2012 Group Project 1 - Revision history

Z8600021: Protected "2012 Group Project 1" ([edit=sysop] (indefinite) [move=sysop] (indefinite))

2012-10-05T08:29:27Z

Protected "2012 Group Project 1" ([edit=sysop] (indefinite) [move=sysop] (indefinite))

← Older revision	Revision as of 18:29, 5 October 2012
(No difference)

Z3370664: /* Image Gallery */

2012-10-05T05:26:53Z

Image Gallery

← Older revision		Revision as of 15:26, 5 October 2012
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	Image:Galen-eye1.jpg\|The eye according to Galen. Credits: Magnus, 1901.		Image:Galen-eye1.jpg\|The eye according to Galen. Credits: Magnus, 1901.

	Image:Kollmann691.jpg\|The blue part at the bottom is the endoderm. The pink middle layer is the mesoderm. The top yellow layer is the ectoderm. The fold labelled as 'augenfeld' is the place where the optic vesicle will form. Credits: ~~Kohlmann~~, J. (1907)		Image:Kollmann691.jpg\|The blue part at the bottom is the endoderm. The pink middle layer is the mesoderm. The top yellow layer is the ectoderm. The fold labelled as 'augenfeld' is the place where the optic vesicle will form. Credits: Kollmann, J. (1907)

	Image:Kollmann692.jpg\|The eye area (augenfeld) is a bowl shaped bulge still located on the side walls. Credits: ~~Kohlmann~~, J. (1907)		Image:Kollmann692.jpg\|The eye area (augenfeld) is a bowl shaped bulge still located on the side walls. Credits: Kollmann, J. (1907)


	Image:Kollmann693.jpg\| The neural tube is shown after removal of all of the ectoderm and ventral organs, such as heart, gut tube, etc. The primary optic vesicle forms a slightly flattened hollow protrusion on the forebrain. Credits: ~~Kohlmann~~, J. (1907)		Image:Kollmann693.jpg\| The neural tube is shown after removal of all of the ectoderm and ventral organs, such as heart, gut tube, etc. The primary optic vesicle forms a slightly flattened hollow protrusion on the forebrain. Credits: Kollmann, J. (1907)


	Image:Kollmann694.jpg\|The lateral surface of the primary optic vesicle is slightly depressed, showing the first sign of the emergence of the secondary optic vesicle. Credits: ~~Kohlmann~~, J. (1907)		Image:Kollmann694.jpg\|The lateral surface of the primary optic vesicle is slightly depressed, showing the first sign of the emergence of the secondary optic vesicle. Credits: Kollmann, J. (1907)

	Image:Kollmann695.jpg\|The bulging lateral wall of the primary optic vesicle is covered by a fairly well demarcated lens plate, a direct continuation of the ectoderm. Between the optic vesicle and the lens pit are some flattened spindle-shaped cells. In the adjoining mesoderm are cross-sections of capillaries. Credits: ~~Kohlmann~~, J. (1907)		Image:Kollmann695.jpg\|The bulging lateral wall of the primary optic vesicle is covered by a fairly well demarcated lens plate, a direct continuation of the ectoderm. Between the optic vesicle and the lens pit are some flattened spindle-shaped cells. In the adjoining mesoderm are cross-sections of capillaries. Credits: Kollmann, J. (1907)

	Image:Kollmann697.jpg\|The lens still hangs together with the ectoderm. The primary eye vesicle is indented with respect to the lens. Between the lens and the lateral plate of the optic vesicle is a narrow space, which allows area to further develop later. Credits: ~~Kohlmann~~, J. (1907)		Image:Kollmann697.jpg\|The lens still hangs together with the ectoderm. The primary eye vesicle is indented with respect to the lens. Between the lens and the lateral plate of the optic vesicle is a narrow space, which allows area to further develop later. Credits: Kollmann, J. (1907)

	Image:Kollmann698.jpg\|4th Week of development. The internal organisation shows the secondary optic vesicle. A: The rear wall of lens is noticeable and is enveloped by mesoderm. B: The edges of the lens pit is already grown and the lens vesicles are formed, which is still related to the remaining ectoderm. Credits: ~~Kohlmann~~, J. (1907)		Image:Kollmann698.jpg\|4th Week of development. The internal organisation shows the secondary optic vesicle. A: The rear wall of lens is noticeable and is enveloped by mesoderm. B: The edges of the lens pit is already grown and the lens vesicles are formed, which is still related to the remaining ectoderm. Credits: Kollmann, J. (1907)

	Image:Kollmann699.jpg\|The lens has now cut off from the ectoderm, but is still very superficial. Between it and the lateral lamina of the optic cup, there is a considerable space. The eye stalk has become longer and is enclosed together with the optic cup and lens of the mesoderm. The cornea, sclera and choroid make gradual development. Credits: ~~Kohlmann~~, J. (1907)		Image:Kollmann699.jpg\|The lens has now cut off from the ectoderm, but is still very superficial. Between it and the lateral lamina of the optic cup, there is a considerable space. The eye stalk has become longer and is enclosed together with the optic cup and lens of the mesoderm. The cornea, sclera and choroid make gradual development. Credits: Kollmann, J. (1907)

	Image:5months-gestation-retina.jpg\|The layers of the retina in the fifth month of development. Credits: Webvision [http://www.ncbi.nlm.nih.gov/pubmed/21413389 PMID:21413389] [PubMed]		Image:5months-gestation-retina.jpg\|The layers of the retina in the fifth month of development. Credits: Webvision [http://www.ncbi.nlm.nih.gov/pubmed/21413389 PMID:21413389] [PubMed]

Z3370664: /* Brief Timeline of Historical Developments on the Eye and its Embryology */

