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J Buritova

Publications and source records attributed to J Buritova.

27 records · Page 2Linked to original sources

When is the maximal effect of pre-administered systemic morphine on carrageenin evoked spinal c-Fos expression in the rat?

This study evaluated, in awake rats, the time course of the expression of c-Fos in spinal cord neurons, in the L4-L5 segments, at various time points after intraplantar carrageenin (0.5 h, 1 h, 1.5 h, 2 h and 2.5 h). In addition, the effects of pre-administered morphine (3 mg/kg, i.v.) on the c-Fos expression, at the various time points, were studied. Very few Fos-like immunoreactive (Fos-LI) neurons were observed 0.5 h after carrageenin. However, spinal c-Fos expression increased initially (at 1 h), in the superficial laminae (I-II) of the spinal dorsal horn, and incrementally increased both in the superficial and deep (V-VI) laminae at later time points after carrageenin. Systemic morphine did not significantly decrease the number of superficial Fos-LI neurons observed 1 h after carrageenin, whereas it significantly reduced the number of superficial Fos-LI neurons induced at 1.5 h and 2 h after carrageenin (58 +/- 3% and 57 +/- 10% reduction, P < 0.001, respectively). In addition, morphine reduced the number of deep Fos-LI neurons at 1.5 h and 2 h after carrageenin (86 +/- 4%, P < 0.01 and 82 +/- 8%, P < 0.001 reduction as compared to control carrageenin expression, respectively). In contrast, morphine was less efficacious in decreasing the number of Fos-LI neurons observed in the superficial and deep laminae at 2.5 h after carrageenin (34 +/- 6% and 59 +/- 6% reduction, P < 0.001, respectively). Thus, the peak effect of pre-administered morphine on carrageenin evoked c-Fos expression was observed 1.5 h and 2 h after intraplantar carrageenin, with a weaker effect observed at 2.5 h after carrageenin. The pharmacokinetic complications between the time course of the antinociceptive effects of morphine and c-Fos expression is discussed. These results clearly demonstrate that studies of c-Fos expression with pharmacological investigations should take into consideration this finding since one delay after the stimulation does not give a full indication of the full potential of the drug tested.

Analgesics, Opioid↗

7-Nitro-indazole, a selective inhibitor of neuronal nitric oxide synthase, reduces formalin evoked c-Fos expression in dorsal horn neurons of the rat spinal cord.

The effect of intravenous 7-nitro-indazole (7NI), a selective inhibitor of neuronal nitric oxide synthase, on intraplantar formalin evoked spinal expression of c-Fos was studied. The spinal expression of c-Fos in the superficial laminae of the dorsal horn was not significantly altered by 7NI. In contrast formalin evoked c-Fos expression in the deep laminae was reduced by 15 mg/kg of 7NI (42 +/- 8% reduction of control, P < 0.05). Formalin evoked inflammation was not influenced by 7NI. Our results implicate a functional relationship between c-Fos expression and nitric oxide, at the spinal level, under inflammatory conditions.

Animals↗

Carrageenan oedema and spinal Fos-LI neurones are reduced by piroxicam in the rat.

Intraplantar carrageenan induced a peripheral oedema and c-Fos like immunoreactivity (Fos-LI) in L4-L5 segments in the dorsal horn (DH) of the rat spinal cord. The total number of carrageenan evoked Fos-LI neurones was 153 +/- 10 per section, with a predominant localization in the superficial and deep laminae of the DH (46 +/- 4% and 32 +/- 2%, respectively). Pre-administered piroxicam (1, 2.5 and 5 mg kg-1, p.o.) dose-dependently reduced the number of Fos-LI neurones in both the superficial and deep laminae of DH, with effects being significantly strongest on the deep laminae Fos-LI neurones. The effects of piroxicam on the number of spinal Fos-LI neurones and on ankle oedema were positively correlated.

Animals↗

Concurrent reduction of inflammation and spinal Fos-LI neurons by systemic diclofenac in the rat.

