Article date: June 1996
By: Jong Hoon Ryu, Kazuhiko Yanai, Xiao‐Lan Zhao, Takehiko Watanabe, in Volume 118, Issue 3, pages 585-592
The binding of [3H]‐(R)α‐methylhistamine and [3H]‐Nα‐methylhistamine to histamine H3‐receptors, [3H]‐SCH23390 to dopamine D1‐receptors, and [3H]‐YM09151‐2 to dopamine D2‐receptors was investigated by quantitative receptor autoradiography in the rat brain following 6‐hydroxydopamine injection into the substantia nigra.
The levels of [3H]‐(R)α‐methylhistamine binding sites in the denervated striatum and substantia nigra were significantly higher than those in the contralateral side from 1 week to 12 weeks after nigral lesions. The H3‐receptor binding was maximal at 3 weeks after nigral lesions and maintained until 12 weeks.
The increased number of histamine H3‐receptors was decreased to the level of the contralateral side by chronic treatment with a selective dopamine D1 agonist, SKF38393, but not modified by a selective dopamine D2 agonist, quinpirole.
Dopamine D1‐ and D2‐receptors in the striatum were similarly up‐regulated after unilateral nigral lesion. On the other hand, the number of dopamine D2‐receptors in the substantia nigra was markedly decreased after administration of 6‐hydroxydopamine.
The treatment with (S)α‐fluoromethylhistidine increased the H3‐receptor binding in both the ipsilateral and contralateral sides. As a result, the magnitude of the ratio of the H3‐receptor binding between ipsilateral and contralateral sides was partially attenuated by treatment with (S)‐α‐fluoromethylhistidine.
These results strongly suggest that the expression of histamine H3‐receptors in the striatum and substantia nigra is influenced through D1‐receptors by tonic nigrostriatal dopaminergic inputs.
The binding of [3H]‐(R)α‐methylhistamine and [3H]‐Nα‐methylhistamine to histamine H3‐receptors, [3H]‐SCH23390 to dopamine D1‐receptors, and [3H]‐YM09151‐2 to dopamine D2‐receptors was investigated by quantitative receptor autoradiography in the rat brain following 6‐hydroxydopamine injection into the substantia nigra.
The levels of [3H]‐(R)α‐methylhistamine binding sites in the denervated striatum and substantia nigra were significantly higher than those in the contralateral side from 1 week to 12 weeks after nigral lesions. The H3‐receptor binding was maximal at 3 weeks after nigral lesions and maintained until 12 weeks.
The increased number of histamine H3‐receptors was decreased to the level of the contralateral side by chronic treatment with a selective dopamine D1 agonist, SKF38393, but not modified by a selective dopamine D2 agonist, quinpirole.
Dopamine D1‐ and D2‐receptors in the striatum were similarly up‐regulated after unilateral nigral lesion. On the other hand, the number of dopamine D2‐receptors in the substantia nigra was markedly decreased after administration of 6‐hydroxydopamine.
The treatment with (S)α‐fluoromethylhistidine increased the H3‐receptor binding in both the ipsilateral and contralateral sides. As a result, the magnitude of the ratio of the H3‐receptor binding between ipsilateral and contralateral sides was partially attenuated by treatment with (S)‐α‐fluoromethylhistidine.
These results strongly suggest that the expression of histamine H3‐receptors in the striatum and substantia nigra is influenced through D1‐receptors by tonic nigrostriatal dopaminergic inputs.
DOI: 10.1111/j.1476-5381.1996.tb15441.x
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