Foraging activity and dietary spectrum of the Argentine ant (Hymenoptera: Formicidae) in invaded natural areas of the northeast Iberian Peninsula.

We analyzed the foraging activity and the dietary spectrum of the Argentine ant (Linepithema humile Mayr) and select native ants on cork oaks from Mediterranean open cork oak (Quercus suber) secondary forests. The study areas included invaded and noninvaded zones in close proximity. The Argentine ant's daily foraging activity was correlated to the abiotic factors studied, whereas the seasonal foraging activity was related not only to the variations in the average air temperature, but also to the trophic needs of the colony. Argentine ant workers focused their attention on protein foods during the queens' oviposition periods and during the larvae development phase, and on carbohydrate foods, such as honeydew, when males and workers were hatching. There were no significant differences over the entire year in the quantity of liquid food collected by the Argentine ant workers in comparison with the native ants studied. The solid diet of the Argentine ant on cork oaks is composed of insects, most of which are aphids. Our results have clear applications for control methods based on toxic baits in the invaded natural ecosystems of the Iberian Peninsula.

[Automatic analysis of the alternate movements of the arms in patients with type 2 spino cellular ataxia]. / Análisis automático de los movimientos alternativos de miembros superiores en pacientes con ataxia espinocerebelosa tipo 2.

INTRODUCTION: A patient with type 2 spino cerebellar ataxia has difficulty in carrying out alternate movements such as pronation and supination. OBJECTIVES. To evaluate the function of an automatized system for measuring disorders of alternate movements. PATIENTS AND METHODS: We studied the measurement of diadochokinesia in two groups of healthy patients, a first group (64 persons) to determine the normal intervals and a second group to validate the test (52 persons). We also studied 100 patients for validation of the system. A further 53 patients were evaluated before and after rehabilitation. RESULTS: Analysis of the basic measurements for diagnosis of duodochokinesia showed that the higher the cut off point, the greater the sensitivity of the test, whereas the opposite occurred with the specificity. Thus, regarding a higher cut off, there is a five times greater probability of a positive results in the patients than in healthy persons. However, the probability of a normal result is six times higher in healthy than in affected persons. The results of variant analysis done on patients before and after rehabilitation suggest that the presence of quantitative changes in the second study was due to the positive effect of neuro rehabilitation. CONCLUSION: The technique used is effective for differentiation of affected from healthy persons and its use is justified in the evaluation of co ordination ability after rehabilitation

[Quantitative evaluation of disorders of coordination in patients with Cuban type 2 spinocerebellar ataxia]. / Evaluación cuantitativa de los trastornos de la coordinación en pacientes con ataxia espinocerebelosa tipo 2 cubana.

INTRODUCTION: Implementation of quantitative techniques to study disorders of coordination of movements in hereditary ataxias permits an objective description of the disease. OBJECTIVES: To make an objective evaluation of the main disorders of coordination in patients with ataxia and compare healthy persons with those affected. PATIENTS AND METHODS: We made a prospective transverse study of 43 normal persons and 50 patients with type 2 spinocerebellar ataxia (SCA2). In all cases we made a qualitative examination of Romberg's sign in two stages to increase the sensitivity. We observed how long the person could keep his balance or whether he swayed and fell. The finger-nose test and diadochokinesia were also quantitatively analyzed using a specially designed system connected to a computer which permitted quantitative analysis. RESULTS: We showed that the patients with SCA2 swayed when standing upright. However, they swayed and fell more when the test became more sensitive. This showed loss of postural sense. The maximum variables of the period and standard deviation were increased, whilst the effectiveness was significantly reduced in the group of patients (finger-nose test). Quantitative examination of diadochokinesia showed increased values for the maximum period, standard deviation and integral. CONCLUSIONS: The techniques developed allow measurement of the main disorders of coordination in patients with SCA2, help to differentiate affected persons from healthy ones and are useful for the detection of moderate changes in severity during progression of the disorder.

Attenuated severity of new acute ischemic events in patients with previous coronary heart disease receiving long-acting nitrates.