Intraplantar carrageenan induced a peripheral inflammation and c-Fos like immunoreactivity (Fos-LI) in the dorsal horn, L4-L5 segments, of the rat spinal cord. The total number of control carrageenan evoked Fos-LI neurons was 126 +/- 6 per section, which were predominately located in the superficial and deep laminae (41 +/- 2% and 39 +/- 2% of the total number of Fos-LI neurons per section) of the dorsal horn. Pre-administered diclofenac (3, 6, 9 mg/kg i.v.) dose dependently reduced the number of Fos-LI neurons, with effects being strongest on the deep laminae Fos-LI neurons. The effects of diclofenac (9 mg/kg) on the number of Fos-LI neurons (68 +/- 2% reduction) and inflamed ankle (72 +/- 7% reduction) and paw (49 +/- 6% reduction) diameters, were positively correlated.

Animals↗

Indomethacin reduces both Krox-24 expression in the rat lumbar spinal cord and inflammatory signs following intraplantar carrageenan.

This study evaluated the 'evoked' expression of Krox-24 protein in the lumbar spinal cord after peripheral carrageenan-induced inflammation and its modification by preadministration of indomethacin, a non-steroidal anti-inflammatory drug, in freely moving rats. Three h after intraplantar carrageenan (6 mg/150 microliters saline) a maximal 'evoked' Krox-24 expression was observed in L2-L6 segments of the dorsal horn ipsilateral to carrageenan inflammation. A maximal number of 'evoked' Krox-24 neurons was observed in L4-L5 segments, predominantly in the superficial laminae (I-II) and to a lesser extent in the medial part of neck (laminae V-VI) of the dorsal horn. Such an increase was not observed after an intraplantar injection of control vehicle saline. increase doses of carrageenan (1, 3 and 6 mg) induced a dose-dependent increase (r2 = 0.617, P < 0.0001) in the number of evoked' Krox-24 neurons observed in the superficial dorsal horn 3 h after carrageenan. Systemic preadministration of indomethacin (1, 2.5 and 5 mg/kg) dose-dependently reduced (r2 = 0.508, P < 0.0001) the total number of carrageenan (6 mg at 3 h)-'evoked' Krox-24 neurons (29 +/- 5, 45 +/- 4 and 57 +/- 2% reduction as compared with control, respectively). Systemic indomethacin dose-dependently reduced the inflamed paw and ankle diameter (16 +/- 8, 34 +/- 12, 54 +/- 6% and 48 +/- 14,. 75 + 16, 90 +/- 7% reduction as compared with the control carrageenan inflammation, respectively). There was a positive correlation between the effect of systemic indomethacin on both 'evoked' Krox-24 expression in superficial laminae and the inflammatory signs (r2 = 0.25, P < 0.01 for the paw diameter; r2 = 0.22, P < 0.05 for the ankle diameter). In addition, the total number of 'evoked' Krox-24 neurons was significantly reduced (43 +/- 5% reduction as compared with control) by an oral pretreatment of indomethacin (10 + 10 mg/kg). Oral indomethacin totally blocked the ankle diameter and reduced the paw diameter (100 + 14 and 30 +/- 6% reduction of the control carrageenan inflammation, respectively).

Animals↗

Carrageenin-evoked c-Fos expression in rat lumbar spinal cord: the effects of indomethacin.

This study evaluated the effects of systemic indomethacin on carrageenin evoked c-Fos expression in rat lumbar spinal cord neurons. Fos-like immunoreactivity was not observed after the intraplantar injection of the control vehicle saline. 2 h after administration of carrageenin (6 mg/150 microliters) into the hind limb, Fos-like immunoreactive neurons were observed in the lumbar spinal cord (64 labelled neurons per L4-L5 sections) and were numerous in the superficial laminae (I-II), whereas at 3-4 h both superficial and deeper laminae (V, VI and ventral horn) were labelled. 3 h after carrageenin administration, maximal Fos-like immunoreactivity was observed (104 labelled neurons per L4-L5 sections). At later time points Fos-like immunoreactivity was observed predominantly in the deeper laminae. Fos-like immunoreactivity was rarely observed within laminae III-IV at any of the time points. At 24 h, the number of Fos-like immunoreactive neurons decreased (36 labelled neurons per L4-L5 sections). With increasing doses of carrageenin, an increase in the number of Fos-like immunoreactive neurons was observed. The number of Fos-like immunoreactive neurons induced by the carrageenin stimulation (6 mg, at 3 h) was clearly reduced by oral pretreatment with indomethacin (20 mg/kg). In addition, i.v. indomethacin (1, 2.5 or 5 mg/kg) dose dependently reduced the number of Fos-like immunoreactive neurons and the inflammation of the paw and the ankle of the injected foot. A strong relationship between the effect of indomethacin on c-Fos expression and its effect on inflammatory processes was observed. These results suggest that Fos-like immunoreactivity induced by carrageenin inflammation may be a very useful tool to study the effects of anti-inflammatory drugs, at both peripheral and central levels of inflammation.

