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Biomedical subjects

P Oliva

Publications and source records attributed to P Oliva.

16 recordsLinked to original sources

Metabotropic and NMDA glutamate receptors participate in the cannabinoid-induced antinociception.

The purpose of this study was to evaluate the possible contribution of metabotropic glutamate receptors (mGluRs) to cannabinoid-induced antinociception in the periaqueductal grey (PAG) matter of rats. Intra-PAG microinjection of WIN 55,212-2, a cannabinoid receptor agonist, increased the latency of the nociceptive reaction (NR) in a dose-dependent fashion in the plantar test. This effect was prevented by pretreatment with SR141716A, a selective antagonist of CB1 receptors. When injected alone, SR141716A produced, with the highest dosage used, a significant reduction in the latency of the NR. CPCCOEt, a selective mGlu1 receptor antagonist, was unable to prevent the analgesia produced by WIN 55,212-2. On the contrary, MPEP, a selective mGlu5 receptor antagonist, completely antagonized the effect of WIN 55,212-2. However, the analgesia induced by CHPG, a selective mGlu5 receptor agonist, was blocked by MPEP but not by SR141716A. When injected alone, CPCOOEt produced no effect, whereas MPEP produced, with the highest dosage used, a significant reduction in the latency of the NR. These data emphasize that mGlu5 receptors, but not mGluR1, may modulate nociception in the PAG. Similarly, a pretreatment with either 2-(S)-alpha-EGlu or (RS)-alpha-MSOP, selective antagonists for group II and III mGluRs, respectively, prevented the WIN 55,212-2-induced analgesia. When the higher dosage of (RS)-alpha-MSOP was used a decrease in the latency of the NR was observed. This was not the case for 2-(S)-alpha-EGlu. Pretreatment with DL-AP5, a selective antagonist of N-methyl-D-aspartate (NMDA) receptors, blocked the effect of WIN 55,212-2, and by increasing the dosage strongly reduced per se the latency of the NR. This study suggests that endogenous glutamate could tonically modulate nociception through mGlu and NMDA receptors in the PAG matter. In particular, the physiological stimulation of these receptors seems to be required for the cannabinoid-induced analgesia in this midbrain area.

Analgesics↗

Neurochemical changes after morphine, dizocilpine or riluzole in the ventral posterolateral thalamic nuclei of rats with hyperalgesia.

A number of studies suggest the involvement of glutamate in central hyperalgesia through NMDA receptors in animal models of inflammation. Most studies analyze glutamate effects at the spinal cord level. In this work, the effects of morphine, dizocilpine and riluzole on the hyperalgesia induced by carrageenan administration in the rat paw model were investigated. The effects of morphine and riluzole on the release of glutamate and aspartate and on the concentrations of citrulline and arginine in dialysates of the ventral posterolateral nucleus of the thalamus were also examined. All three drugs decreased hyperalgesia when administered prior to carrageenan injection. Morphine decreased the glutamate concentration in dialysates of the ventral posterolateral nucleus but did not affect the concentrations of the other amino acids. The effect of morphine was observed in the absence of painful stimulation and when pressure applied to the rat paw induced a nociceptive reaction. Riluzole decreased the concentrations of glutamate and aspartate and those of citrulline and arginine in the presence or absence of painful stimulation. These experiments suggest that morphine and riluzole attenuate the hyperalgesia induced by injection of carrageenan in the rat hind paw, at least partly, by decreasing glutamate release in the ventral posterolateral thalamic nucleus.

Analysis of Variance↗

Periaqueductal gray matter metabotropic glutamate receptors modulate formalin-induced nociception.

The role played by periaqueductal gray (PAG) matter metabotropic glutamate receptors (mGluRs) in the modulation of persistent noxious stimulation was investigated in mice. The formalin test was used as a model of persistent pain. Intra-PAG microinjections of (S)-3, 5-DHPG (25 and 50 nmol/mouse) and L-CCG-I (30 and 60 nmol/mouse), agonists of group I and group II mGluRs, respectively, decreased the nociceptive response (-92+/-6% and -89+/-8%, respectively) during the late phase. No change of the early nociceptive phase was observed after (S)-3,5-DHPG or L-CCG-I treatments. These effects were antagonized by a pretreatment with CPCCOEt (40 nmol/mouse) and (2S)-alpha-EGlu (30 nmol/mouse). CPCCOEt is a selective antagonist of group I mGlu receptors, while (2S)-alpha-EGlu is an antagonist of group II. Intra-PAG microinjections of L-SOP (60 and 120 nmol/mouse), a selective agonist of group III mGluRs, induced an increase of the nociceptive response (+95+/-7%) during the late hyperalgesic phase. (R,S)-alpha-M-SOP (70 nmol/mouse), a selective antagonist of group III mGluRs, completely antagonized the L-SOP-induced effect. These results show that PAG mGluRs participate in modulating the late hyperalgesic behaviours induced by formalin. It seems, therefore, possible that group I and group II mGluRs positively modulate PAG antinociceptive descending pathway following a persistent noxious stimulation, while group III mGluRs modulate it negatively.