BACKGROUND: Platelet aggregation and secondary vasoconstriction are key events in the genesis of acute coronary syndromes. HYPOTHESIS: Since nitrates have vasodilatory and antiaggregant effects, treatment with long-acting nitrates at the time of onset of acute coronary syndromes could be associated with attenuation of their severity. METHODS: A consecutive series of 533 patients with acute coronary syndrome and past history of coronary artery disease admitted to the Cardiology Service of a general hospital was studied. A specific questionnaire assessed the use of nitrates and other relevant drugs, as well as other clinical variables. The diagnosis of unstable angina or acute myocardial infarction (MI) was established according to clinical, electrocardiographic, and enzymatic criteria. RESULTS: In the whole cohort, 169 patients had MI and 364 had unstable angina. Previous use of long-acting nitrates was significantly more common in patients with unstable angina (56%) than in those with MI (37%) (p < 0.0001). Multivariate analysis identified being a nonsmoker [odds ratio: 95%, confidence limits (CL) 0.37, 0.23-0.59], previous unstable angina (CL 0.62, 0.41-0.92), use of aspirin (CL 0.58, 0.41-0.92), and use of long-acting nitrates (CL 0.61, 0.40-0.93) as the independent predictors of the development of unstable angina rather than MI; of these the combination of nitrates and aspirin was the strongest predictor. CONCLUSIONS: Long-acting nitrates as well as aspirin are suggested to have a protective or modifying effect on the development of acute coronary syndromes, favoring unstable angina rather than acute MI.

Cholinergic modulation of the picrotoxin-induced electrocorticographical events and behavioral "pain-like" symptoms at somatomotor cortical level in the rat.

In this study, we examined the modulation by acetylcholine of electrocorticographical (ECoG) ictal events and spontaneous pain-like behaviors following cortical application of the GABA(A) antagonist picrotoxin in the awake rat. Distilled water as vehicle, the cholinomimetic substance eserine, and the general muscarinic antagonist atropine were microinjected 10 min before the second microinjection of 2 microg picrotoxin into the hind paw region of the somatomotor cortex (SmI). Under these conditions, we observed that eserine (physostigmine, 1 microg, 10 microg, and 20 microg) did not consistently modify the number of the picrotoxin-induced ECoG spikes and bursts, but instead produced a massive enhancement of the number of hind paw licks compared with vehicle at 10 microg and, to a lesser extent, the number of the stereotyped "turn-in" and "neglected" paws following picrotoxin. In contrast, atropine (1 microg, 10 microg, and 20 microg) increased the number of the picrotoxin-induced spikes and bursts at 10 microg and, at all doses, decreased the number of the picrotoxin-induced pain-like symptoms. Statistically significant changes for the number of paw lifts, licks, and "turn-in" paws were observed only with 10 microg. These results tend to show that epilepsy and pain are not strictly related to each other and also emphasize the cortex as a target for interactions between GABA and acetylcholine relative to "central" pain.

Picrotoxin produces a "central" pain-like syndrome when microinjected into the somato-motor cortex of the rat.

In this study, we report the possibility of producing marked electrocorticographic changes and "pain-like" reactions, when the GABAA antagonist picrotoxin is microinjected unilateraly into the rat somato-motor Sml cortex in the region of the hind paw. After the microinjection, we observed continuous seizure isolated spikes, spikes-and-waves, bursts, and pain-like reactions, almost exclusively confined to the hind paw. These reactions considered of lifting off the floor, licking of the paw palm or digits, biting, paw tremors, and a peculiar paw position that we called "turn-in" paw. We also noted other behaviors, such as "limping," "neglected" paw, or rearing. The "pain-like" character of these manifestations was suggested by the fact that similar qualitative and quantitative data occurred consequent to the administration of 2.5% diluted formalin into the palm of the hind paw in different rats. Bringing together the electrocorticographic events and the behavioral reactions produced by Sml picrotoxin indicated that there was no obvious correlation between the phenomena, except that the tremor was always associated with the bursts. Sensory denervation of the hind paw, produced by sciatic and saphenous nerve transections, did not significantly modify either the ictal activity or the behavior. Finally, microinjection of naloxone prior to picrotoxin did not change the cortical events, but greatly diminished the "pain-like" reactions. All these results favor the cortical microinjection of a GABAA receptor antagonist as a good rat model for studying pain of "central" origin. They emphasize the possible role of the Sml cortex in such a phenomenon, and the deficit of cortical GABAergic processing, which can include an opioid link.