Animals↗

Cholecystokinin B receptor antagonism enhances the ability of a low dose of morphine to reduce c-Fos expression in the spinal cord of the rat.

Three hours after intraplantar carrageenin (6 mg/150 microliters) Fos-like immunoreactivity was predominantly observed in the superficial and deep laminae of the L4-L5 segments of the dorsal horn of the spinal cord in the rat. The total number of Fos-like immunoreactive neurons was equally divided between the superficial (laminae I-II) and deep laminae (laminae V-VI), 99 +/- 3 and 102 +/- 7 Fos-like immunoreactive neurons per section, respectively. In the absence of carrageenin stimulation a negligible number of Fos-like immunoreactive neurons were observed. Pre-administered systemic morphine (0.3 mg/kg) did not significantly influence the total number of Fos-like immunoreactive neurons 3 h after carrageenin. However, pre-administration of a higher dose of morphine (3 mg/kg) significantly reduced the total number of Fos-like immunoreactive neurons (28 +/- 8% reduction, P < 0.001, as compared with control carrageenin Fos-like immunoreactive expression), with this effect being equally divided between the superficial and deep laminae (29 +/- 5 and 29 +/- 6% reduction, respectively, P < 0.001, as compared with control carrageenin Fos-like immunoreactive expression, for both). Pre-administration of the selective cholecystokinin B receptor antagonist, L-365-260 (0.2 mg/kg), alone did not influence the total number of Fos-like immunoreactive neurons 3 h after carrageenin.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Reduction of carrageenin oedema and the associated c-Fos expression in the rat lumbar spinal cord by nitric oxide synthase inhibitor.

1. Three hours after intraplantar carrageenin (6 mg/150 microliters of saline) Fos-like immunoreactivity (Fos-LI) was mainly observed in L4 and L5 segments of the dorsal horn. Both superficial (I-II) and deep laminae (V-VI) neurones were labelled. 2. We have studied the effect of systemic administration of a nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME) on carrageenin evoked c-Fos expression and thus the contribution of nitric oxide to this expression. 3. Pre-administration of L-NAME (10, 25, 50, 100 mg kg-1, i.v.) dose-dependently reduced the number of superificial and deep laminae Fos-LI neurones, 100 mg kg-1 produced a 63 +/- 2% and 72 +/- 4% reduction of Fos-LI neurones respectively, P < 0.0001 for both superficial and deep neurones. 4. Pre-administered L-NAME dose-relatedly reduced the carrageenin-evoked paw and ankle oedema, with 100 mg kg-1 of L-NAME resulting in a 74 +/- 2% and 103 +/- 2% reduction respectively. 5. Post-administration of L-NAME (10 mg kg-1, i.v.) reduced the number of superficial and deep laminae Fos-LI neurones (65 +/- 7% and 53 +/- 8% reduction respectively, P < 0.01 for both superficial and deep neurones). 6. Post-administered L-NAME reduced both the paw and ankle oedema (52 +/- 8% and 62 +/- 10% reduction respectively, P < 0.0001 for both paw and ankle). 7. Pre-administered D-NAME (100 mg kg-1, i.v.), the inactive isomer of L-NAME, produced a weak reduction of the number of superficial laminae Fos-LI neurones (26 +/- 8% reduction, P<0.05), without influencing the deep Fos-LI neurones (5 +/- 8% enhancement) or the oedema.8. Systemic L-arginine (1200 mg kg-1) did not reverse the reduction of the total number of Fos-LI neurones induced by 100mg kg-1 of L-NAME, or the effect of L-NAME on the paw and ankle oedema.9. Intraplantar L-arginine (30 mg) did not reverse the effect of L-NAME (100 mg kg-1) on the total number of Fos-LI neurones. However, the inhibitory effects of L-NAME on the paw and ankle oedema were partially reversed by intraplantar L-Arginine (34 +/- 9% and 45 +/- 11% reduction of carrageenin oedema respectively) with these effects being significant as compared to the effect of L-NAME alone(P<0.05 for both).10. There is a strong correlation between the reduction of the number of Fos-LI neurones and the oedema by L-NAME, clearly demonstrating a predominant role of peripheral NO in the development of one of the signs of carrageenin inflammation.

