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1 General aspects (0)   1.1 Epidemiology (10)   1.2 Population genetics (7)   1.3 Pathogenesis (3)   1.4 Quality of life (3)   1.5 Glaucomas as cause of blindness (2)   1.6 Prevention and screening (5) 2 Anatomical structures in glaucoma (0)   2.1 Conjunctiva (0)   2.2 Cornea (1)   2.3 Sclera (0)   2.4 Anterior chamber angle (0)   2.5 Meshwork (3)     2.5.1 Trabecular meshwork (10)     2.5.2 Schlemms canal (0)     2.5.3 Scleral outlet channels (0)   2.6 Aqueous humor dynamics (0)     2.6.1 Production (0)     2.6.2 Outflow (1)       2.6.2.1 Trabecular meshwork (1)       2.6.2.2 Uveoscleral (0)     2.6.3 Compostion (3)   2.7 Episcleral veins and venous pressure (1)   2.8 Iris (4)   2.9 Ciliary body (3)   2.10 Lens (0)   2.11 Vitreous body (0)   2.12 Choroid, peripapillary choroid, peripapillary atrophy (2)   2.13 Retina and retinal nerve fibre layer (20)   2.14 Optic disc (18)   2.15 Optic nerve (2)   2.16 Chiasma and retrochiasmal central nervous system (1)   2.17 Stem cells (0)   2.20 Other (0) 3 Laboratory methods (2)   3.1 Microscopy (3)   3.2 Electron microscopy (2)   3.3 Immunohistochemistry (8)   3.4 Molecular genetics (2)     3.4.1 Linkage studies (8)     3.4.2 Gene studies (3)   3.5 Molecular biology incl. 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Abstract #8937 Published in IGR 5-2

Omega conotoxin: a subtype specific calcium channel ligand with therapeutic potential in glaucoma?

Chu TC; Potter DE
Research Communications in Pharmacology and Toxicology 2001; 6: 263-275

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The purpose of this study was to use Ω conotoxin GVIA (CgTx) to define the potential roles of N type Ca²⁺ channels in modulating: 1. intraocular pressure (IOP), pupil diameter and aqueous humor flow rate of rabbits; and 2. electrically-induced norepinephrine release from sympathetic neurons in iris ciliary bodies. CgTx was injected into the vitreous of normal and surgically sympathectomized eyes; contralateral (normal) eyes were injected with saline. Aqueous humor flow rate was quantified by fluorophotometry. Perfused, electrically stimulated iris ciliary bodies were utilized to investigate the effects of CgTx on ³H norepinephrine oveflow. Results showed that CgTx induced dose related ocular hypotension and a reduction of aqueous humor flow rate in normal rabbits. The effects of CgTx (3.3 μg) on ocular hydrodynamics were greater in normal than sympathetically denervated eyes. Miosis was observed in normal rabbit eyes at all doses of CgTx. In iris ciliary body, CgTx (1, 10, 100 nm) caused concentration related suppression (50, 75, 97%) of electrically evoked norepinephrine release. Following pretreatment with CgTx (10 nM), moxonidine (1 μm), an α₂/I₁ receptor agonist, caused no additional reduction in norepinephrine release beyond the effect of CgTx alone. Pretreatment with an α₂/I₁ receptor antagonist, efaroxan (10 μm), prevented the inhibitory effect of moxonidine but did not affect the suppressive effect of CgTx. It is concluded that CgTx induced inhibition of N type Ca²⁺ channels can suppress IOP and aqueous flow rate in rabbits and that these effects are mediated, in part, by suppression of sympathetic nerve activity in the iris ciliary body. Additional studies are needed to determine if conotoxins have other properties that would prove useful in the therapy of glaucoma.

Dr. T.C. Chu, Department of Pharmacology, Morehouse School of Medicine, 720 Westview Drive SW, Atlanta, GA 30310 1495, USA. tc@msm.edu

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Classification:

11.14 Investigational drugs; pharmacological experiments (Part of: 11 Medical treatment)

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