Animals↗

Periaqueductal gray matter glutamate and GABA decrease following subcutaneous formalin injection in rat.

Glutamate and GABA are important nociception modulating transmitters in specific brain regions, i.e. the spinal cord, the thalamic nuclei and the periaqueductal gray (PAG). However, quantitative and topographical changes in glutamate and GABA release in these brain regions during peripheral inflammation episodes have not been characterized in awake animals. To address this issue, an in vivo microdialysis study was carried out in freely moving rats in order to analyze PAG extracellular glutamate and GABA concentrations following unilateral formalin injection into the dorsal skin of the right hind-paw. Both glutamate and GABA release decreased after the injection of formalin during phase I and phase II of hyperalgesia. Because naloxone prevented the decrease of GABA and glutamate release induced by formalin, this study shows that, in vivo, a nociceptive stimulation may activate opioidergic fibres into the PAG. The increased release of endogenous opioids may, in turn, inhibit the activity of the GABAergic neurons (i.e. opioid disinhibition). Formalin injection also decreased extracellular glutamate concentration. However, we found that intra-PAG perfusion with tetrodotoxin only decreased GABA, but not glutamate dialysate values. Although it should be reasonable to speculate that opioids also inhibit glutamate fibres, further investigation is needed to clarify whether or not the dialysate glutamate we measured reflects change in the metabolism or neurotransmitter pool of this amino acid.

Analysis of Variance↗

Role of vasopressin on excitatory amino acids mediated pressor responses in the periaqueductal gray area.

In order to evaluate the role played by vasopressin on pressor responses elicited by stimulation of the periaqueductal gray (PAG) area by excitatory amino acids we carried out in vivo studies in genetically vasopressin deficient rats (Brattleboro). Microinjections of 1-glutamic acid (glutamate, 0.6 to 60 nmol/rat) or N-methyl-d-aspartic acid (NMDA, 0.07 to 7 nmol/rat) into the PAG area of freely moving Brattleboro rats induced increases of arterial blood pressure values significantly lower than those obtained in Long Evans rats (control) (glutamate in Brattleboro rats: from +2+/-1 mmHg to 16+/-3 mmHg; glutamate in Long Evans rats: from +16+/-2 mmHg to +36+/-4 mmHg; NMDA in Brattleboro rats: from +5+/-2 mmHg to +34 +/-8 mmHg; NMDA in Long Evans rats: from +18+/-7 mmHg to 80+/-9 mmHg; n=5). Similarly, in anaesthetized Brattleboro rats (urethane 1.2 g/kg i.p.) pressor responses to NMDA microinjections (0.7 nmol/rat) into the PAG area were significantly lower than in Long Evans rats (controls) (+15+/-3 mmHg vs +24+/-4 mmHg). In Long Evans rats NMDA injection also reversed blood pressure decrease induced by ganglionic blocker, hexamethonium and/or losartan (3 mg/kg i.v.), an AT1 receptor antagonist. In Brattleboro rats, NMDA injection did not reverse blood pressure decreases induced by hexamethonium (5 mg/kg i.v.). Moreover, hexamethonium induced blood pressure decrease was not reversed by acetylcholine injection (137 nmol/rat) into the PAG area of anaesthetized Long Evans rats, but if injected before hexamethonium, acetylcholine was able to increase blood pressure (+25+/-3 mmHg). Our results document: i) the importance of the PAG area in the control of cardiovascular system; ii) the involvement of excitatory amino acids in the neural control of vasopressin release; iii) the close relationship between glutamate and vasopressin in the central blood pressure regulation.

Acetylcholine↗

Questionable validity of 'dissociative amnesia' in trauma victims. Evidence from prospective studies.

BACKGROUND: We reviewed evidence from prospective studies to test whether individuals can develop amnesia for traumatic experiences, a process variously termed 'repression', 'dissociative amnesia' or 'psychogenic amnesia'. METHOD: Using specified criteria, we selected and analysed studies which prospectively assessed memory in victims of documented traumatic experiences. RESULTS: In studies in which people were asked directly about a past traumatic experience, they consistently reported memories. Non-reporting occurred only in studies where subjects were not asked directly about the experience. This latter design leaves open the well-documented possibility that subjects simply did not disclose events that they actually remembered. Some prospective studies were also limited by incomplete documentation of trauma and failure to rule out other more ordinary causes of amnesia. CONCLUSIONS: Prospective data as yet fail to demonstrate that individuals can develop dissociative amnesia for traumatic events.