Intimal injury in a transiently occluded coronary artery increases myocardial necrosis. Effect of aspirin.

This study tested the hypothesis that intimal injury in a transiently occluded coronary artery limits myocardial salvage. The effect of intimal injury on reactive hyperaemia was investigated in 17 pigs submitted to a 30-min occlusion of the left anterior descending coronary artery (LAD), not resulting in myocardial infarction. Catheter-induced intimal damage increased local platelet deposition (99mTc) and reduced hyperaemia, but did not modify myocardial platelet or polymorphonuclear leucocyte content (myeloperoxidase activity) after 6 h reperfusion. To investigate the influence of intimal injury on the extent of myocardial necrosis secondary to a more prolonged coronary occlusion, and the role of platelets on this influence, 52 pigs were submitted to a double randomization (2x2 factorial design) to 250 mg i.v. aspirin vs. placebo and to coronary intimal injury vs. no coronary damage before a 48-min occlusion of the LAD and 6 h of reperfusion. After excluding 12 animals with reocclusion, coronary intimal injury was associated with larger infarcts (triphenyltetrazolium reaction) in animals receiving placebo (36.2+/-7.0% of the area at risk in animals with intimal injury vs. 10.8+/-3.9% in animals without coronary injury, P=0.006) but not in those receiving aspirin (20.3+/-6.5 vs. 21.7+/-6.5% of the area at risk in animals with and without intimal injury respectively). These results suggest that coronary intimal injury in the reperfused artery may have adverse effects on myocardial salvage by mechanisms other than reocclusion or embolization of platelet aggregates.

Myocardial segment shrinkage during coronary reperfusion in situ. Relation to hypercontracture and myocardial necrosis.

We have investigated the changes in myocardial segment length induced by reperfusion, and their relation to myocyte hypercontracture and contraction band necrosis. Regional wall function was monitored by ultrasonic gauges in 39 pigs submitted to 48-min occlusion of the left anterior descending coronary artery (LAD) and 6h of reperfusion. Infarct size (triphenyltetrazolium reaction), the extent of contraction band necrosis (quantitative histology) and myocardial water content (desiccation) were measured. Reperfusion induced a marked reduction in end-diastolic length of the LAD segment in all animals, maximal within 15 min after reflow. After 30 min of reperfusion, end-diastolic length of the LAD segment remained below the basal value in 15 animals. The 15 animals that showed shrinkage of the reperfused segment did not differ from the remaining animals in heart rate, aortic pressure, or control segment variables, but had larger infarcts (mean +/- SEM: 32.1 +/- 5.4 vs 12.1 +/- 3.2% of the area at risk, P = 0.003). There was an inverse correlation between end-diastolic length of the LAD segment after 30 min of reperfusion and infarct percentage (r = -0.72) or the extent of contraction band necrosis (r = -0.71). End-diastolic length reduction was more pronounced in larger infarcts despite a more severe myocardial oedema. Neither systolic shortening of the LAD segment nor end-diastolic length or systolic shortening of the control segment, or haemodynamic variables after 30 min of reperfusion correlated to infarct percentage or to the extent of contraction band necrosis. It is concluded that myocardial segment shrinkage during reperfusion reflects myocyte hypercontracture leading to contraction band necrosis.

The "plantar test" apparatus (Ugo Basile Biological Apparatus), a controlled infrared noxious radiant heat stimulus for precise withdrawal latency measurement in the rat, as a tool for humans?

