Placing a translucent diffuser over the eye of a chick causes the eye to grow excessively, resulting in form-deprivation myopia. For chickens kept on a 12:12 h light/dark cycle, removing the diffuser for 3 h during the light period protects against the excessive growth, but if the bird is kept in the dark for this 3-h period, the protective effect is abolished. Injecting dopamine agonists into the eye during this 3-h dark period restores the protective effect, which can be blocked by dopamine antagonists injected just prior to diffuser removal in the light. These responses are mediated by D2 receptors, suggesting that the protective effect of normal vision against form-deprivation is mediated through the stimulation of dopamine release and activation of D2-dopamine receptors.

As the malaria parasite, Plasmodium falciparum, grows within its host erythrocyte it induces an increase in the permeability of the erythrocyte membrane to a range of low-molecular-mass solutes, including Na+ and K+ (ref. 1). This results in a progressive increase in the concentration of Na+ in the erythrocyte cytosol. The parasite cytosol has a relatively low Na+ concentration and there is therefore a large inward Na+ gradient across the parasite plasma membrane. Here we show that the parasite exploits the Na+ electrochemical gradient to energize the uptake of inorganic phosphate (P(i)), an essential nutrient. P(i) was taken up into the intracellular parasite by a Na+-dependent transporter, with a stoichiometry of 2Na+:1P(i) and with an apparent preference for the monovalent over the divalent form of P(i). A P(i) transporter (PfPiT) belonging to the PiT family was cloned from the parasite and localized to the parasite surface. Expression of PfPiT in Xenopus oocytes resulted in Na+-dependent P(i) uptake with characteristics similar to those observed for P(i) uptake in the parasite. This study provides new insight into the significance of the malaria-parasite-induced alteration of the ionic composition of its host cell.

Increases in the expression of the immediate early gene ZENK in the retina, measured by changes in the levels of mRNA and protein immunoreactivity, are amongst the most rapid responses so far measured to conditions that decrease the rate of eye growth in chickens. Our aim was to determine whether atropine, a muscarinic cholinergic antagonist, and 2-amino-6,7-dihydroxy-1,2,3,4-tetrahydronaphthalene hydrobromide, a dopamine agonist, which are known to block excessive eye growth, produce similar changes in ZENK expression. Form-deprivation resulted in significant down-regulation of the expression of retinal ZENK mRNA within 1 h of fitting the diffusers, whereas removal of the diffusers from the eyes of chickens that had developed form-deprivation myopia resulted in significant up-regulation of retinal ZENK expression within 1 h. When atropine (10 microL of 25 mM solution) and 2-amino-6,7-dihydroxy-1,2,3,4-tetrahydronaphthalene hydrobromide (10 microL of a 10 mM solution) were injected intravitreally, just prior to fitting the diffusers, the down-regulation of retinal ZENK mRNA caused by form-deprivation was reversed. This resulted in levels of ZENK mRNA higher than in control or contralateral control eyes. The doses were chosen because they are known to block the excessive axial elongation induced by form-deprivation, without affecting the growth of control eyes. Neither agent had any effect on retinal ZENK expression within this time period when injected into control eyes. These results suggest that both muscarinic acetylcholine antagonists and dopamine agonists act early in the signal cascade controlling eye growth, possibly within the retina itself.

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