PubMed Health⌕ Search

Biomedical subjects

I G Morgan

Publications and source records attributed to I G Morgan.

At least 19 recordsLinked to original sources
PubMed2006

Dopaminergic agents affect the ability of brief periods of normal vision to prevent form-deprivation myopia.

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.

Animals↗
PubMed2001

Localization of voltage-sensitive L-type calcium channels in the chicken retina.

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 alpha1 subunits of L-type calcium channels in chicken retina, using antibodies to the alpha1c, alpha1d and alpha1f subunits of L-type calcium channels. The alpha1c-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 alpha1d subunits labelled most, if not all, cell bodies. The antibody to a human alpha1f 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 distributons of these alpha1-subunits suggests subtle functional differences in their roles at different cellular locations.

Animals↗
PubMed1999

Colchicine causes excessive ocular growth and myopia in chicks.

Colchicine has been reported to destroy ganglion cells (GCs) in the retina of hatchling chicks. We tested whether colchicine influences normal ocular growth and form-deprivation myopia, and whether it affects cells other than GCs. Colchicine greatly increased axial length, equatorial diameter, eye weight, and myopic refractive error, while reducing corneal curvature. Colchicine caused DNA fragmentation in many GCs and some amacrine cells and photoreceptors, ultimately leading to the destruction of most GCs and particular sub-sets of amacrine cells. Colchicine-induced ocular growth may result from the destruction of amacrine cells that normally suppress ocular growth, and corneal flattening may result from the destruction of GCs whose central pathway normally plays a role in shaping the cornea.

Animals↗
PubMed1998

Cholinergic amacrine cells are not required for the progression and atropine-mediated suppression of form-deprivation myopia.

Muscarinic cholinergic pathways have been implicated in the visual control of ocular growth. However, the source(s) of acetylcholine and the tissue(s) which regulate ocular growth via muscarinic acetylcholine receptors (mAChRs) remain unknown. We sought to determine whether retinal sources of acetylcholine and mAChRs contribute to visually guided ocular growth in the chick. Cholinergic amacrine cells were ablated by intraocular injections of either ethylcholine mustard aziridinium ion (ECMA; a selective cholinotoxin) or quisqualic acid (QA; an excitotoxin that destroys many amacrine cells, including those that release acetylcholine). Disruption of cholinergic pathways was assessed immunocytochemically with antibodies to the acetylcholine-synthesizing enzyme choline acetyltransferase (ChAT) and three different isoforms of mAChR, and by biochemical assay for ChAT activity. ECMA (25 nmol) destroyed two of the four subtypes of cholinergic amacrine cells and attenuated retinal ChAT activity, but left retinal mAChR-immunoreactivity intact. QA (200 nmol) destroyed the majority of all four subtypes of cholinergic amacrine cells, and ablated most mAChR-immunoreactivity and ChAT activity in the retina. ECMA and QA had no apparent effect on mAChRs or cholinergic fibres in the choroid, only marginally reduced choroidal ChAT activity, and had little effect on ChAT activity in the anterior segment. Toxin-treated eyes remained emmetropic and responded to form-deprivation by growing excessively and becoming myopic. Furthermore, daily intravitreal injection of 40 microg atropine for 6 days into form-deprived toxin-treated eyes completely prevented ocular elongation and myopia. We conclude that neither cholinergic amacrine cells nor mAChRs in the retina are required for visual regulation of ocular growth, and that atropine may exert its growth-suppressing influence by acting upon extraretinal mAChRs, possibly in the choroid, retinal pigmented epithelium, or sclera.

Animals↗
PubMed1998

Enkephalin, neurotensin and somatostatin increase cAMP levels in the chicken retina.

PURPOSE: Enkephalin, neurotensin and somatostatin are released at high rates in the dark and at low rates in the light n the chicken retina. The present study examines the effects of these peptide transmitters on retinal cAMP METHODS: Chicken retinas were incubated in vitro with various drugs for 10min. Cyclic AMP was extracted with acidified ethanol and retinal levels of cAMP were measured using a radioassay kit. RESULTS/CONCLUSIONS: These peptides increased cAMP levels in the chicken retina in vitro, which is surprising as their receptors are generally thought to be negatively coupled to adenylate cyclase. The paradoxical increase in retinal cAMP may be due to unique types of peptide receptors that are positively coupled to adenylate cyclase. A more plausible explanation is that these peptides act indirectly and change the rate of release of another transmitter, whose receptor is coupled to adenylate cyclase.