2012-10-05T05:24:31Z

Brief Timeline of Historical Developments on the Eye and its Embryology

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	\| John Clement Heisler published his book ‘A Text-book of embryology’. It contains a chapter detailing the embryonic development of the eye, according to the knowledge current at that time. The book’s copyright has expired, so it can be viewed free online: [http://archive.org/details/atextbookembryo01heisgoog]		\| John Clement Heisler published his book ‘A Text-book of embryology’. It contains a chapter detailing the embryonic development of the eye, according to the knowledge current at that time. The book’s copyright has expired, so it can be viewed free online: [http://archive.org/details/atextbookembryo01heisgoog]

	Julius ~~Kollman~~ also published his book 'Atlas of the Development of Man'. It contained very detailed description and illustrations showing the embryonic development of the human according to the knowledge current at that time. His illustrations were reused by many others after his time and built upon for further refined understanding of the embryology of the human.		Julius Kollmann also published his book 'Atlas of the Development of Man'. It contained very detailed description and illustrations showing the embryonic development of the human according to the knowledge current at that time. His illustrations were reused by many others after his time and built upon for further refined understanding of the embryology of the human.

	Here are examples of Julius Kollman's excellent illustrations showing eye development in various stages:		Here are examples of Julius Kollman's excellent illustrations showing eye development in various stages:

Z3370664: /* Image Gallery */

2012-10-05T05:18:21Z

Image Gallery

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 Image:Eye_diagram_bandw.jpg‎ | Basic structure of the human eye.
 Image:Eyediagramcolour1.JPG | Basic anatomy of the eye.
 Image:Stage14 sem2b-limb.jpg | A Stage 14 embryo showing the location of an otic placode.
 Image:Stage 13 image 060.jpg | A cross section showing the organisation of the developing brain, the optic vesicle and the lens (optic) placode.

Z3370664: /* The impact of visible light on the immature retina */

2012-10-05T04:33:14Z

The impact of visible light on the immature retina

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	Article Source: <pubmed>22405869</pubmed>		Article Source: <pubmed>22405869</pubmed>

	The authors mentioned in this article <ref name="PMID22405869"><pubmed>22405869</pubmed></ref> that they were interested in investigating the effect of light on postnatal eye development in mice, because mice are born with fused eyelids, which separate 12 days after birth. Before the eyelids separate, the retina develops in mice with very little radiation from light. It is believed that the darkness plays a role in the development of the retina in mice, which is why their eyelids are fused for 12 days after birth. Therefore the authors were interested to see what effect light would have on postnatal retinal development of mice, with special interest in retinal ganglion cells (RGC). In their experiment, they surgically opened the eyelids on the right eyes of some of the mice to expose them to visible light 12 hours per day, while they left some other mice in the dark after surgical separation of their eyelids. They also kept the left eyes of the mice naturally fused as controls in the experiment. Their results showed that early light exposure in mice causes a decrease in retinal ganglion cells because it affects cellular apoptosis in the retina. The authors also observed that early exposure to light in mice causes lumican mRna transcription to resume and to quickly increase. (Lumican normally stays silent in retina after birth).		The authors mentioned in this article <ref name="PMID22405869"><pubmed>22405869</pubmed></ref> that they were interested in investigating the effect of light on postnatal eye development in mice, because mice are born with fused eyelids, which separate 12 days after birth. Before the eyelids separate, the retina develops in mice with very little radiation from light. It is believed that the darkness plays a role in the development of the retina in mice, which is why their eyelids are fused for 12 days after birth. Therefore the authors were interested to see what effect light would have on postnatal retinal development of mice, with special interest in retinal ganglion cells (RGC). In their experiment, they surgically opened the eyelids on the right eyes of some of the mice to expose them to visible light 12 hours per day, while they left some other mice in the dark after surgical separation of their eyelids. They also kept the left eyes of the mice naturally fused as controls in the experiment. Their results showed that early light exposure in mice causes a decrease in retinal ganglion cells because it affects cellular apoptosis in the retina. The authors also observed that early exposure to light in mice causes lumican mRna transcription to resume and to quickly increase. (Lumican normally stays silent in retina after birth). <ref name="PMID22405869"/>


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	===GABA Maintains the Proliferation of Progenitors and Non-Pigmented Ciliary Epithelium===		===GABA Maintains the Proliferation of Progenitors and Non-Pigmented Ciliary Epithelium===

Z3370664: /* Current Research */

2012-10-05T04:30:28Z

Current Research

← Older revision		Revision as of 14:30, 5 October 2012
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	===The impact of visible light on the immature retina===		===The impact of visible light on the immature retina===

	<pubmed>22405869</pubmed>		Article Source: <pubmed>22405869</pubmed>

	The authors mentioned in this article <ref name="PMID22405869"><pubmed>22405869</pubmed></ref> that they were interested in investigating the effect of light on postnatal eye development in mice, because mice are born with fused eyelids, which separate 12 days after birth. Before the eyelids separate, the retina develops in mice with very little radiation from light. It is believed that the darkness plays a role in the development of the retina in mice, which is why their eyelids are fused for 12 days after birth. Therefore the authors were interested to see what effect light would have on postnatal retinal development of mice, with special interest in retinal ganglion cells (RGC). In their experiment, they surgically opened the eyelids on the right eyes of some of the mice to expose them to visible light 12 hours per day, while they left some other mice in the dark after surgical separation of their eyelids. They also kept the left eyes of the mice naturally fused as controls in the experiment. Their results showed that early light exposure in mice causes a decrease in retinal ganglion cells because it affects cellular apoptosis in the retina. The authors also observed that early exposure to light in mice causes lumican mRna transcription to resume and to quickly increase. (Lumican normally stays silent in retina after birth).		The authors mentioned in this article <ref name="PMID22405869"><pubmed>22405869</pubmed></ref> that they were interested in investigating the effect of light on postnatal eye development in mice, because mice are born with fused eyelids, which separate 12 days after birth. Before the eyelids separate, the retina develops in mice with very little radiation from light. It is believed that the darkness plays a role in the development of the retina in mice, which is why their eyelids are fused for 12 days after birth. Therefore the authors were interested to see what effect light would have on postnatal retinal development of mice, with special interest in retinal ganglion cells (RGC). In their experiment, they surgically opened the eyelids on the right eyes of some of the mice to expose them to visible light 12 hours per day, while they left some other mice in the dark after surgical separation of their eyelids. They also kept the left eyes of the mice naturally fused as controls in the experiment. Their results showed that early light exposure in mice causes a decrease in retinal ganglion cells because it affects cellular apoptosis in the retina. The authors also observed that early exposure to light in mice causes lumican mRna transcription to resume and to quickly increase. (Lumican normally stays silent in retina after birth).
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	===GABA Maintains the Proliferation of Progenitors and Non-Pigmented Ciliary Epithelium===		===GABA Maintains the Proliferation of Progenitors and Non-Pigmented Ciliary Epithelium===

