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Biomedical subjects

I G Morgan

Publications and source records attributed to I G Morgan.

At least 55 records · Page 3Linked to original sources
PubMed1987

Cholinergic amacrine cells in the rabbit retina synapse onto other cholinergic amacrine cells.

Cholinergic amacrine cells in the rabbit retina have been detected by localizing choline acetyltransferase-like immunoreactivity. The characteristic array of normally placed and displaced amacrine cells was detected, as were two major synaptic plexuses in the inner plexiform layer. At the ultrastructural level, the most striking feature was the existence of contacts between the processes of cholinergic amacrine cells. Since this feature has also been detected in chicken and goldfish retina, it needs to be taken into account in any model which seeks to explain how the cholinergic amacrine cells are involved in generating directional selectivity at the ganglion cell level.

Animals↗
PubMed1987

Cholinergic amacrine cells of the chicken retina: a light and electron microscope immunocytochemical study.

Cholinergic amacrine cells of the chicken retina were detected by immunohistochemistry using an antiserum against affinity-purified chicken choline acetyltransferase. Three populations of cells were detected: type I cholinergic amacrine cells had cell bodies on the border of the inner nuclear and inner plexiform layers and formed a prominent laminar band in sublamina 2 of the inner plexiform layer, while type II cholinergic amacrine cells had cell bodies in the ganglion cell layer, and formed a prominent laminar band in sublamina 4 of the inner plexiform layer. Type III cholinergic amacrine cell bodies were located towards the middle of the inner nuclear layer, and their processes were more diffusely distributed in sublaminas 1 and 3-5 of the inner plexiform layer. Type I and type II cells were present at densities of over 7000 cells/mm2 in central areas declining to less than 2000 cells/mm2 in the temporal retinal periphery. The cells were organized locally in a non-random mosaic, with regularity indices ranging from 3 peripherally to over 5 centrally. Neither at the light nor electron microscopic levels was a lattice of cholinergic dendrites of the kind reported by Tauchi and Masland [J. Neurosci. 5, 2494-2501 (1985)] detectable. Within the two prominent dendritic plexuses, a major feature of the synaptic interactions of the type I and type II cholinergic cells was extensive synaptic interaction between cholinergic processes. Apart from this, there was little, if any, input to cholinergic processes from non-cholinergic amacrine cells, but there was input from bipolar cells. Output from the cholinergic amacrine cell processes was directed towards non-cholinergic amacrine cells as well as other cholinergic amacrine cells, and ganglion cells.

Animals↗
PubMed1987

The toxic effects of ethylcholine mustard aziridinium ion on cholinergic cells in the chicken retina.

The chicken retina has been used to examine the toxicity of a highly reactive chemical analog of choline, ethylcholine mustard aziridinium ion (ECMA). Following a single intravitreal injection, retinas were analyzed biochemically for CAT and AChE activities, and GABA, glycine, and dopamine levels. Retinas were also examined using histofluorescence for dopamine histochemistry, for AChE, and immunohistochemistry with antibodies to CAT, tyrosine hydroxylase, GABA, 5-HT, Leu-enkephalin, and somatostatin. A dose of 50 nmol ECMA caused a prolonged 70% depletion of CAT activity and a 40% depletion of AChE activity. The other biochemical parameters were unchanged. This result corresponds to the morphological finding that 2 populations of cholinergic cells were destroyed and that the AChE activity associated with their terminal arbors was lost. A third population of cholinergic cells, located towards the middle of the inner nuclear layer, was resistant to the toxic effects of ECMA. The other cell types, except for somatostatin-immunoreactive cells and photoreceptors, which showed transient effects, were unaffected. ECMA therefore appears to be a highly specific toxin for cholinergic cells in the retina.

Acetylcholine↗
PubMed1986

Somatostatin-immunoreactive amacrine cells of chicken retina: retinal mosaic, ultrastructural features, and light-driven variations in peptide metabolism.