In the present study, we precisely and automatically measured the withdrawal latency to noxious radiant heat application in unrestrained male rats and in human subjects of both sexes, by means of the "plantar test" apparatus (Ugo Basile Biological Apparatus). The infrared light stimulus of this tool was applied underneath the hindpaws of rats and the middle fingers of human subjects. With one right and one left stimulation every 10 min, we observed a decrease in latency over a 40-min testing period in rats; the latency reached a mean value of 5.08 +/- 0.25 sec after 40 min with a 36-W stimulus, which corresponded to 46.5 degrees C. In pilot experiments, also performed on rats, we showed that the opiate morphine (10 mg/kg, i.p.) produced remarkable increases of the withdrawal latency only in "naive" animals (i.e., ones that had never experienced the plantar test stimulus) and not in animals "habituated" to it. Among humans, we noted gender differences, such as less sensitivity to the infrared noxious radiant heat for women, particularly during the menstrual period. A difference from rats was that there was no significant latency modification along the 40-min testing period for either women or men, with a mean latency of 5.61 +/- 0.18 sec (47.5 degrees C) for the women and 4.39 +/- 0.10 sec (45.5 degrees C) for the men. These data confirm the reliability of the plantar test in rats, and demonstrate the possible use of an infrared source in human subjects as a noxious heat stimulus; the withdrawal reaction to this stimulus is emphasized as a good index of nociception in humans.

Administration of lipid-emulsion versus conventional amphotericin B in patients with neutropenia.

OBJECTIVE: To evaluate the usefulness of a 20% lipid emulsion as a delivery system for amphotericin B (1 mg/mL) administered over 1 hour to patients with neutropenia with hematologic malignancies compared with amphotericin B (0.1 mg/mL) administered in dextrose 5% solution over the same time. DESIGN: A prospective, comparative, randomized, labeled study. SETTING: Hematology unit, pharmacy service, university general hospital. PARTICIPANTS: Twenty patients with neutropenia with hematologic malignancies and proven or suspected fungal infections, 10 in the fat emulsion group (group 1) and 10 in the dextrose 5% group (group 2). MAIN OUTCOME MEASURES: Clinical tolerance (i.e., fever, shaking chills, nausea, blood pressure, pulse rate) and biologic tolerance (i.e., urea, creatinine, sodium, potassium). RESULTS: Clinical tolerance was comparable in both groups although amphotericin B in fat emulsion was better tolerated. Medication for symptoms related to the administration of amphotericin B was given in 6 cases in group 1 and in 8 cases in group 2. There was a statistically significant difference in the urea concentrations between the 2 groups (p = 0.023); there was an observed increase between the initial and the final serum urea (56.8 mg/d in group 1, 79.8 mg/dL in group 2). Statistically significant differences in creatinine serum concentrations (84.9 mumol/L in group 1, 123.8 mumol/L in group 2) (p = 0.047) were found. No differences were found in the antifungal efficacy of the treatment. However, as amphotericin B was started in the majority of cases (75%) as empiric treatment for fever unresponsive to antibiotic therapy, it is difficult to compare the efficacy of both preparations. CONCLUSIONS: The clinical tolerance of lipid-emulsion infusions is similar to that of conventionally administered amphotericin B therapy. Renal toxicity appears to be decreased when the drug is administered in a fat emulsion. This type of preparation permits the reduction of the volume and the time of administration for amphotericin B therapy.

Previous aspirin use may attenuate the severity of the manifestation of acute ischemic syndromes.

BACKGROUND: The present study was designed to investigate whether the prior use of aspirin could influence the severity of the manifestation of acute coronary artery syndromes, given the well-documented observations that aspirin can prevent myocardial infarction, stroke, and death in cardiovascular disease. METHODS AND RESULTS: A series of 539 consecutive patients admitted to the Coronary Care Unit of a General Hospital was carefully characterized in a study with an ambidirectional design, with regard to previous medical history, aspirin use, and subsequent hospital diagnosis. Among the 214 patients previously taking aspirin, the hospital diagnosis was myocardial infarction in 24% and unstable angina in 76% compared with 54% and 46%, respectively, among the 325 not taking aspirin (P < .0001), for a reduction in the odds ratio of myocardial infarction with aspirin of 72% (95% CI, 59% to 90%). The decrease in odds was homogeneous in all subsets studied and independent of age, sex, previous angina, or previous myocardial infarction. The myocardial infarction was of a Q-wave type in 62% of aspirin users compared with 76% of nonusers (P < .05). By multivariate analysis, previous aspirin use was a strong predictor of unstable angina versus myocardial infarction and the only independent predictor of non-Q-wave versus Q-wave myocardial infarction. CONCLUSIONS: This study, thus, suggests a shift to less severe manifestation of acute coronary syndromes with aspirin use, implying that the failure of the drug in many patients with an acute coronary syndrome is only partial and that aspirin has the potential of attenuating the severity of the underlying acute thrombotic disease process.

