Summary
Mice injected with DSP-4 [N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine], a selective noradrenergic neurotoxin, had marked depletions of central noradrenaline and an attenuated post-decapitation reflex. DSP-4-treated mice exhibited an increased sensitivity to the α2-adrenoceptor agonist clonidine as measured by inhibition of the pinna reflex, but normal sensitivity as measured by hypothermia. This differential sensitivity may reflect the presence of supersensitive postsynaptic α2-adrenoceptors in some, but not all, CNS regions after DSP-4 treatment.
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Acknowledgments. The authors gratefully acknowledge the excellent technical assistance of Mr P. E. Richards. DSP-4 hydrochloride and clonidine hydrochloride were synthesized by Beecham Pharmaceuticals Research Division.
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Lerner, U., Larsson, Å. The bisphosphonates HEBP and AHPrBP but not AHBP inhibit mineral mobilization and lysosomal enzyme release from mouse calvarial bones in tissue culture. Experientia 40, 963–965 (1984). https://doi.org/10.1007/BF01946460
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DOI: https://doi.org/10.1007/BF01946460