	<pubmed>22590629</pubmed>		Article Source: <pubmed>22590629</pubmed>

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	===MIP/Aquaporin 0 Represents a Direct Transcriptional Target of PITX3 in the Developing Lens===		==="MIP/Aquaporin 0 Represents a Direct Transcriptional Target of PITX3 in the Developing Lens"===

	<pubmed>21698120</pubmed>		Article Source: <pubmed>21698120</pubmed>


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	===Activation of c-Jun N-terminal kinase (JNK) during mitosis in retinal progenitor cells.===		==="Activation of c-Jun N-terminal kinase (JNK) during mitosis in retinal progenitor cells."===



	<pubmed>22496813</pubmed>		Article Source: <pubmed>22496813</pubmed>


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	\| In the past, most studies about c-Jun N-terminal kinase (JNK) in the retina have been in relation to neurodegeneration~~. <ref name="PMID22496813"><pubmed>22496813</pubmed></ref> Therefore~~ the authors in this article were interested in investigating the function of c-Jun N-terminal kinase in the retinal progenitor cells in neonatal rats. <ref name="PMID22496813"/> In the experiment, they took retinal tissue from newborn rats and fixed them, and subsequently examined them using confocal microscopy and fluorescence to discover c-Jun N-terminal kinase ‘phosphorylation by immunohistochemistry’. <ref name="PMID22496813"/> Mitotic cells in the retina were identified during the experiment. The results of their experiment revealed that c-Jun N-terminal kinase is phosphorylated in the developing retina of neonatal rats during the mitosis of progenitor cells. This shows that c-Jun N-terminal kinase can control the proliferation of progenitor cells in the developing retina. Their experiment also revealed that inhibiting c-Jun N-terminal kinase causes disruptions to the mitotic cell cycle by reducing the cell numbers in anaphase. However, inhibiting c-Jun N-terminal kinase did not change the cell numbers in metaphase or prophase. <ref name="PMID22496813"/>		\| In the past, most studies about c-Jun N-terminal kinase (JNK) in the retina have been in relation to neurodegeneration; therefore the authors in this article were interested in investigating the function of c-Jun N-terminal kinase in the retinal progenitor cells in neonatal rats. <ref name="PMID22496813"><pubmed>22496813</pubmed></ref> In the experiment, they took retinal tissue from newborn rats and fixed them, and subsequently examined them using confocal microscopy and fluorescence to discover c-Jun N-terminal kinase ‘phosphorylation by immunohistochemistry’. <ref name="PMID22496813"/> Mitotic cells in the retina were identified during the experiment. The results of their experiment revealed that c-Jun N-terminal kinase is phosphorylated in the developing retina of neonatal rats during the mitosis of progenitor cells. This shows that c-Jun N-terminal kinase can control the proliferation of progenitor cells in the developing retina. Their experiment also revealed that inhibiting c-Jun N-terminal kinase causes disruptions to the mitotic cell cycle by reducing the cell numbers in anaphase. However, inhibiting c-Jun N-terminal kinase did not change the cell numbers in metaphase or prophase. <ref name="PMID22496813"/>


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	===LRP5 is required for vascular development in deeper layers of the retina===		==="LRP5 is required for vascular development in deeper layers of the retina"===


	<pubmed>20652025</pubmed>		Article Source: <pubmed>20652025</pubmed>

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	<pubmed>20686684</pubmed>		Article Source: <pubmed>20686684</pubmed>

Z3370664: /* Current Research */

2012-10-05T04:17:02Z

Current Research

← Older revision		Revision as of 14:17, 5 October 2012
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	Not only are there still many important processes and components of eye development that we would like to understand, this knowledge also contributes to the development of treatments for eye disorders and technologies such as the bionic eye.		Not only are there still many important processes and components of eye development that we would like to understand, this knowledge also contributes to the development of treatments for eye disorders and technologies such as the bionic eye.

			Below are summaries of some current research articles.


