PubMed · 7827534
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K Long, R Long. 1994. Treating open-angle glaucoma.. https://pubmed.ncbi.nlm.nih.gov/7827534/
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In this study we investigated whether a selective pattern of norepinephrine loss potentiates methamphetamine-induced striatal dopamine depletion in rats. We also evaluated whether chronic norepinephrine depletion reduces the threshold dose of methamphetamine necessary to induce long-lasting striatal dopamine loss in mice and in rats. Pre-treatment with the selective noradrenergic neurotoxin DSP-4 (50 mg/kg, i.p.) in mice and in rats significantly enhanced methamphetamine-induced striatal dopamine depletion. Administration of a low dose of methamphetamine (1 x 5 mg/kg and 3 x 5 mg/kg, respectively, i.p., at 2-h interval) to C57B1/6N mice and Sprague-Dawley rats did not decrease striatal dopamine levels when injected alone but produced a significant decrease in striatal dopamine when given to rodents carrying a long-lasting norepinephrine depletion previously induced by DSP-4. Our results suggest that norepinephrine loss might both enhance neurotoxic damage and decrease the threshold for neurotoxicity to nigrostriatal dopaminergic neurons in different animal species.
Binding properties of [3H]dexmedetomidine [(+)-(S)-4-[1-(2,3-dimethylphenyl)ethyl]-1H-imidazole] as an agonist-type radioligand for alpha 2-adrenoceptors were characterised for the first time in tissues relevant to its analgesic (spinal cord from neonatal or adult rats) and behavioural (rat cerebral cortex) actions. In membranes of rat cerebral cortex (KdHigh 0.2 +/- 0.03 nM, KdLow 8.8 +/- 1.4 nM with Bmax High 130 +/- 11 fmol/mg protein, RHigh 16%) and neonatal spinal cord (KdHigh 0.3 +/- 0.04 nM, KdLow 14 +/- 3.7 nM with Bmax High 290 +/- 40 fmol/mg protein, RHigh 25%) Gpp(NH)p modifies the biphasic binding to monophasic and binding is competed with specifically by alpha 2-adrenoceptor compounds. Binding to rat cerebral cortex is not modified by pretreatment with the noradrenergic neurotoxin, DSP-4 (N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine). In contrast, [3H]dexmedetomidine binding to adult rat spinal cord membranes is more complex and both saturation analysis and competition experiments indicate the presence of a non-adrenergic component of binding (about 40% of total binding) which is sensitive to imidazole-type compounds. This non-adrenergic component of [3H]dexmedetomidine binding can be defined as a novel type of imidazole binding site such that, of the imidazoline I1 or I2 receptor ligands, only cimetidine has relatively high affinity. In conclusion, [3H]dexmedetomidine shows very complex binding characteristics that limit its use as an agonist-type radioligand for alpha 2-adrenoceptors but it may be a useful tool for imidazoline receptor characterisation.
The present study examined whether reserpine-induced oral dyskinesia is mediated by release of residual endogenous dopamine. Amphetamine produced a dose-dependent change in reserpine-induced oral dyskinesia in which the response was exacerbated by 0.6 mg/kg amphetamine and inhibited by 1 mg/kg. The latter dose also produced stereotypy that may have interfered with expression of reserpine-induced oral dyskinesia. Nigrostriatal 6-hydroxydopamine lesions attenuated expression of reserpine-induced oral dyskinesia. These lesions did not reduce locomotor activity, however, indicating that the attenuation of reserpine-induced oral dyskinesia was not due to a general depressant effect of the lesions on motor behavior. These results suggest that increasing dopamine release by administration of amphetamine exacerbates reserpine-induced oral dyskinesia, whereas decreasing the amount of releasable dopamine in the striatum by 6-hydroxydopamine lesions attenuates reserpine-induced oral dyskinsia. These findings may have implications for understanding tardive dyskinesia and L-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia.