Meeuwis K. Boelen
La Trobe University
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Featured researches published by Meeuwis K. Boelen.
Visual Neuroscience | 1996
Ian G. Morgan; Meeuwis K. Boelen
We propose that there exists within the avian, and perhaps more generally in the vertebrate retina, a two-state nonadapting flip-flop circuit, based on reciprocal inhibitory interactions between the photoreceptors, releasing melatonin, the dopaminergic amacrine cells, and amacrine cells which contain enkephalin-, neurotensin-, and somatostatin-like immunoreactivity (the ENSLI amacrine cells). This circuit consists of two loops, one based on the photoreceptors and dopaminergic amacrine cells, and the other on the dopaminergic and ENSLI amacrine cells. In the dark, the photoreceptors and ENSLI amacrine cells are active, with the dopaminergic amacrine cells inactive. In the light, the dopaminergic amacrine cells are active, with the photoreceptors and ENSLI amacrine cells inactive. The transition from dark to light state occurs over a narrow (< 1 log unit) range of low light intensities, and we postulate that this transition is driven by a graded, adapting pathway from photoreceptors, releasing glutamate, to ON-bipolar cells to dopaminergic amacrine cells. The properties of this pathway suggest that, once released from the reciprocal inhibitory controls of the dark state, dopamine release will show graded, adapting characteristics. Thus, we postulate that retinal function will be divided into two phases: a dopamine-independent phase at low light intensities, and a dopamine-dependent phase at higher light intensities. Dopamine-dependent functions may show two-state properties, or two-state properties on which are superimposed graded, adapting characteristics. Functions dependent upon melatonin, the enkephalins, neurotensin, and somatostatin may tend to show simpler two-state properties. We propose that the dark-light switch may have a role in a range of light-adaptive phenomena, in signalling night-day transitions to the suprachiasmatic nucleus and the pineal, and in the control of eye growth during development.
Neurochemistry International | 2006
P. Megaw; Mary G. Boelen; Ian G. Morgan; Meeuwis K. Boelen
The retinal dopaminergic system appears to play a major role in the regulation of global retinal processes related to light adaptation. Although most reports agree that dopamine release is stimulated by light, some retinal functions that are mediated by dopamine exhibit circadian patterns of activity, suggesting that dopamine release may be controlled by a circadian oscillator as well as by light. Using the accumulation of the dopamine metabolite dihydroxyphenylacetic acid (DOPAC) in the vitreous as a measure of dopamine release rates, we have investigated the balance between circadian- and light control over dopamine release. In chickens held under diurnal light:dark conditions, vitreal levels of DOPAC showed daily oscillations with the steady-state levels increasing nine-fold during the light phase. Kinetic analysis of this data indicates that apparent dopamine release rates increased almost four-fold at the onset of light and then remained continuously elevated throughout the 12h light phase. In constant darkness, vitreal levels of DOPAC displayed circadian oscillations, with an almost two-fold increase in dopamine release rates coinciding with subjective dawn/early morning. This circadian rise in vitreal DOPAC could be blocked by intravitreal administration of melatonin (10 nmol), as predicted by the model of the dark-light switch where a circadian fall in melatonin would relieve dopamine release of inhibition and thus be responsible for the slight circadian increase in dopamine release. The increase in vitreal DOPAC in response to light, however, was only partially suppressed by melatonin. The activity of the dopaminergic amacrine cell in the chicken retina thus appears to be dominated by light-activated input.
Clinical and Experimental Ophthalmology | 2001
Sally I. Firth; Ian G. Morgan; Meeuwis K. Boelen; Catherine W. Morgans
L‐type calcium channels have been associated with synaptic transmission in the retina, and are a potential site for modulation of the release of neurotransmitters. The present study documents the immunohistochemical localization of neuronal α1 subunits of L‐type calcium channels in chicken retina, using antibodies to the α1c, α1d and α1f subunits of L‐type calcium channels. The α1c‐like subunits were localized to Müller cells, with predominantly radial processes, and a prominent band of horizontal processes in the outer plexiform layer. The antibody to α1d subunits labelled most, if not all, cell bodies. The antibody to a human α1f subunit strongly labelled photoreceptor terminals. Fainter immunoreactivity was detected in the inner segments of the photoreceptors, a subset of amacrine cells, two bands of labelling in the inner plexiform layer and many ganglion cells. The differential cellular distributions of these α1‐subunits suggests subtle functional differences in their roles at different cellular locations.