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	\| GABA is an ‘inhibitory neurotransmitter’ in the central nervous system of adults. <ref name="PMID22590629"><pubmed>22590629</pubmed></ref> It is responsible for controlling proliferation of stem cells and progenitor cells. The authors of this article <ref name="PMID22590629"/> was interested to find the effects of GABA on proliferation of progenitor cells and non-pigmented ciliary epithelial cells (NPE) in the retina. Their study focused on progenitor cells and non-pigmented epithelium of the ciliary body in chickens. Non-pigmented epithelial cells in chickens arise from the neuroepithelium of the optic cup. They share similar functions as progenitors of the early retina, such as expression of Chx10 and Pax6 genes. It is not agreed upon whether epithelial cells of the ciliary body have stem cell properties. However, it has been found that these cells can be cultured and transplanted into retinas that are injured, in order to replace neurons that were previously lost. However, there is not much known about what factors regulate the proliferation of stem cells. Hence the authors were interested in finding the effects of GABA on proliferation of retinal cells. Their results showed that non-pigmented epithelial cells in chickens ‘express extrasynaptic-like GABAA receptors’ that have the ability to regulate cell proliferation. It has been found that inhibiting these ‘GABAA receptors’ also causes a decrease in proliferation of retinal progenitor cells and non-pigmented epithelial cells in 'the intact E8 retina’. <ref name="PMID22590629"/>		\| GABA is an ‘inhibitory neurotransmitter’ in the central nervous system of adults. <ref name="PMID22590629"><pubmed>22590629</pubmed></ref> It is responsible for controlling proliferation of stem cells and progenitor cells. The authors of this article <ref name="PMID22590629"/> was interested to find the effects of GABA on proliferation of progenitor cells and non-pigmented ciliary epithelial cells (NPE) in the retina. Their study focused on progenitor cells and non-pigmented epithelium of the ciliary body in chickens. Non-pigmented epithelial cells in chickens arise from the neuroepithelium of the optic cup. They share similar functions as progenitors of the early retina, such as expression of Chx10 and Pax6 genes. It is not agreed upon whether epithelial cells of the ciliary body have stem cell properties. However, it has been found that these cells can be cultured and transplanted into retinas that are injured, in order to replace neurons that were previously lost. <ref name="PMID22590629"/> However, there is not much known about what factors regulate the proliferation of stem cells. Hence the authors were interested in finding the effects of GABA on proliferation of retinal cells. Their results showed that non-pigmented epithelial cells in chickens ‘express extrasynaptic-like GABAA receptors’ that have the ability to regulate cell proliferation. It has been found that inhibiting these ‘GABAA receptors’ also causes a decrease in proliferation of retinal progenitor cells and non-pigmented epithelial cells in 'the intact E8 retina’. <ref name="PMID22590629"/>


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	[[File:Gaba-effects-retina.JPG\|thumbnail\|250px\|'''GABAA receptor mediated effects on retinal progenitor cell proliferation'''		[[File:Gaba-effects-retina.JPG\|thumbnail\|250px\|'''"GABAA receptor mediated effects on retinal progenitor cell proliferation"''' <ref name="PMID22590629"/>
	]]		]]
	\|}		\|}
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	\|PITX3 plays a siginificant role in the development of lens in vertebrates. If there is a deficiency is PITX3, it causes a range of problems in humans such as microphthalmia, Peter’s anomaly, or isolated cataracts. Mutation of PITX3 also causes degeneration of the lens in zebrafish and mice. It is therefore important to understand what factors may affect the decrease in PITX3, as a normal level of PITX3 is needed to maintain normal eye development. The authors wanted to investigate specific genes which are affected by PITX3. Previous research has shown that MIP and Aquaporin causes defects in the lens in both mice and humans. MIP and Aquaporin are targeted by PITX3, so their imbalance is interrelated in the cause of defects in the lens. Therefore it has been previously proven that PITX3 is needed for normal development of the lens. However, there has not been much information previously known regarding the exact effect that PITX3 has, or the specific genes it targets. Since MIP and Aquaporin is common genes found in humans, mice and zebrafish, the authors ~~<ref name="PMID21698120"><pubmed>21698120</pubmed></ref>~~ chose to study these genes to understand the pathway that PITX3 takes and its exact involvement in the development of the lens. Their results proved that deficiency in MIP and Aquaporin indeed affects normal development of the lens, and it is indeed related to deficiency in PITX3. However, there is still more research needed to understand PITX3 and the genes it interacts with, and their effect in ocular development.		\|The authors in this article <ref name="PMID21698120"><pubmed>21698120</pubmed></ref> mentioned that PITX3 plays a siginificant role in the development of lens in vertebrates. If there is a deficiency is PITX3, it causes a range of problems in humans such as microphthalmia, Peter’s anomaly, or isolated cataracts. Mutation of PITX3 also causes degeneration of the lens in zebrafish and mice. It is therefore important to understand what factors may affect the decrease in PITX3, as a normal level of PITX3 is needed to maintain normal eye development. The authors wanted to investigate specific genes which are affected by PITX3. Previous research has shown that MIP and Aquaporin causes defects in the lens in both mice and humans. MIP and Aquaporin are targeted by PITX3, so their imbalance is interrelated in the cause of defects in the lens. Therefore it has been previously proven that PITX3 is needed for normal development of the lens. However, there has not been much information previously known regarding the exact effect that PITX3 has, or the specific genes it targets. Since MIP and Aquaporin is common genes found in humans, mice and zebrafish, the authors chose to study these genes to understand the pathway that PITX3 takes and its exact involvement in the development of the lens. Their results proved that deficiency in MIP and Aquaporin indeed affects normal development of the lens, and it is indeed related to deficiency in PITX3. However, there is still more research needed to understand PITX3 and the genes it interacts with, and their effect in ocular development.


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	[[File:Mip1-expression-in-pitx3.jpg\|thumbnail\|250px\|'''Analysis of mip1 expression in pitx3-mo and control embryos via in situ hybridization and RT-PCR''']]		[[File:Mip1-expression-in-pitx3.jpg\|thumbnail\|250px\|'''"Analysis of mip1 expression in pitx3-mo and control embryos via in situ hybridization and RT-PCR"''' <ref name="PMID21698120"/>
			]]
	\|}		\|}

