Effect of postnatal light deprivation on the ontogenesis of dopamine neurons in rat retina.

In rats raised from birth under a regular dark-light cycle, retinal dopamine (DA) levels were low at 12 days, increased progressively and steeply at 16, 20, 30 and 60 days and peaked at about 75 days postnatally. Dark-rearing from birth suppressed the magnitude of the normal developmental pattern of DA concentrations in retina and at 20, 30 and 60 days of age they were markedly smaller compared with those in age-matched controls grown under regular cyclic illumination. In adult rats reared up to the age of 60 days in regular cyclic lighting and then transferred to complete darkness for additional periods of 7-60 days, there were marked reductions in retinal DA levels. In rats reared in total darkness for 16, 20 or 30 days after birth and then transferred to regular dark-light conditions for additional periods of up to 30 or 60 days, retinal DA levels were always higher than those in animals with continuous light deprivation. They were similar to or even higher than those in rats grown under regular dark-light cycle. Findings suggest that light stimulation is essential for the postnatal ontogenetic increases of synthesis and storage of DA within retinal DAergic neurons. Suppressed DA accumulation in retina induced by dark-rearing from birth is not irreversible and can be completely corrected by re-exposure to regular lighting conditions regardless of the durations of postnatal light deprivation.

Dopamine turnover in rat retina: a 24-hour light-dependent rhythm.

To examine the pattern of retinal dopamine (DA) turnover during 24 h, DA and 3,4-dihydroxyphenylacetic acid (DOPAC) were measured at 2-h intervals in rats kept in a regular 12-h light-dark cycle. DA and DOPAC were higher during the light and lower during the dark hours. These rhythmic variations were abolished and DA and DOPAC remained low during 24 h of light deprivation. Findings indicate that DA turnover in the retina is accelerated during the light and suppressed during the dark phases of the diurnal light-dark cycle. These fluctuations in retinal DA neuronal activity are not truly circadian but are dependent on environmental lighting as an external stimulator.

Differential effect of acute and chronic haloperidol administration on dopamine turnover in rat nigrostriatal and retinal dopaminergic neurons.

Haloperidol-induced increases in DOPAC and HVA declined in the striatum but remained unchanged in the retina after chronic pretreatment with haloperidol (1-4 weeks). DA concentrations were unaffected in the striatum but decreased in the retina after acute or chronic haloperidol administration. Light stimulation increased both retinal DA and DOPAC. The findings indicate that acute and chronic haloperidol affect nigrostriatal and retinal DA neurons differentially. In addition, DA neurons in retina respond differently to activations by haloperidol and light.

Mesolimbic dopaminergic neurons are not spared by MPTP neurotoxicity in mice.

In C57 black mice, MPTP (N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) (30 mg/kg X 2, 20 mg/kg X 15, 30 mg/kg X 15, or 35 mg/kg X 1) depleted DA in both striatum and accumbens but not in frontal cortex, hypothalamus and retina. DA decreases were more pronounced in striatum than in accumbens, were maximal at 2 days, partially reversed later but persisted up to 30 days after treatment. DA depletions in nigra were smaller earlier and maximal later. The study suggests that, in mice, MPTP damages nigrostriatal and mesolimbic projections but spares other DA neurons.

Uveal coloboma associated with amniotic band syndrome.

A baby girl had constriction bands and digital amputations typical of the amniotic band syndrome, as well as a typical uveal coloboma in a slightly microphthalmic eye. A small, free-floating amniotic band may have lodged in the fetal uveal cleft at 5 to 6 weeks of gestation, preventing closure of the cleft and thus resulting in this first reported instance of an association between amniotic band syndrome and an isolated uveal coloboma.

Amniotic band syndrome and strabismus.

Three patients with various manifestations of the amniotic band syndrome associated with strabismus are presented and discussed. All three cases demonstrate a paralytic strabismus due to a unilateral paresis-paralysis of the medial rectus in one case and of the superior rectus in another. The third case showed a bilateral lateral rectus paralysis. In two cases, the strabismus was accompanied by other ocular manifestations, while in one patient strabismus and amblyopia were the sole ophthalmological findings. In two of the cases, a direct association between the mesodermal bands and the strabismus could be established, while in one case this association might have been incidental. Careful ophthalmological followup and treatment of these cases prevented needless loss of vision while appropriate muscle surgery restored acceptable cosmetic appearance in one case.

The dopaminergic amacrine system and its response to light stimulation in rats with inherited retinal dystrophy.

In both the RCS mutant strain of rats with hereditary progressive retinal dystrophy and in controls, concentrations of dopamine (DA) and its metabolic DOPAC increased steeply in retina from 14 to 60 days postnatally with no further elevations in older animals indicating normal dopaminergic system evolution in the RCS rats. In 60-, 90-, and 135-day-old but not in younger (14- and 30-day-old) RCS rats killed in the light phase of the light-dark cycle, retinal DA, and more markedly DOPAC levels, were lower than those in age-matched controls. In normal rats aged 24, 35 and 70 days that were dark-adapted for 24 hr, 2-hr light exposure increased DA and mainly DOPAC levels in retina. LIght stimulation after dark adaptation elevated retinal DA and DOPAC only in 24- but not in 35- or 70-day-old RCS rats. In RCS rats with advanced retinal dystrophy, decreases in retinal DA and DOPAC levels and lack of response of DA amacrine cells to light exposure are probably secondary to degeneration or impairment of photoreceptors which are no longer capable of transmitting light stimuli onto DA neurons in retina.