An association between clotting factor concentrates use and mortality in human immunodeficiency virus-infected hemophilic patients.

There is much evidence that clotting factor concentrates (CFC), especially the so-called intermediate-purity preparations, exert an immunomodulating effect in vitro. The impact of this effect on the outcome of human immunodeficiency virus (HIV) infection in hemophiliacs is still controversial. In this retrospective cohort study, the effects of treatment with CFC on mortality and progression to acquired immunodeficiency syndrome (AIDS) were estimated while controlling for individual risk factors. Logistic regression and survival analysis, including the Cox proportional-hazards regression model, were performed with data from a 11-year follow-up of 225 hemophilic patients seropositive for HIV type 1 (HIV-1) of two hemophilia centers. Mortality and progression to AIDS rates were strongly associated with lower administration of CFC. After adjusting for age, a statistically significant and robust association was observed. The use of CFC was negatively associated with progression to AIDS (P = .0252) and mortality (P = .0033). The adjusted relative hazards of mortality and progression to AIDS rate between the most treated patients (> 700 IU/kg/yr) versus the least treated (< or = 700 IU/kg/yr) were 0.53 (confidence limits, 0.33 to 0.86) and 0.57 (0.39 to 0.84), respectively. Although the effects of other unmeasured risk factors cannot be excluded with certainty, these results suggest that there is a negative association between treatment with CFC and progression to AIDS and mortality.

Does barbiturate anesthesia modify the neuronal properties of the somatosensory thalamus? A single-unit study related to nociception in the awake-pentobarbital-treated rat.

By means of extracellular recordings, we studied thalamic ventrobasal complex neurons of rats tested first awake, and then anesthetized with pentobarbital. In both conditions, we found two groups of units in both states. The first group, displaying a spontaneous bursting activity, was not obviously responding to peripheral stimuli. Another group, displaying a single-spike activity, was almost exclusively activated by innocuous and/or noxious and innocuous mechanical stimuli. Still in this group, units specifically driven by noxious stimuli were only found under pentobarbital. These data, different from classical findings, emphasize the interest of the awake preparation in order to study nociceptive cellular mechanisms at the thalamic level.

[Effects of reoxygenation-induced osmotic edema on cell viability. Study using isolated myocytes]. / Efecto del edema osmótico durante la reoxigenación sobre la viabilidad celular. Estudio en el miocito aislado.