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	\| In the past, most studies about c-Jun N-terminal kinase (JNK) in the retina have been in relation to neurodegeneration. <ref name="PMID22496813"><pubmed>22496813</pubmed></ref> Therefore the authors in this article were interested in investigating the function of c-Jun N-terminal kinase in the retinal progenitor cells in neonatal rats. <ref name="PMID22496813"/> In the experiment, they took retinal tissue from newborn rats and fixed them, and subsequently examined them using confocal microscopy and fluorescence to discover c-Jun N-terminal kinase ‘phosphorylation by immunohistochemistry’. <ref name="PMID22496813"/> Mitotic cells in the retina were identified during the experiment. The results of their experiment revealed that c-Jun N-terminal kinase is phosphorylated in the developing retina of neonatal rats during the mitosis of progenitor cells. ~~<ref name="PMID22496813"/>~~ This shows that c-Jun N-terminal kinase can control the proliferation of progenitor cells in the developing retina. Their experiment also revealed that inhibiting c-Jun N-terminal kinase causes disruptions to the mitotic cell cycle by reducing the cell numbers in anaphase. ~~<ref name="PMID22496813"/>~~ However, inhibiting c-Jun N-terminal kinase did not change the cell numbers in metaphase or prophase. <ref name="PMID22496813"/>		\| In the past, most studies about c-Jun N-terminal kinase (JNK) in the retina have been in relation to neurodegeneration. <ref name="PMID22496813"><pubmed>22496813</pubmed></ref> Therefore the authors in this article were interested in investigating the function of c-Jun N-terminal kinase in the retinal progenitor cells in neonatal rats. <ref name="PMID22496813"/> In the experiment, they took retinal tissue from newborn rats and fixed them, and subsequently examined them using confocal microscopy and fluorescence to discover c-Jun N-terminal kinase ‘phosphorylation by immunohistochemistry’. <ref name="PMID22496813"/> Mitotic cells in the retina were identified during the experiment. The results of their experiment revealed that c-Jun N-terminal kinase is phosphorylated in the developing retina of neonatal rats during the mitosis of progenitor cells. This shows that c-Jun N-terminal kinase can control the proliferation of progenitor cells in the developing retina. Their experiment also revealed that inhibiting c-Jun N-terminal kinase causes disruptions to the mitotic cell cycle by reducing the cell numbers in anaphase. However, inhibiting c-Jun N-terminal kinase did not change the cell numbers in metaphase or prophase. <ref name="PMID22496813"/>


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	[[File:JNK1.png\|thumbnail\|300px\|'''"JNK is phosphorylated during mitosis of retinal progenitor cells."''']]		[[File:JNK1.png\|thumbnail\|300px\|'''"JNK is phosphorylated during mitosis of retinal progenitor cells."''' <ref name="PMID22496813"/>]]
	\|}		\|}

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	The ~~lipoprotein receptor-related protein 5 (LRP5) has a significant function~~ in ~~the development of retinal vasculature.~~<ref name="PMID20652025"><pubmed>20652025</pubmed></ref> Research has shown that mutations of the LRP5 causes loss of function, due to incomplete development of retinal vessel network, in both humans and mice. The authors investigated how mutations occur in the LRP5, which leads to abnormal development of the retinal vasculature. They have studied retinal endothelial cells in mutant mice in their study. Their results showed that in retina with mutated LRP5, endothelial cells in the retinal vasculature primarily produced cell clusters in the inner-plexiform layer instead of migrating into deeper layers of the retina to form normal retinal vasculature. The authors also discovered that there was a decrease in Slc38a5, which is “a Müller cell-specific glutamine transporter”, in mice with mutated LRP5. Their results lead the authors to conclude that normal LRP5 is very important in the development of normal retinal vasculature due to their role in causing migration of retinal endothelial cells in the deeper layers of the retina. LRP5 is also important for retinal interneurons and Müller cells to function correctly.		The authors in this article <ref name="PMID20652025"><pubmed>20652025</pubmed></ref> mentioned that lipoprotein receptor-related protein 5 (LRP5) has a significant function in the development of retinal vasculature. Research has shown that mutations of the LRP5 causes loss of function, due to incomplete development of retinal vessel network, in both humans and mice. The authors investigated how mutations occur in the LRP5, which leads to abnormal development of the retinal vasculature. They have studied retinal endothelial cells in mutant mice in their study. Their results showed that in retina with mutated LRP5, endothelial cells in the retinal vasculature primarily produced cell clusters in the inner-plexiform layer instead of migrating into deeper layers of the retina to form normal retinal vasculature. The authors also discovered that there was a decrease in Slc38a5, which is “a Müller cell-specific glutamine transporter”, in mice with mutated LRP5. <ref name="PMID20652025"/> Their results lead the authors to conclude that normal LRP5 is very important in the development of normal retinal vasculature due to their role in causing migration of retinal endothelial cells in the deeper layers of the retina. LRP5 is also important for retinal interneurons and Müller cells to function correctly.


	\|		\|
	[[File:Retina-cell-clusters.JPG\|350px\|thumbnail\|'''Endothelial cells form thick clusters in the LRP5 mutant retina''']]		[[File:Retina-cell-clusters.JPG\|350px\|thumbnail\|'''"Endothelial cells form thick clusters in the LRP5 mutant retina"''' <ref name="PMID20652025"/>]]
	\|}		\|}