Somatostatin-like immunoreactive amacrine cells of the chicken retina have been characterized by immunohistochemistry at the light and electron microscope levels. The cell bodies were set back from the junction of the inner nuclear and inner plexiform layers, and prominent fibre plexuses were found in sublaminas 1 and 3-5 of the inner plexiform layer. The cells were distributed across the retinal surface with a centroperipheral gradient of cell density. Locally, the cells were organized in a non-random mosaic. Ultrastructurally, immunohistochemical reaction product was found throughout the cytoplasm of the cell bodies, particularly associated with membranous structures, including the cytoplasmic surfaces of the Golgi apparatus, and within large dense-core vesicles. In dendritic varicosities in the inner plexiform layer, reaction product was associated with the external surfaces of small, clear synaptic vesicles. The synaptic relationships of the somatostatin-immunoreactive terminals in sublamina 1 were distinct from those in sublaminas 3-5. Those in sublamina 1 received input predominantly, possibly exclusively, from bipolar cells. Feedback synapses onto bipolar terminals or to the other amacrine cell process at a synaptic dyad were observed. In sublaminas 3-5, input came predominantly, possibly exclusively, from other, non-immunoreactive amacrine cells, and output was primarily onto other amacrine cells. No synaptic contacts with ganglion cells or with other somatostatin-immunoreactive amacrine cells were identified. Changes in levels of somatostatin-like immunoreactivity in retinas of chicks kept on 12:12 light:dark cycles were detected by radioimmunoassay, and by light and electron microscopic immunohistochemistry. Levels of retinal somatostatin-like immunoreactivity increased in the light and decreased in the dark. The changes appear to be light-driven rather than circadian, since with prolonged exposure to light or dark, the levels of somatostatin-like immunoreactivity continued to increase or decrease until plateaus were reached. The light-driven change in levels of somatostatin-like immunoreactivity may be related to the predominance of bipolar input to the immunoreactive processes in sublamina 1 of the inner plexiform layer. The reduction in peptide levels in the dark may indicate greater release of somatostatin-like immunoreactivity from the amacrine cells in the dark, resulting in an inability of peptide synthesis to keep pace with breakdown. In the light, release of somatostatin-like immunoreactivity may be lower, leading to a net synthesis of peptide.

Animals↗
PubMed1985

Cholinergic and acetylcholinesterase-containing neurons of the chicken retina.

In the chicken retina, choline acetyltransferase-like immunoreactivity (ChAT-LI) defines three populations of cholinergic amacrine cells and two terminal bands in the inner plexiform layer (IPL). Acetylcholinesterase (AChE) histochemistry defines two prominent bands within the IPL which corresponded to those containing ChAT. Other AChE-positive bands in the IPL are not associated with cholinergic transmission sites. Cholinergic cell bodies contain AChE, but the most intensely AChE-positive cells do not appear to be cholinergic. AChE histochemistry may be used to define the major cholinergic synaptic sites in the IPL, and may be a useful marker of IPL lamination.

Acetylcholinesterase↗
PubMed1984

A physiologically active kainic acid-preferring receptor in chicken retina.

Neurotoxicity induced by intravitreal injections of kainic acid in the chicken retina was effectively antagonized by piperidine 2,3-dicarboxylic acid and to a lesser extent D-gamma-glutamylglycine. 2-Amino-5-phosphonovaleric acid and glutamic acid diethyl ester were much less effective antagonists. These effects probably result from interactions with a kainic acid-preferring receptor localized on the OFF-centre bipolar cells. Piperidine 2,3-dicarboxylic acid and D-gamma-glutamylglycine also blocked selectively the OFF-responses of ganglion cells while glutamic acid diethyl ester was without effect. 2-Amino-5-phosphonovaleric acid rapidly blocked ON and, much more slowly, OFF-responses. These results are consistent with a role for kainic acid-preferring receptors located on the OFF-centre bipolar cells in chicken retina in physiological transmission between photoreceptors and the OFF-centre bipolar cells.

2-Amino-5-phosphonovalerate↗
PubMed1984

The concentration of enkephalin-like material in the chick retina is light dependent.

The enkephalin-like immunoreactivity in the retina of chicks has been studied using immunohistochemical and radioimmunoassay techniques. The histochemical experiments showed that the immunoreactivity was confined to a subpopulation of amacrine cells in the inner nuclear layer which projected processes into sublaminae 1 and 3-5 of the inner plexiform layer. The distribution of the immunoreactivity was markedly influenced by the ambient lighting conditions: it was reduced in the dark and restored by a period in the light. The reactivity was lost from both cell soma in the inner nuclear layer and from the processes. Radioimmunoassays showed that the quantity of enkephalin-like material was reduced by more than 60% after 12 h in the dark. Attempts to entrain a rhythm by keeping chicks on 12/12 h light/dark cycles for up to 4 days were largely unsuccessful. A rhythm may have been partially entrainable, but the major factor involved was light. These results highlight the lability of the neuropeptide in the retina and the need for controlled lighting conditions in studies of this kind. They also indicate that this system may be a fruitful model to explore two important issues: (i) it could allow studies of neuropeptide metabolism in a physiologically intact system; (ii) the role of particular amacrine cells in visual processing could be determined by depleting them of their neurotransmitter/neuromodulator.