Animals↗
PubMed1997

Development of the enkephalin-, neurotensin- and somatostatin-like (ENSLI) amacrine cells in the chicken retina.

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.

Animals↗
PubMed1997

Localization of D1 dopamine receptors in the chicken retina.

PURPOSE: The localization of dopamine D1 receptors (DIR) in the chicken retina was examined using an anti-human DIR monoclonal antibody and PAP techniques. RESULTS: A clear band of staining was seen in the outer plexiform layer, as well as cellular staining in the outer-most part of the inner nuclear layer, probably in a subset of horizontal cells. Many different amacrine cell bodies were labelled in the inner one-third of the inner nuclear layer. There was also extensive staining in the inner plexiform layer, which showed some striation. Occasional labelled ganglion cells were also detected. CONCLUSION: Localization of D1-dopamine receptors has been shown in the chicken retina.

Animals↗
PubMed1997

A light-driven rhythm in neurotensin-like immunoreactivity in the chicken retina.

PURPOSE: To determine if the pattern of release of neurotensin from the enkephalin-, neurotensin- and somatostatin-like immunoreactive amacrine cells in response to light and dark is the same as that of the enkephalins and somatostatin. METHODS/RESULTS: Both the enkephalins and somatostatin are released at high rates in the dark and at lower rates in the light, and these rate changes are reflected in increasing intracellular levels of the peptides in vivo in the light and decreasing levels in the dark. The levels of neurotensin-like immunoreactivity show a similar diurnal light-driven and non-circadian rhythm in vivo. CONCLUSION: This implies that the actual release rates of neurotensin follow the same patterns as those demonstrated in vitro for the enkephalins and somatostatin.

Adaptation, Ocular↗
PubMed1997

A fundamental step-transition in retinal function at low light intensities.

There appears to be a fundamental step-transition in retinal function at low light intensities, close to the scotopic-mesopic transition. This step-transition is observed for elements of the retinal dark-light switch, which has been described in the chicken retina. Over the same range of light intensities, there is a step-transition in photoreceptor retinomotor movements and in the coupling of horizontal and All amacrine cells, which suggests a switch in retinal circuitry from rod-processing to cone-processing regimes. A similar step-transition in pineal function suggests that the retinal step-transition signals to the central circadian systems. Finally, this step-transition may also inhibit eye growth, and thus be responsible for the reported diurnal rhythm in eye growth. Disturbances to this step-transition may be the initial cause of disordered eye growth in the form-deprivation myopia paradigm.

Adaptation, Ocular↗
PubMed1997

Dopaminergic behaviour in chicken retina and the effect of form deprivation.

PURPOSE: Dopamine (DA) is considered to be a neurotransmitter involved in light-adaptive responses in the retina and has been implicated in the control of the eye growth induced by form deprivation. Vitreal DOPAC was shown to be a good indicator of retinal dopaminergic activity. METHODS/RESULTS: Dopaminergic activity was highest during the light; with vitreal DOPAC levels rising within 3 h of light exposure. Form deprivation attenuated dopaminergic activity, as the rise in vitreal DOPAC levels on light exposure was reduced in form-deprived eyes, compared with control eyes. CONCLUSION: The lack of sustained activation of DA release may explain the role of DA in the control of eye-growth.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1995

Neural barriers affect the action of nitric oxide synthase inhibitors in the intact chicken retina.

Nitric oxide synthase (NOS) activity, as measured by the formation of L-[3H]citrulline from L-[3H]arginine, was blocked by micromolar concentrations of NOS inhibitors in retinal homogenates, but concentrations approximately 20-3000 times higher were needed in intact retina. The higher concentrations could be related to transport of the NOS inhibitors into neuronal cells and/or their sequestration within glial cells. NG-monomethyl-L-arginine and N-iminoethyl-L-ornithine significantly inhibited L-[3H]arginine uptake, whereas N omega-nitro-L-arginine methyl ester and N omega-nitro-L-arginine had little or no effect on L-[3H]arginine uptake. The high concentrations of the inhibitors needed to inhibit nitric oxide production in intact tissue and their different interactions with arginine uptake systems may explain some of the conflicting results on the activity of NOS inhibitors on a range of physiological parameters in vivo.

Animals↗
PubMed1995

Parallel suppression of retinal and pineal melatonin synthesis by retinally mediated light.

We have recently shown that light, over a narrow range of low intensities suppresses the activity of the enkephalin-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.

Animals↗
PubMed1995

Pineal activity is under the control of retinal D1-dopaminergic pathways.

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.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