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	~~Vascular~~ endothelial growth factor (VEGF) has an important role in normal development of retinal vasculature. <ref name="PMID20686684"><pubmed>20686684</pubmed></ref> In the process of vascularisation of the retina, the retinal astrocytes (both vascularised and not yet vascularised) expresses the vascular endothelial growth factor. ~~<ref name="PMID20686684"/>~~ This fact indicates that vascular endothelial growth factor that are derived from astrocytes of the retina plays an important role in vessel maturation and angiogenesis. ~~<ref name="PMID20686684"/>~~ Therefore the authors wanted to test the role of vascular endothelial growth factor that are derived from astrocytes to find further confirmation. ‘Cre-lox technology’ was used in the experiment to remove the vascular endothelial growth factor from mice retinal astrocytes in the developmental period. <ref name="PMID20686684"/> The results showed that removing vascular endothelial growth factor that are derived from astrocytes caused ‘the regression of smooth muscle cell-coated radial arteries and veins’ from the effects of hyperoxia. <ref name="PMID20686684"/> Hence, this result indicates that vascular endothelial growth factor plays an important role in stabilising blood vessels during the development of the retinal vasculature. ~~<ref name="PMID20686684"/>~~ It has been suggested that this finding may be of relevance to retinopathy in premature neonatal humans. <ref name="PMID20686684"/>		The authors in this article mentioned that "vascular endothelial growth factor" (VEGF) has an important role in normal development of retinal vasculature. <ref name="PMID20686684"><pubmed>20686684</pubmed></ref> The authors explained that in the process of vascularisation of the retina, the retinal astrocytes (both vascularised and not yet vascularised) expresses the vascular endothelial growth factor. This fact indicates that vascular endothelial growth factor that are derived from astrocytes of the retina plays an important role in vessel maturation and angiogenesis. Therefore the authors wanted to test the role of vascular endothelial growth factor that are derived from astrocytes to find further confirmation. ‘Cre-lox technology’ was used in the experiment to remove the vascular endothelial growth factor from mice retinal astrocytes in the developmental period. <ref name="PMID20686684"/> The results showed that removing vascular endothelial growth factor that are derived from astrocytes caused ‘the regression of smooth muscle cell-coated radial arteries and veins’ from the effects of hyperoxia. <ref name="PMID20686684"/> Hence, this result indicates that vascular endothelial growth factor plays an important role in stabilising blood vessels during the development of the retinal vasculature. It has been suggested that this finding may be of relevance to retinopathy in premature neonatal humans. <ref name="PMID20686684"/>

	[[File:Astrocyte-vegf-deletion.JPG\|250px\|thumbnail\|'''"Astrocyte specific deletion of VEGF." ''']]		[[File:Astrocyte-vegf-deletion.JPG\|250px\|thumbnail\|'''"Astrocyte specific deletion of VEGF." ''' <ref name="PMID20686684"/>]]
	\|		\|
	[[File:Effect-of-vegf-on-retinal-vasculature.JPG\|250px\|thumbnail\|'''"Effects of astrocyte-derived VEGF on retinal vascular development."''']]		[[File:Effect-of-vegf-on-retinal-vasculature.JPG\|250px\|thumbnail\|'''"Effects of astrocyte-derived VEGF on retinal vascular development."''' <ref name="PMID20686684"/>]]
	[[File:Vegf-protects-vessels.JPG\|250px\|thumbnail\|'''Astrocyte-derived VEGF protects vessels from hyperoxia. ''']]		[[File:Vegf-protects-vessels.JPG\|250px\|thumbnail\|'''"Astrocyte-derived VEGF protects vessels from hyperoxia." '''<ref name="PMID20686684"/>]]

	\|}		\|}

Z3370664: /* Introduction */

2012-10-05T03:55:55Z

Introduction

← Older revision		Revision as of 13:55, 5 October 2012
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			===Basic Anatomy of the eye===

	The main anatomical structures of the eye are as follows:		The main anatomical structures of the eye are as follows:
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	The '''retina''' is a light-sensitive layer located towards the back of the internal surface of the eye, which contains photoreceptors (rods and cones) which detects visual information and transmits it to the brain through the optic nerve. The retina is made up of approximately 10 layers as follows: retinal pigment epithelium, photoreceptor cell layer, external limiting membrane, outer nuclear layer, outer plexiform layer, inner nuclear layer, inner plexiform layer, ganglion cell layer, nerve fiber layer, and internal limiting membrane. <ref name="Remington L.A. (2012) Clinical Anatomy of the Visual System. 3rd Ed. Elsevier 2012."/>		The '''retina''' is a light-sensitive layer located towards the back of the internal surface of the eye, which contains photoreceptors (rods and cones) which detects visual information and transmits it to the brain through the optic nerve. The retina is made up of approximately 10 layers as follows: retinal pigment epithelium, photoreceptor cell layer, external limiting membrane, outer nuclear layer, outer plexiform layer, inner nuclear layer, inner plexiform layer, ganglion cell layer, nerve fiber layer, and internal limiting membrane. <ref name="Remington L.A. (2012) Clinical Anatomy of the Visual System. 3rd Ed. Elsevier 2012."/>

			'''Macula''' is a pigmented oval region in the central area of the retina, important for maintaining visual acuity. '''Fovea''' is the central point in the macula, which is concentrated with cones for sharp colour vision. <ref name="Remington L.A. (2012) Clinical Anatomy of the Visual System. 3rd Ed. Elsevier 2012."/>


	{\|		{\|
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	Credits: Webvision <ref name="Kolb H, Fernandez E, Nelson R. '''The Organization of the Retina and Visual System ''' (Online Book). PMID:[http://www.ncbi.nlm.nih.gov/pubmed/21413389 21413389] [PubMed]"/> ]]		Credits: Webvision <ref name="Kolb H, Fernandez E, Nelson R. '''The Organization of the Retina and Visual System ''' (Online Book). PMID:[http://www.ncbi.nlm.nih.gov/pubmed/21413389 21413389] [PubMed]"/> ]]
	\|}		\|}


	'''Macula''' is a pigmented oval region in the central area of the retina, important for maintaining visual acuity. '''Fovea''' is the central point in the macula, which is concentrated with cones for sharp colour vision. <ref name="Remington L.A. (2012) Clinical Anatomy of the Visual System. 3rd Ed. Elsevier 2012."/>

