Abstract
Based on previous work, it has been hypothesized that the energetics of ultraviolet (UV) light disrupts effects induced by receptor-binding ligands. If this hypothesis is true, then UV light should (i) disrupt a broad variety of endpoints and (ii) disrupt effects produced by ligands that bind to diverse receptor types. This was tested directly in the present study by using ligands selective for four different receptors (one ionotropic, three metabotropic) and three different behavioral endpoints. The selective dopamine D2 receptor antagonist (–)sulpiride (0.1 uM) dose-relatedly decreased spontaneous locomotor velocity, the selective nicotinic acetylcholine receptor agonist nicotine (1, 3, 5 mM) and the selective muscarinic acetylcholine receptor agonist pilocarpine (20, 30, 50 mM) induced seizure-like activity, and the selective-opioid receptor agonist U-50,488H (10 uM) produced physical dependence (manifested as abstinence-induced withdrawal) in planarian models. Each of these diverse ligand and receptor-mediated effects were attenuated by UV light (254 nm = 7.83 × 10–19 J = 4.89 eV). These findings provide further evidence that UV light disrupts ligand-receptor mediated interactions and that UV light might provide a useful tool for examining drug-receptor interactions.
Highlights
A photodynamic effect is produced whenever an isolated rabbit thoracic aorta, which has been previously contracted to a steady-state isometric tension by an adrenoceptor agonist, is exposed to ultraviolet (UV) light [1,2]
Dopamine D1- and D2-receptor agonists, antagonists, or inhibitors of neuronal dopamine reuptake alter planarian locomotor activity (“motility”)
We have shown that a decrease in planarian spontaneous locomotor velocity produced by the selective dopamine D2 receptor antagonist sulpiride (5-(Aminosufonyl)-N-[(1-ethyl-2-pyrrolidinyl)methyl]-2-methoxy benzamide) occurs in an enantiomeric-selective-((–)sulpiride >> (+)sulpiride) and in a dose-dependent manner
Summary
A photodynamic effect is produced whenever an isolated rabbit thoracic aorta, which has been previously contracted to a steady-state isometric tension by an adrenoceptor agonist, is exposed to ultraviolet (UV) light [1,2]. Dopamine D1- and D2-receptor agonists, antagonists, or inhibitors of neuronal dopamine reuptake alter planarian locomotor activity (“motility”) (e.g., [11,12,14,15,16,17,18]; anticonvulsants inhibit seizure-like activity (pSLA) [19]; and abstinence- and antagonistinduced withdrawal signs are elicited in planarian model of physical dependence [20,21,22,23]. Attenuation of these effects by receptor-selective antagonists supports recaptor-mediated mechanisms
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call