamic range neurons (WDR) to iontophoretically applied N-methyl-D-aspartic acid (NMDA) and quisqualic acid (QUIS) were studied in anesthetized, paralysed rats. The results show that lidocaine induced (i) potentiation of the NMDA excitation, reversible by 7-chloro-kynurenate (7-Cl-KYNA), a selective antagonist of the glycine binding site on the NMDA receptor; (ii) reduction of the QUIS excitation, reversible by strychnine (STRYCH), a glycine antagonist at its receptor. These findings, supporting a glycine-like action of lidocaine, are discussed together with data on the role of excitatory amino acids (EAAs) and the analgesic effect of lidocaine on neuropathic pain.

Animals↗
PubMed1993

Central effects of systemic lidocaine mediated by glycine spinal receptors: an iontophoretic study in the rat spinal cord.

The objective of this investigation was to demonstrate the possible interactions of systemic lidocaine (lido) with inhibitory receptors in the spinal cord. In the lumbar dorsal horn of anesthetized and curarized rats, 60 physiologically identified, wide dynamic range (WDR) neurons, were recorded extracellularly. Glutamate, glycine and its selective antagonist, strychnine, were iontophoretically applied onto the neurons either singularly or concurrently. The effects of systemic lido on the drug-induced frequency changes and the interaction with the glycine receptors, using strychnine as a probe, were studied. It was consistently found that: (i) lido (3-4 mg/kg) inhibited the excitatory responses to iontophoretic glutamate, (ii) this inhibition was significantly antagonized by concurrent iontophoretic strychnine, (iii) iontophoretic glycine induced comparable glutamate inhibition that was reversed by strychnine. In contrast, no effect on glutamate-induced excitations was observed when lido was applied by micropressure or a different local anesthetic was systemically administered. The results suggest that central inhibitory effects of lido could be mediated by spinal strychnine-sensitive glycine receptors, activated by lido itself or possibly by its glycine residue-bearing metabolites.

Animals↗
PubMed1992

Effect of systemic lidocaine on dorsal horn neuron hyperactivity following chronic peripheral nerve injury in rats.

Systemic lidocaine (3-4 mg/kg) was tested for its effect on identified spinal cord wide-dynamic-range (WDR) neurons in rats with a unilateral chronic neuropathy induced by two different peripheral nerve injuries (section or compression by ligatures). In both cases, neurons on the side ipsilateral to the injuries showed a spontaneous firing frequency higher than that of the opposite intact side (23.5 +/- 3.4 vs 4.2 +/- 1.5 spikes/sec). The hyperactivity was not affected by a sensory block of the peripheral receptive field. It was consistently found that lidocaine suppressed or reduced the spontaneous neuronal hyperactivity on the ipsilateral side, whereas it had no effect on the normal spontaneous activity of the neurons on the intact side. In all recordings, the hyperactivity returned to the prelidocaine injection rates within 20 min. These results indicate a preferential action of subanesthetic doses of lidocaine on the hyperactive WDR neurons. Such preferential action is related to a susceptibility acquired by WDR neurons of the peripherally injured side and is not simply attributable to the increased frequency of firing.

Animals↗
PubMed1991

Facilitatory role of calcitonin gene-related peptide (CGRP) on excitation induced by substance P (SP) and noxious stimuli in rat spinal dorsal horn neurons. An iontophoretic study in vivo.

The effects of iontophoretically applied calcitonin gene-related peptide (CGRP) and/or substance P (SP) onto physiologically identified neurons in the rat lumbar dorsal horn were studied. The consistent excitatory effects of SP found on the spontaneous and the noxious evoked activity were significantly potentiated by CGRP application. This peptide facilitated the noxious evoked activity and did not affect the spontaneous activity of the neurons. The responses to non-noxious stimuli were unaffected in all cases.

Action Potentials↗
PubMed1991

Effects of lateral reticular nucleus stimulation on trigeminal sensory and motor neuron activity related to the jaw opening reflex.

The effects of lateral reticular nucleus (LRN) stimulation on the responses to tooth pulp (TP) stimulation of neurons located in the trigeminal (V) sensory (39 units) and motor (33 units) nuclei were assessed in anesthetized rats. Only neurons which responded to TP stimulation with bursts of spikes that were in a constant temporal relationship with the digastric EMG signal were studied. The LRN-stimulating electrodes were positioned at optimal sites to suppress the TP-evoked jaw-opening reflex (JOR) recorded simultaneously with the neuronal activity related to it. It was found that: (1) the neurons in the V nucleus oralis responded to TP stimulation with 3-8 msec latency excitatory responses that were suppressed during LRN conditioning stimulation with a time course comparable to that of the JOR suppression, and (2) the neurons in the V nucleus motor responded to TP stimulation with 5-15 msec latency excitatory responses. This activity was suppressed during LRN-conditioning stimulation with a time course that parallels the inhibition of the activity of nucleus oralis neurons and of the JOR. However, assuming that the excitatory interneurons for the V motoneurons are located in the nucleus oralis, the suppression of this input by LRN may account for the lack of response in V motor neurons. Thus, we suggest that LRN inhibits the TP-evoked JOR by acting on the sensitive afferent limb of the reflex.

Animals↗
PubMed1991

Selective inhibition by systemic lidocaine of noxious evoked activity in rat dorsal horn neurons.

The effect of systemically injected lidocaine (3-4 mg kg-1) on the responses to noxious and non-noxious stimuli on 28 wide dynamic range (WDR) neurons in the dorsal horn was studied in anesthetized and curarized rats. It was consistently found that lidocaine reduced or suppressed the responses to noxious stimuli whereas it did not act on the responses to non-noxious stimulation and on the spontaneous activity. Furthermore the noxious stimuli were completely ineffective from 10-15 min following the lidocaine injection while the non-noxious stimuli maintained their efficacy. The control responses, in all the cases, returned within 20 min. The results suggest that lidocaine exerts a selective inhibitory effect on nociceptive transmission at the spinal level.

Animals↗
PubMed1990

Bulbar influences on the periaqueductal gray. Potential role in nociception.

Unit activity was recorded from 96 neurons in the periaqueductal gray (PAG) in response to focal electrical stimulation of the lateral reticular nucleus (LRN) and the nucleus gigantocellularis (NGC), in anesthetized, curarized rats. Consistent with anatomical studies showing direct projections from these nuclei to PAG, short latency excitatory responses (less than 5 ms) were found in 63 neurons and inhibition of the activity in 28 neurons. Peripheral noxious heat stimulation was effective in altering the activity in 36 of these neurons (38%). The LRN and NGC stimuli inhibited the noxious evoked responses in 26 of these neurons. The inhibition could also be induced when the dorsolateral funiculi (DLFs) were cut. These results indicate that LRN and NGC can have a direct influence on PAG neurons, which are probably involved in the processing of noxious information.

Animals↗
PubMed1989

Cortical influences on neurons of the lateral reticular nucleus responding to noxious stimuli.

The effect of frontoparietal sensorimotor (FPSM) cortex stimulation on both the spontaneous and the noxious evoked activity of neurons in the lateral reticular nucleus (LRN) was tested in barbiturate-anesthetized rats. Ninety-three LRN neurons that responded to a noxious heat stimulus (HS) were recorded (72% antidromically fired from the cerebellum). Of these, 66 neurons altered their spontaneous firing rates in response to cortical stimulation. Two patterns of responses were found: either an excitation followed by a suppression of spontaneous activity (52 neurons), or a pure suppression of spontaneous activity lasting 50-400 msec (14 neurons). In 46 of these neurons, it was found that cortical stimulation reduced HS-evoked activity to near the baseline level. Furthermore, it was found that when applied after a prolonged cortical stimulation, the HS was ineffective. It is concluded that FPSM cortex can influence nociceptive information in LRN neurons that respond to its stimulation, possibly interfering with the mechanisms underlying stimulation-produced analgesia (SPA). In this context, it is proposed that the cortex can modulate the activity of LRN neurons that activate, through local loops, a descending antinociceptive system and also a separate projection system to the cerebellum.

Action Potentials↗