OBJECTIVE: To investigate the hypothesis that reperfusion edema may kill myocytes. METHODS: Adult Sprague-Dawley rat hearts were perfused with a calcium free dissociation buffer containing collagenase 0.03% in a Langedorff system. Intact cells were selected and myocytes were cultured in adherent pretreated dishes. After 3 hours, 80% of cells were rod-shaped. Anoxia was simulated by means of metabolic inhibition by adding NaCN 2 mM to the control media, and reoxygenation by substituting this media with one of the following media non containing NaCN: 1) normo-osmotic (312 mOsm); 2) hypoosmotic (80 mOsm); 3) normo-osmotic with low Na+ (312 mOsm). A group of cells was kept with control media without metabolic inhibition and then submitted to simulated reoxygenation with hypoosmotic media (control group). The number of rod, square and round-shaped cells was monitored, and cell viability was assessed after 5 min of reoxygenation by the Trypan blue test. RESULTS: After 60 min of metabolic inhibition there were no differences in the % of cells without hypercontracture among groups reoxygenated with normo-osmotic, hypoosmotic, low Na+ normo-osmotic and control media (84 +/- 16, 74 +/- 10, 76 +/- 14 and 90 +/- 6% respectively (p = NS). After 5 min of reoxygenation, these values decreased (p < 0.001) to 19 +/- 6, 11 +/- 9 and 13 +/- 3% (p = NS), respectively, in groups with normo-osmotic, hypoosmotic, and low Na+ normo-osmotic reoxygenation, but were not modified in the control group (78 +/- 4). The % of viable cells (Trypan negative) preserved after 5 min of reoxygenation was 67 +/- 29% in the group with normo-osmotic reoxygenation, 31 +/- 23% in the group with hypoosmotic reoxygenation, and 85 +/- 12% in the group with low Na+ normo-osmotic reoxygenation (p < 0.001). Exposing cells without metabolic inhibition to hypoosmotic media resulted in no significative reduction of cell viability. CONCLUSION: Hypoosmotic reoxygenation following prolonged metabolic inhibition may kill viable myocytes. This effect is not due to the low Na+ concentration in the hypoosmotic medium.

Single-unit recordings at dorsal raphe nucleus in the awake-anesthetized rat: spontaneous activity and responses to cutaneous innocuous and noxious stimulations.

In this study, we recorded the single-unit activity of the dorsal raphe nucleus (DRN) in rats tested first awake and, a few days later, anesthetized with sodium pentobarbital and recorded again. This was achieved by means of a small chronically implanted device supporting a 25 micron platinum-iridium wire as the recording electrode. In both the awake and anesthetized conditions, and in agreement with most of the studies performed at the DRN level, we found that a vast majority of the units, displaying small amplitude and long-duration action potentials, possessed a low level of spontaneous activity (0.2-4 Hz). Among these units, found in greater number under pentobarbital, it was possible to establish that this activity was regular or irregular, in accordance with the literature reports. However, as opposed to these studies, we determined that the 'regularity' was relative, only noticeable in more or less prolonged phases of activity. In particular, we never recorded the so-called 'clock-like' activity, largely reported as an unambiguous criterion for selecting the serotoninergic neurons. In both the awake and anesthetized conditions, the responses of the DRN neurons to peripheral mechanical innocuous and noxious stimulations were observed in only one-half of the units recorded and were weak in comparison to other results that we obtained at the nucleus raphe magnus level in previous studies. When present, these responses were excitation or inhibition, occurring during or after the stimulus application. These results question the direct involvement of the DRN in acute nociception.

Contraction band necrosis at the lateral borders of the area at risk in reperfused infarcts. Observations in a pig model of in situ coronary occlusion.

The aim of this study was to test the hypothesis that increased mechanical stress at the lateral borders of the area at risk may render this area more susceptible to ischaemia/reperfusion injury in the absence of collateral flow. The spatial distribution of myocardial necrosis within the territory of a transiently occluded left anterior descending coronary artery was investigated in 31 porcine hearts submitted to 48 min of coronary occlusion and 6 h of reperfusion. Immediately before excising the heart, the left anterior descending coronary artery was re-occluded and 10% fluorescein was injected in the left atrium. The area at risk was imaged by ultraviolet illumination of the myocardial slices, and the area of necrosis by incubation in triphenyltetrazolium chloride. The area at risk was divided in four sectors and an index of eccentricity was calculated as the percent of the area of necrosis located in the two lateral sectors of the area at risk. The area of contraction band necrosis was measured in whole heart histological sections. Infarcts were generally small, and were composed almost exclusively of contraction band necrosis. There was a good correlation between the extent of the area of contraction band necrosis and infarct size (r = 0.831, P < 0.0005). The area of necrosis had a patchy appearance and was predominantly distributed along the lateral borders of the area at risk. This eccentric distribution was more prominent in smaller infarcts, and the eccentricity index was inversely correlated with infarct size (r = -0.471, P = 0.007), suggesting that contraction band necrosis occurs first at the interface between control and reperfused myocardium in this model. These results are in agreement with a prominent role of mechanical factors in the genesis of myocardial necrosis during transient coronary occlusion.