	==Research History==		==Research History==

Z3370664: /* Introduction */

2012-10-05T03:52:07Z

Introduction

← Older revision		Revision as of 13:52, 5 October 2012
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	The '''retina''' is a light-sensitive layer located towards the back of the internal surface of the eye, which contains photoreceptors (rods and cones) which detects visual information and transmits it to the brain through the optic nerve. The retina is made up of approximately 10 layers as follows: retinal pigment epithelium, photoreceptor cell layer, external limiting membrane, outer nuclear layer, outer plexiform layer, inner nuclear layer, inner plexiform layer, ganglion cell layer, nerve fiber layer, and internal limiting membrane. <ref name="Remington L.A. (2012) Clinical Anatomy of the Visual System. 3rd Ed. Elsevier 2012."/>		The '''retina''' is a light-sensitive layer located towards the back of the internal surface of the eye, which contains photoreceptors (rods and cones) which detects visual information and transmits it to the brain through the optic nerve. The retina is made up of approximately 10 layers as follows: retinal pigment epithelium, photoreceptor cell layer, external limiting membrane, outer nuclear layer, outer plexiform layer, inner nuclear layer, inner plexiform layer, ganglion cell layer, nerve fiber layer, and internal limiting membrane. <ref name="Remington L.A. (2012) Clinical Anatomy of the Visual System. 3rd Ed. Elsevier 2012."/>

			{\|
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			[[File:Retina-layers-diagram2.jpg\|thumb\|200px\|A diagram of the layers of the retina.
			Credits: Webvision <ref name="Kolb H, Fernandez E, Nelson R. '''The Organization of the Retina and Visual System ''' (Online Book). PMID:[http://www.ncbi.nlm.nih.gov/pubmed/21413389 21413389] [PubMed]"/> ]]
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			[[File:Eye-retina-layers.jpg\|thumb\|200px\|The layers of the retina magnified, showing the direction of the layers of the retina in the back of the eye.
			Credits: Webvision <ref name="Kolb H, Fernandez E, Nelson R. '''The Organization of the Retina and Visual System ''' (Online Book). PMID:[http://www.ncbi.nlm.nih.gov/pubmed/21413389 21413389] [PubMed]"/> ]]

			\|
			[[File:Retina-layers-diagram.jpg\|thumb\|200px\|A diagram of the components of the retina.
			Credits: Webvision <ref name="Kolb H, Fernandez E, Nelson R. '''The Organization of the Retina and Visual System ''' (Online Book). PMID:[http://www.ncbi.nlm.nih.gov/pubmed/21413389 21413389] [PubMed]"/> ]]
			\|}


	'''Macula''' is a pigmented oval region in the central area of the retina, important for maintaining visual acuity. '''Fovea''' is the central point in the macula, which is concentrated with cones for sharp colour vision. <ref name="Remington L.A. (2012) Clinical Anatomy of the Visual System. 3rd Ed. Elsevier 2012."/>		'''Macula''' is a pigmented oval region in the central area of the retina, important for maintaining visual acuity. '''Fovea''' is the central point in the macula, which is concentrated with cones for sharp colour vision. <ref name="Remington L.A. (2012) Clinical Anatomy of the Visual System. 3rd Ed. Elsevier 2012."/>

Z3370664: /* Retina */

2012-10-05T03:44:22Z

Retina

← Older revision		Revision as of 13:44, 5 October 2012
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	The inner wall itself is divided into two components - the inner neuroblastic layer and the outer neuroblastic layer (see Figure 6). The outer neuroblastic layer forms the rod and cone cells while the inner neuroblastic layer forms the remaining cell types found in the retina - the bipolar, ganglion, horizontal, amacrine and glial cells (Figure 7).<ref name="Schoenwolf: Larsen’s Human embryology, 4th ed. Churchill Livingstone, An Imprint of Elsevier. 2008"/> The organisation of the retina is interesting in that incoming light passes through several layers of these neural retina cells before it is detected by rod and cone cells at the back of the retina, and then nerve signals are passed back through the layers of neural retina cells that the light just passed through moments before - a seemingly strange design that the eye does not share with man-made light-capturing devices such as a camera (imagine putting the wires in front of the image sensor!).		The inner wall itself is divided into two components - the inner neuroblastic layer and the outer neuroblastic layer (see Figure 6). The outer neuroblastic layer forms the rod and cone cells while the inner neuroblastic layer forms the remaining cell types found in the retina - the bipolar, ganglion, horizontal, amacrine and glial cells (Figure 7).<ref name="Schoenwolf: Larsen’s Human embryology, 4th ed. Churchill Livingstone, An Imprint of Elsevier. 2008"/> The organisation of the retina is interesting in that incoming light passes through several layers of these neural retina cells before it is detected by rod and cone cells at the back of the retina, and then nerve signals are passed back through the layers of neural retina cells that the light just passed through moments before - a seemingly strange design that the eye does not share with man-made light-capturing devices such as a camera (imagine putting the wires in front of the image sensor!).


	Differentiation of the neuroblastic layers into neural retina cells occurs in a pattern both within the layers and across the retina. Cells differentiate from the inner neuroblastic layer to the outer neuroblastic layer, and differentiate from the central retina to the peripheral retina.<ref name="PMID18168748"/> The macula is first identifiable in week 22 when ganglion cells start to form multiple rows, and the primitive fovea begins to form at approximately the same time as a depression in the macula.<ref><pubmed>6462623</pubmed></ref> It is not until 15-45 months after birth that this area becomes exclusively populated by cone cells and becomes the fovea centralis - the area of the retina with the highest visual acuity.		Differentiation of the neuroblastic layers into neural retina cells occurs in a pattern both within the layers and across the retina. Cells differentiate from the inner neuroblastic layer to the outer neuroblastic layer, and differentiate from the central retina to the peripheral retina.<ref name="PMID18168748"/> The macula is first identifiable in week 22 when ganglion cells start to form multiple rows, and the primitive fovea begins to form at approximately the same time as a depression in the macula.<ref><pubmed>6462623</pubmed></ref> It is not until 15-45 months after birth that this area becomes exclusively populated by cone cells and becomes the fovea centralis - the area of the retina with the highest visual acuity.
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	[[File:Formation of the retina 1.jpg\|400px\|thumb\|left\|Fig. 6: Cross-section of the primitive retina showing cell types and layers.]] [[File:Formation of the retina 2.jpg\|400px\|thumb\|center\|Fig. 7:Cross-section of a developed retina showing cell types and layers.]]		[[File:Formation of the retina 1.jpg\|400px\|thumb\|left\|Fig. 6: Cross-section of the primitive retina showing cell types and layers.]] [[File:Formation of the retina 2.jpg\|400px\|thumb\|center\|Fig. 7:Cross-section of a developed retina showing cell types and layers.]]