Amino Acid Oxidoreductases↗

The contribution of NMDA receptor activation to spinal c-Fos expression in a model of inflammatory pain.

1. Intraplantar carrageenin (6 mg 150 microliters-1) evoked a high level of spinal c-Fos expression in the dorsal horn, of segments L4-L5 of the spinal cord, and an extensive peripheral oedema; both parameters were assessed 3 h after carrageenin. 2. Two series of experiments were performed, with the mean total number of Fos like-immunoreactive neurones (Fos-LI), after carrageenin, not being significantly different for the two series of experiments (266 +/- 17 and 332 +/- 31 Fos-LI neurones). For both series of experiments Fos-LI neurones were predominantly located in the superficial and deep laminae, only 10% of the total number of Fos-LI neurones were located in the nucleus proprius and 10% were located in the ventral horn. 3. Pre-administration of the N-methyl-D-aspartate (NMDA) receptor antagonist, (+)-HA966 (0.5 mg kg-1 and 2.5 mg kg-1, s.c.), 30 min before carrageenin, did not significantly influence the total number of Fos-LI neurones, as compared to control carrageenin expression. 4. Pre-administration of the highest dose of (+)-HA966 (10 mg kg-1) significantly reduced the number of deep laminae Fos-LI neurones (28 +/- 3% reduction of control number of Fos-LI neurones after carrageenin, P < or = 0.05), without influencing the number of superficial Fos-LI neurones. There was a tendency towards a reduction of the number of Fos-LI neurones in the nucleus proprius by the highest concentration of pre-administered (+)-HA966, (31 +/- 8% reduction), but this effect did not reach significance. 5. Pre-plus post-administered (+)-HA966 (0.5 mg kg-1), 30 min before and again 45 min afterintraplantar carrageenin, did not significantly influence the total number of Fos-LI neurones, as compared to control carrageenin expression.6. Pre- plus post-administration of 2.5 mg kg-1 (+)-HA966 significantly reduced the total number of Fos-LI neurones, as compared to control carrageenin expression. This effect was reflected by a significant reduction in the number of Fos-LI neurones in the nucleus proprius (36+/-7% reduction of control carrageenin c-Fos expression respectively, P<0.05).7. Pre-plus post-administration of 10 mg kg-1 of (+)-HA966 significantly reduced the number of Fos-LI neurones in the superficial laminae, nucleus proprius, deep laminae and ventral horn (33 +/-0.5%,55+/-6%, 40+/-4% and 51+/-4% reduction of control carrageenin c-Fos expression, respectively, P<0.05,for all areas).8. A single post-administration of (+)-HA966 (10 mg kg-1), 45 min after intraplantar carrageenin, did not significantly influence the number of Fos-LI neurones in the superficial, deep laminae or ventral horn, but significantly reduced the number of Fos-LI neurones in the nucleus proprius, as compared tocontrol carrageenin expression (39+-/8% reduction of control carrageenin c-Fos expression, P <0.05).9 None of the concentrations of (+)-HA966 studied, irrespective of the timing of administration,influenced the peripheral carrageenin oedema. Our results illustrate a contribution of central NMDA receptor activation to carrageenin-evoked spinal c-Fos expression. These results extend previous studies demonstrating the contribution of the NMDA receptor to central hyperalgesia and the expression of c-Fos.

Animals↗