Adult↗

Ion Adsorption and Agglomeration Mechanism in Si3N4/H2O(l) Dispersions Compatible with Thermodynamical Stability

Adsorption isotherms from aqueous liquid phase of H+ and/or OH- ions onto Si3N4 solid surface agglomerates have been derived through titration measurements (Beruto et al., J. Chem. Soc., Faraday Trans. 91(2), 323 (1995)). The isotherms exhibit S-shape and can be fitted with Freundlich as well as with Langmuir type isotherms. In order to explain the agglomeration process based on the decrease of total solid-liquid interfacial energy, a model (ISD) has been developed. The agreement between numerical data derived by this model and the experimental data is quite good. Isotherm equation and agglomeration law should obey also the dispersion thermodynamic stability criterion. This condition yields an extra equation to select the pair of functions, thus providing a criterion to choose between the several equations that fit adsorption and agglomeration data fairly well. The solution of the problem mentioned above, from the mathematical point of view, is based on the Dini implicit function theorem (Mezzasalma and Oliva, Appl. Math. Lett., submitted). The results indicate that Van der Waals adsorption isotherm coupled with the ISD model are compatible with the thermodynamic stability of the aqueous Si3N4 dispersions.

Journal Article↗

Very long-term users of marijuana in the United States: a pilot study.

The authors recruited a sample of 37 Americans, aged 30-74, who had smoked marijuana on at least 5,000 separate occasions. These subjects were found to span a wide range of ethnic groups, educational backgrounds, occupations, and annual income; they did not display any obvious features which distinguished them from the population as a whole. They typically began smoking in the 1960s or early 1970s, and then continued to smoke heavily into middle adulthood because they felt that marijuana relieved unpleasant feeling states such as anxiety or depression. To our knowledge, individuals of this type have not previously been examined; further studies of older, long-term American marijuana users are needed.

Adult↗

Fat-free mass index in users and nonusers of anabolic-androgenic steroids.

We calculated fat-free mass index (FFMI) in a sample of 157 male athletes, comprising 83 users of anabolic-androgenic steroids and 74 nonusers. FFMI is defined by the formula (fat-free body mass in kg) x (height in meters)-2. We then added a slight correction of 6.3 x (1.80 m - height) to normalize these values to the height of a 1.8-m man. The normalized FFMI values of athletes who had not used steroids extended up to a well-defined limit of 25.0. Similarly, a sample of 20 Mr. America winners from the presteroid era (1939-1959), for whom we estimated the normalized FFMI, had a mean FFMI of 25.4. By contrast, the FFMI of many of the steroid users in our sample easily exceeded 25.0, and that of some even exceeded 30. Thus, although these findings must be regarded as preliminary, it appears that FFMI may represent a useful initial measure to screen for possible steroid abuse, especially in athletic, medical, or forensic situations in which individuals may attempt to deny such behavior.

Adipose Tissue↗

Evaluation of vaginal microflora in patients infected with HIV.

HIV infection is thought to exacerbate the virulence of normal saprophytic vaginal microflora. We studied the vaginal ecosystem of HIV patients to detect the quantitative and qualitative variation of vaginal microorganisms. 15 patients (5 with AIDS and 10 with ARC) were investigated. Vaginal candidiasis was more frequent in this group than in the control groups. Gardnerella was present in 60% of patients generally in association with anaerobic bacteria and Mycoplasma. Among anaerobia, Bacteroides sp and other Gram-negative rods were the most common bacteria. Neisseria gonorrhoeae was absent in all patients tested. Chlamydia trachomatis was recovered in two out of the 15 HIV-positive patients. Aerobic Gram-negative flora was 100-fold that of the control group and anaerobic Gram-negative flora 10-fold.

AIDS-Related Complex↗

Refractory ergonovine-induced coronary vasospasm: importance of intracoronary nitroglycerin.

Recent experience has suggested that the ergonovine maleate test is a safe procedure for the diagnosis of variant angina pectoris, because ergonovine-induced coronary vasospasm has generally been reversible by sublingual nitroglycerin. This report describes five cases of ergonovine-induced coronary vasospasm that were refractory to sublingual nitroglycerin. Four of these patients had cardiac arrest. In two patients the vasospasm was responsive to intracoronary nitroglycerin administration. Three patients died as a reuslt of the test. The two survivors differed from the nonsurvivors in the total dose or ergonovine given (0.1 and 0.15 mg versus 0.17, 0.3 and 0.3 mg, respectively) and in the method of administration of ergonovine. The survivors were given serial doses of 0.05 mg each whereas the three nonsurvivors received either larger initial doses (0.1 followed by 0.07 mg) or progressive incremental doses (0.05, 0.1 and 0.15 mg serially). Sublingual nitroglycerin, given to all five patients, and intravenous nitroglycerin, given to three of the five, were ineffective in reversing vasospasm. Intracoronary nitroglycerin favorably altered the course of the survivors. Thus, the ergonovine maleate test is not benign and may cause severe coronary vasospasm that is unresponsive to sublingual and intravenous nitroglycerin, but may be reversed by intracoronary nitroglycerin.

Administration, Oral↗