Dissociation between anti-infarct effect and anti-edema effect of ischemic preconditioning.

This study tested the hypothesis that preconditioning, by reducing catabolite accumulation during ischemia, reduces osmotic swelling and myocardial necrosis during subsequent reperfusion. Farm pigs were randomly allocated to one of three groups of treatment: a control group undergoing a 48-min coronary occlusion (CO) of the middle left anterior descending artery, a preconditioned group (2 cycles of 5-min CO and 5-min reperfusion before the 48-min CO), or an intracoronary perfusion group receiving a substrate-free anoxic buffer perfusion into the area at risk between minutes 5 and 10 of the prolonged CO. Animals were killed after 30 min (n = 23) or 6 h (n = 31) of reperfusion. Compared with the control group, both ischemic preconditioning and washout of ischemic by-products by transient anoxic perfusion reduced myocardial edema after 30 min of reperfusion (P < 0.002) by 35 and 32%, respectively, but only ischemic preconditioning reduced final infarct size (by 55%, P < 0.006). Myocardial lactate content before reperfusion, measured in an additional series of 12 experiments, was reduced by 35% in animals receiving preconditioning or intracoronary perfusion. Thus ischemic preconditioning has a marked protective effect against reperfusion edema, and this effect can be explained by reduced catabolite accumulation during ischemia. However, there is no evidence from this study indicating that reduced catabolite accumulation and limited reperfusion edema explain the important anti-infarct effect of ischemic preconditioning.

The GABAA receptor antagonist picrotoxin induces a 'pain-like' behavior when administered into the thalamic reticular nucleus of the behaving rat: a possible model for 'central' pain?

In this study, we reported that the microinjection of the GABAA antagonist picrotoxin into the rat thalamic reticular nucleus produced a 'pain-like' behavior. This behavior was primarily characterized by repetitive lifting off the hindpaw from the floor contralateral to the injection site, sometimes accompanied by extension of the leg and maximal fingers separation. Surprisingly, these manifestations were not occurring when picrotoxin was applied to the ventrobasal complex itself, alternatively producing 'wet-dog' shakes. These data show that the local administration of picrotoxin is a relevant approach for studying pain of 'central' origin and complex GABAergic modulatory mechanisms within the thalamic sensory complex.

Are ventromedial medulla neuronal properties modified by chronic peripheral inflammation? A single-unit study in the awake, freely moving polyarthritic rat.

In the present work, we recorded the neuronal properties of the ventromedial medulla, a brainstem structure involved in the descending spinal control systems related to nociception, in awake, freely moving healthy and polyarthritic rats. These animals were rendered polyarthritic with a subcutaneous administration of the Freund's adjuvant into the tail, and studied at 20 and 30 days post-inoculation. At the ventromedial medulla level, the single-unit activities were recorded by means of a chronically implanted device supporting a 50 microns platinum-iridium wire as the recording electrode. With a total of 308 recorded neurons, we determined that in both healthy rats, i.e. animals having received mineral oil only and arthritic rats, there were ventromedial medulla units with common physiological properties, but also changes. In agreement with the results from anesthetized arthritic rats at spinal and thalamic levels, the systematic analysis of the responses to light touch and mechanical shock revealed that the 'multimodal, multireceptive' units, excited by innocuous and noxious stimuli, were much more responsive to both modalities in arthritic rats. Approximately 7% of these neurons displayed a 'paroxysmal' spontaneous activity, also reported in the literature for other structures. In addition, we recorded a significant number of neurons inhibited or excited-inhibited by innocuous and noxious cutaneous stimulations, and a few with a regular spontaneous activity, also responding, which has never been the case in healthy rats. We conclude that a peripheral chronic inflammation, such as arthritis, can produce changes of the ventromedial medulla neuronal properties, as compared to healthy animals. Consequently, in addition to its classical role in the spinal control of nociception, the ventromedial medulla is able to develop some form of plasticity in the case of persistent pain of peripheral origin.