			[[File:5months-gestation-retina.jpg\|thumb\|center\|400px\|The layers of the retina in the fifth month of development. Credits: Webvision <ref name="Kolb H, Fernandez E, Nelson R. '''The Organization of the Retina and Visual System ''' (Online Book). PMID:[http://www.ncbi.nlm.nih.gov/pubmed/21413389 21413389] [PubMed]"/> ]]

	===Ciliary Body===		===Ciliary Body===

← Older revision		Revision as of 15:26, 5 October 2012
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	Image:Galen-eye1.jpg\|The eye according to Galen. Credits: Magnus, 1901.		Image:Galen-eye1.jpg\|The eye according to Galen. Credits: Magnus, 1901.

	Image:Kollmann691.jpg\|The blue part at the bottom is the endoderm. The pink middle layer is the mesoderm. The top yellow layer is the ectoderm. The fold labelled as 'augenfeld' is the place where the optic vesicle will form. Credits: ~~Kohlmann~~, J. (1907)		Image:Kollmann691.jpg\|The blue part at the bottom is the endoderm. The pink middle layer is the mesoderm. The top yellow layer is the ectoderm. The fold labelled as 'augenfeld' is the place where the optic vesicle will form. Credits: Kollmann, J. (1907)

	Image:Kollmann692.jpg\|The eye area (augenfeld) is a bowl shaped bulge still located on the side walls. Credits: ~~Kohlmann~~, J. (1907)		Image:Kollmann692.jpg\|The eye area (augenfeld) is a bowl shaped bulge still located on the side walls. Credits: Kollmann, J. (1907)


	Image:Kollmann693.jpg\| The neural tube is shown after removal of all of the ectoderm and ventral organs, such as heart, gut tube, etc. The primary optic vesicle forms a slightly flattened hollow protrusion on the forebrain. Credits: ~~Kohlmann~~, J. (1907)		Image:Kollmann693.jpg\| The neural tube is shown after removal of all of the ectoderm and ventral organs, such as heart, gut tube, etc. The primary optic vesicle forms a slightly flattened hollow protrusion on the forebrain. Credits: Kollmann, J. (1907)


	Image:Kollmann694.jpg\|The lateral surface of the primary optic vesicle is slightly depressed, showing the first sign of the emergence of the secondary optic vesicle. Credits: ~~Kohlmann~~, J. (1907)		Image:Kollmann694.jpg\|The lateral surface of the primary optic vesicle is slightly depressed, showing the first sign of the emergence of the secondary optic vesicle. Credits: Kollmann, J. (1907)

	Image:Kollmann695.jpg\|The bulging lateral wall of the primary optic vesicle is covered by a fairly well demarcated lens plate, a direct continuation of the ectoderm. Between the optic vesicle and the lens pit are some flattened spindle-shaped cells. In the adjoining mesoderm are cross-sections of capillaries. Credits: ~~Kohlmann~~, J. (1907)		Image:Kollmann695.jpg\|The bulging lateral wall of the primary optic vesicle is covered by a fairly well demarcated lens plate, a direct continuation of the ectoderm. Between the optic vesicle and the lens pit are some flattened spindle-shaped cells. In the adjoining mesoderm are cross-sections of capillaries. Credits: Kollmann, J. (1907)

	Image:Kollmann697.jpg\|The lens still hangs together with the ectoderm. The primary eye vesicle is indented with respect to the lens. Between the lens and the lateral plate of the optic vesicle is a narrow space, which allows area to further develop later. Credits: ~~Kohlmann~~, J. (1907)		Image:Kollmann697.jpg\|The lens still hangs together with the ectoderm. The primary eye vesicle is indented with respect to the lens. Between the lens and the lateral plate of the optic vesicle is a narrow space, which allows area to further develop later. Credits: Kollmann, J. (1907)

	Image:Kollmann698.jpg\|4th Week of development. The internal organisation shows the secondary optic vesicle. A: The rear wall of lens is noticeable and is enveloped by mesoderm. B: The edges of the lens pit is already grown and the lens vesicles are formed, which is still related to the remaining ectoderm. Credits: ~~Kohlmann~~, J. (1907)		Image:Kollmann698.jpg\|4th Week of development. The internal organisation shows the secondary optic vesicle. A: The rear wall of lens is noticeable and is enveloped by mesoderm. B: The edges of the lens pit is already grown and the lens vesicles are formed, which is still related to the remaining ectoderm. Credits: Kollmann, J. (1907)

	Image:Kollmann699.jpg\|The lens has now cut off from the ectoderm, but is still very superficial. Between it and the lateral lamina of the optic cup, there is a considerable space. The eye stalk has become longer and is enclosed together with the optic cup and lens of the mesoderm. The cornea, sclera and choroid make gradual development. Credits: ~~Kohlmann~~, J. (1907)		Image:Kollmann699.jpg\|The lens has now cut off from the ectoderm, but is still very superficial. Between it and the lateral lamina of the optic cup, there is a considerable space. The eye stalk has become longer and is enclosed together with the optic cup and lens of the mesoderm. The cornea, sclera and choroid make gradual development. Credits: Kollmann, J. (1907)

	Image:5months-gestation-retina.jpg\|The layers of the retina in the fifth month of development. Credits: Webvision [http://www.ncbi.nlm.nih.gov/pubmed/21413389 PMID:21413389] [PubMed]		Image:5months-gestation-retina.jpg\|The layers of the retina in the fifth month of development. Credits: Webvision [http://www.ncbi.nlm.nih.gov/pubmed/21413389 PMID:21413389] [PubMed]