Article date: January 1995
By: Prisca Honoré, Victoria Chapman, Jaroslava Buritova, Jean‐Marie Besson, in Volume 114, Issue 1, pages 77-84
Three hours after intraplantar carrageenin (6 mg/150 μl 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.
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.
Pre‐administration of l‐NAME (10, 25, 50, 100 mg kg−1, i.v.) dose‐dependently reduced the number of superficial 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.
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.
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).
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).
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.
Systemic l‐arginine (1200 mg kg−1) did not reverse the reduction of the total number of Fos‐LI neurones induced by 100 mg kg−1 of l‐NAME, or the effect of l‐NAME on the paw and ankle oedema.
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).
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.
Three hours after intraplantar carrageenin (6 mg/150 μl 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.
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.
Pre‐administration of l‐NAME (10, 25, 50, 100 mg kg−1, i.v.) dose‐dependently reduced the number of superficial 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.
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.
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).
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).
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.
Systemic l‐arginine (1200 mg kg−1) did not reverse the reduction of the total number of Fos‐LI neurones induced by 100 mg kg−1 of l‐NAME, or the effect of l‐NAME on the paw and ankle oedema.
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).
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.
DOI: 10.1111/j.1476-5381.1995.tb14908.x
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