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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

Drug-induced regulation of [125I]iodocyanopindolol-labeled 5-hydroxytryptamine1B receptor binding sites in the central nervous system.

Little is known about the regulation of 5-hydroxytryptamine1B (5-HT1B) receptors, a putative terminal autoreceptor in the central nervous system. We studied the regional responses of [125I]iodocyanopindolol ([125I]ICYP)-labeled central 5-HT1B sites to chronic treatment with 5-HT agonists and antagonists at a dose of 10 mg/kg/d IP for 30 consecutive days in the rat. In controls, there were 3.4-fold regional differences in Bmax, with a rank order of brainstem > hippocampus > cortex, striatum > spinal cord, and Kas were slightly lower in striatum and spinal cord. RU 24969 significantly reduced Bmax 23 to 63% in cortex, hippocampus, striatum, brainstem, and spinal cord without a change in Ka except for a 1.7-fold increase in cortex and spinal cord. The putative 5-HT1B agonist (m-trifluoromethyl-phenylpiperazine (TFMPP), but not [1-(3-chlorophenyl)piperazine] (m-CPP) or the 5-HT1B antagonists pindolol or quipazine, reduced the Bmax of cortical 5-HT1B sites (-16%). Chronic treatment with the 5-HT antagonists methysergide, pindolol, propranolol, ritanserin, metergoline, or methiothepin did not significantly affect striatal Bmax or Kd compared to respective vehicles. The data demonstrate significant changes in maximum number of 5-HT1B receptors in response to chronic agonist but not antagonist treatments at the dose studied.[1]

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