Animals↗
PubMed1983

Intravitreal kainic acid permanently eliminates off-pathways from chicken retina.

Kainic acid rapidly suppresses both ON- and OFF-visually evoked responses in the tectum after injection into the vitreous of chicken eyes. One week after injection the OFF-responses were still suppressed, while ON-responses were detected of similar magnitude but of simplified form to those of control eyes. It is suggested that kainic acid selectively destroys OFF- rather than ON-bipolar cells, while the simplification of the ON-responses is due to the destruction of amacrine cells.

Animals↗
PubMed1983

Dose-dependent effects of intravitreal kainic acid on specific cell types in chicken retina.

In chicken retina, approximately two thirds of the bipolar cells and most amacrine cells are destroyed after intravitreal injection of from 20 to 60 nmoles of kainic acid. These cells, plus horizontal cells are destroyed after intravitreal injections of 120 nmoles of kainic acid. One third of the bipolar cells, Müller glial cells, photoreceptors and ganglion cells seem to be much more resistant. The resistance of the ganglion cells to intravitreal kainic acid is unusual and is not found in mammalian retinas. Dopaminergic amacrine cells may also be resistant to kainic acid. It is suggested that kainic acid interacts directly with bipolar cells and horizontal cells, depolarising the bipolar cells and horizontal cells and thereby killing them, while hyperpolarizing the ON-bipolar cells. The possibility that amacrine cell death may be an indirect result of kainic acid's effects on bipolar cells is discussed. Whatever the precise way in which kainic acid causes cell death, the technique of causing lesions is useful for defining the localization of retinal and particularly amacrine cell transmitter systems.

Animals↗
PubMed1982

Folic acid derivatives do not reproduce the neurotoxic effects of kainic acid on chicken retina.

Methyltetrahydrofolic acid, formyltetrahydrofolic acid, folic acid and dihydrofolic acid were injected intravitreally into the eyes of chickens. No short-term or long-term signs of neurotoxicity were observed, even when doses 100-200 times those at which kainic acid produces clear neurotoxic effects were injected. The folic acid derivatives neither inhibited nor potentiated the neurotoxic effects. Thus no support is given to the suggestion that folic acid and its derivatives may act as kainic acid agonists or antagonists, even though the receptors involved in kainic acid-induced neurotoxicity appear to be of the kainic acid rather than quisqualic acid or N-methyl-D-aspartic acid type.

Animals↗
PubMed1982

Ganglion cells of chicken retina possess nicotinic rather than muscarinic acetylcholine receptors.

Chicken retinas were exposed to intravitreal kainic acid to destroy amacrine and bipolar cells at low concentrations, and horizontal cells at high concentrations in addition. Ganglion cell were destroyed by intravitreal injections of colchicine. Low doses of kainic acid reduced the number of binding sites for both [3H]quinuclidinyl benzilate (muscarinic acetylcholine receptors) and N-[propionyl-3H]alpha-bungarotoxin (nicotinic acetylcholine receptors), with little additional loss at higher doses. In contrast, colchicine reduced the number of binding sites for N-[propionyl-3H]alpha-bungarotoxin, but had little or no effect on the number of binding sites for [3H]quinuclidinyl benzilate. These results are consistent with the idea that, in chicken retina, cholinergic amacrine cells make contact with ganglion cell dendrites at sites which possess mainly nicotinic acetylcholine receptors, while both types of receptor are involved in interactions between amacrine cells and perhaps bipolar cells.

Animals↗
PubMed1981

Discrete distributions of putative cholinergic and somatostatinergic amacrine cell dendrites in chicken retina.

The distributions of putative cholinergic and somatostatinergic amacrine cells of the chicken retina were compared. Acetylcholinesterase-positive amacrine cell bodies were concentrated at the border between the inner nuclear and plexiform layers. Similar amacrine cell bodies were detected in a displaced position in the ganglion cell layer. Both populations had dendrites joining the 4 bands of acetylcholinesterase activity in the inner plexiform layer. The cell bodies of somatostatin-immunoreactive amacrine cells were distinct from the intensely acetylcholinesterase-positive cell bodies. The immunoreactive terminal bands did not overlap the acetylcholinesterase-positive bands, except in the inner parts of the inner plexiform layer.