Journal of Neurochemistry | 2001
Pam Megaw; Ian G. Morgan; Meeuwis K. Boelen
Dopamine is generally accepted as a major neurotransmitter associated with light‐adaptive processes in the retina. However, little is known about its precise release pattern in vivo, largely due to the lack of an unambiguous method for the determination of dopamine release. We have found that vitreal levels of dihydroxyphenylacetic acid (DOPAC) reflect the rate of dopamine release in chickens. Blocking re‐uptake with nomifensine significantly lowered vitreal DOPAC and retinal dopamine, confirming the retinal origin and reliance of vitreal DOPAC on intact re‐uptake mechanisms. Further, inhibition of monoamine oxidase with pargyline reduced vitreal as well as retinal DOPAC levels, confirming that the DOPAC detected is generated by monoamine oxidase. Finally, we found that DOPAC diffused freely into and out of isolated vitreous bodies and we found the vitreous to be metabolically inert with respect to DOPAC, supporting the idea that vitreal levels of DOPAC are consequential to the retinal metabolism of dopamine. Exposure to light, which is known to increase retinal dopamine release, readily increased vitreal DOPAC levels. The accumulation of DOPAC in the vitreous over 6 h light fitted a mathematical model of DOPAC accumulation based on zero‐order influx (proportional to dopamine release rates) and diffusion driven, first‐order efflux.
Neuroreport | 1995
Ian G. Morgan; Meeuwis K. Boelen; Pat Miethke
WE have recently shown that light, over a narrow range of low intensities suppresses the activity of the enkepha-lin-immunoreactive amacrine cells of the chicken retina. In this paper, we show that over the same range of low light intensities the rate of melatonin synthesis in both the retina and the pineal of the chicken is suppressed. We further show that the effects of light on the pineal at these low intensities are mediated by the retina and not by direct actions on the pineal. Combined with our evidence that dopaminergic pathways within the retina are involved in controlling the state of activity of the pineal, these results suggest, but do not prove, that the change in state of a microcircuit within the retina involving the photoreceptors, dopaminergic amacrine cells and enkephalin-immunoreactive amacrine cells may be causally related to changes in the state of the pineal.
Neuroscience Letters | 1994
Ian G. Morgan; John Wellard; Meeuwis K. Boelen
The functional state of the amacrine cells which contain enkephalin-, neurotensin- and somatostatin-like immunoreactivity of the chicken retina was monitored by measuring the rate of change in the levels of [Leu]enkephalin-like immunoreactivity in the retina. Dark-adapted birds were exposed to lights of different intensities for 12 h. At light levels of < or = 0.03 microW/cm2, the ENSLI amacrine cells were highly active but, by 0.08 microW/cm2, they reached a state of maximum inactivation. Thus, the ENSLI amacrine cells act as flip-flop devices, inactivated by critical levels of light, which correspond to those which inactivate pineal melatonin synthesis. They may, therefore, be involved in retinal pathways which signal the difference between day and night.
Brain Research | 1994
Meeuwis K. Boelen; John Wellard; Mark Dowton; Ian G. Morgan
The activity of the enkephalin-immunoreactive (ENSLI) amacrine cells of the chicken retina is low in the light and high in the dark, resulting in parallel increases and decreases in the levels of the enkephalins. In vivo, the selective dopaminergic D1 antagonist SCH23390 increased the activity of the ENSLI amacrine cells in the light (ED50; 20 pmol), but had a much lesser effect in the dark, whereas the selective dopaminergic D2 antagonist sulpiride had effects only at very high concentrations (ED50; 39 nmol). In contrast, the non-selective dopamine agonist ADTN hardly affected the activity of the ENSLI amacrine cells in the light, but markedly reduced their activity in the dark. This pattern of effects suggests that dopamine actively inhibits the ENSLI amacrine cells in the light, but exerts much less inhibitory activity in the dark, consistent with the idea that dopamine is released during the exposure of the retina to light. Thus dopaminergic controls over the ENSLI amacrine cells appear to contribute to the light:dark differences in activity of the ENSLI amacrine cells. Results obtained on the dopaminergic control of enkephalin release in vitro were generally consistent with this model, except that ADTN appeared to stimulate the ENSLI amacrine cells in the dark.
Neuroreport | 1995
Ian G. Morgan; Meeuwis K. Boelen; Pat Miethke
The role of dopaminergic pathways in the retina in controlling the functional state of the pineal was investigated. Dopaminergic agents were injected into the eyes of dark-adapted chickens which were maintained in the dark. Changes in the activity of N-acetyltransferase (NAT) in the retina and pineal were then monitored. Injection of the non-specific dopamine agonist 6,7-ADTN depressed retinal and pineal NAT. The D1-specific agonist SKF38393 did not affect retinal NAT but depressed pineal NAT. In contrast, quinpirole, a D2-specific agonist, depressed retinal NAT, but did not depress pineal NAT. Thus, D1- rather than D2-dopaminergic pathways in the retina are involved in the retinal circuit which control pineal function.
Brain Research | 1991
Meeuwis K. Boelen; John Wellard; Mark Dowton; Ian W. Chubb; Ian G. Morgan
Retinal levels of [Leu5]enkephalin-like immunoreactivity (LE-LI) increase during the light and decrease during darkness, in vivo15. Intravitreal injection of the GABA antagonist picrotoxin had no effect on the accumulation of LE-LI during the light, suggesting the absence of significant GABAergic control over LE-LI cells. However, injection of the glycine antagonist strychnine, prevented the light-induced increase of retinal levels of LE-LI during 6 h exposure to light, indicating the presence of glycinergic control over the LE-LI neurons. When applied during the dark, strychnine increased the depletion of LE-LI by 34% compared to vehicle-injected eyes, suggesting that the LE-LI neurons receive some glycinergic input during the dark as well. The release of LE-LI from retinas superfused in vitro is depressed by exposing the preparation to light. Superfusing isolated retinas with physiological buffer containing picrotoxin (100 microM), GABA (50 mM), or the GABA agonists muscimol (100 microM), (+)-baclofen (200 microM), or 4,5,6,7-tetrahydroisoxazolo[5,4-c]pyridin-3-ol (THIP) (100 mM), had no effect on the efflux of LE-LI. Strychnine (100 mM) however increased the efflux of LE-LI by 64%, compared to the spontaneous efflux during the light. Glycine (15 and 50 mM) decreased the spontaneous efflux of LE-LI from retinas superfused in darkness by 44-48% and by 31% at 5 mM. These data are consistent with the results from pharmacological manipulations in vivo. We conclude that the LE-LI amacrine cells are under inhibitory control from glycinergic but not from GABAergic neurons.(ABSTRACT TRUNCATED AT 250 WORDS)
Developmental Brain Research | 1997
D.S Yang; Meeuwis K. Boelen; Ian G. Morgan
The development of the enkephalin-, neurotensin- and somatostatin-like immunoreactive (ENSLI) amacrine cells in the chicken retina has been investigated by radioimmunoassay (RIA) and immunocytochemistry (ICC). By RIA, enkephalin-like immunoreactivity (ENK-LI) was detected at embryonic day (E) 5 at only very low levels, which gradually increased until E17. From E18 to E21, there was a relatively rapid increase in ENK-LI levels, and just after hatching, there was a very steep rise. By ICC, the cell bodies of the ENSLI amacrine cells were first detected in the inner nuclear layer on E18, with no immunostaining in the inner plexiform layer (IPL). On E21, more cells were detected and processes in the IPL were visible, but detailed arborisations were not clear. On postnatal day (P) 1, the ENSLI amacrine cells showed a morphology similar to that in mature retina in both the density of cell bodies and the ramification pattern of processes. Antibodies to neurotensin and somatostatin revealed a similar developmental pattern. Thus, the three peptides appear to follow a similar developmental pattern in the ENSLI amacrine cells, suggesting that the three peptides respond similarly to developmental stimuli, just as they are released in parallel in response to physiological stimulation from mature ENSLI amacrine cells. After hatching, higher levels of ENK-LI were detected by RIA and more ENSLI amacrine cell bodies and processes were detected by ICC in animals kept in the light than in those kept in the dark. In retinas kept in the light for 12 h, it was found that immunoreactive processes in the IPL formed strongly stained patches, but this was not observed in retinas kept in the dark for 12 h.