Acetylcholinesterase↗
PubMed1981

Intraocular colchicine selectively destroys immature ganglion cells in chicken retina.

Low doses of colchicine (greater than 0.5 microgram) injected into the eyes of young chickens irreversibly inhibit axonal transport of material labelled with [3H]fucose. This is due to almost total destruction of the retinal ganglion cells, while other retinal cell types, including the displaced amacrine cells found in the same retinal layer, survive the treatment. The neurotoxic effect of colchicine on chick retinal ganglion cells decreases after hatching, and it is suggested that the decrease in sensitivity may be related to myelination of the retinal ganglion cell axons.

Animals↗
PubMed1981

Phenobarbitone binding sites in rat brain synaptosomal membranes.

Phenobarbitone binds to rat brain synaptosomeal membranes at a single class of sites of relatively low affinity (Kd 100 microM) and high density (800 pmol/mg protein). Phenobarbitone can be displaced from these binding sites by a range of substituted barbiturates. For those barbiturates which possess anaesthetic, anticonvulsant or depressant properties, there is an excellent correlation between ability to displace phenobarbitone and ability to enhance the binding of the inhibitory neurotransmitter GABA. On the other hand, convulsant barbiturates are relatively more effective in enhancing GABA binding than would be expected from their ability to displace phenobarbitone. These phenobarbitone binding sites may be involved in the potentiation of GABA-mediated synaptic inhibition by barbiturates, an effect likely to contribute to the pharmacological actions of these substances. These barbiturate sites are distinct from GABA recognition sites and from GABA-activated ionophores, since GABA, bicuculline methochloride, diazepam and picrotoxinin did not influence phenobarbitone binding. Furthermore, extraction of the synaptosomal membranes with Triton X-100 abolishes phenobarbitone binding to the membranes while enhancing GABA binding.

Animals↗
PubMed1981

Kainic acid affects both plexiform layers of chicken retina.

Intraocular injections of kainic acid produce marked lesions of the chicken retina. Low doses (6-20 nmol/retina) appear to cause lesions of the inner part of the retina, primarily involving amacrine cells. At around 60 nmol/retina there is a qualitative change in the nature of the lesion, as the horizontal and bipolar cells begin to degenerate. Higher doses of kainic acid lead to disappearance of both the outer and inner plexiform layers. At all doses used, the photoreceptors and ganglion cells survive exposure to kainic acid. Low doses of kainic acid reduce the content of the amacrine and horizontal cell markers acetylcholine and gamma-amino-butyric acid, but have little effect upon taurine. These results are consistent with a role for glutamic and/or aspartic acid as bipolar cell and photoreceptor transmitters.

Animals↗
PubMed1981

The effects of colchicine and vinblastine on memory in chicks.

Colchicine, injected bilaterally into the forebrain of day-old chicks at times before and after one-trial avoidance learning, produced transient amnesia for one to three hours after learning, that could not be accounted for as a perceptual or attentional defect. The amnesia was dose dependent and was produced only when injections occurred within a limited period before and after learning. No amnesia occurred when injections were given 120 min before or 60 min later than the learning trial, nor at times prior to the retrieval test. During the amnesic period, new learning could occur and be retrieved 15 min later. The amnesia could be overcome by retention-testing or by a new, related, learning experience before or up to 30 min after onset of amnesia. Control birds injected with saline or lumicolchicine, a biologically inactive derivative of colchicine, showed normal retention. Vinblastine sulphate, which also interrupts microtubular networks and hence axonal flow, had no amnesic properties. Colchicine injections had no effect on the levels of acetylcholinesterase, choline acetyltransferase, glutamic acid decarboxylase, and muscarinic acetylcholine receptors in the whole forebrain or in forebrain synaptosomes during the amnesic period. Nor did colchicine injections affect amino acid uptake and protein or glycoprotein synthesis before or during the amnesic period, although there was 10-20% inhibition of protein synthesis 5 h after injection. Thus over the amnesic period, there was no evidence of gross perturbation of brain function. Electron microscopy showed microtubules intact within 1 mm of the injection site 2.5 after injection. Oedema was found at this time in chicks injected with a high dose (100 micrograms) shown to disturb behaviour grossly, but not with a low dose (5 micrograms) which caused amnesia. Transient amnesia for one-trial avoidance learning is most probably caused by secondary effects of colchicine on nerve cell function. We suggest that the amnesic episode represents destruction of one of the stages of a multiple independent parallel process of memory consolidation.

Animals↗