Impaired formation of the inner retina in an AChE knockout mouse results in degeneration of all photoreceptors

Abstract

AbstractBlinding diseases can be assigned predominantly to genetic defects of the photoreceptor/pigmented epithelium complex. As an alternative, we show here for an acetylcholinesterase (AChE) knockout mouse that photoreceptor degeneration follows an impaired development of the inner retina. During the first 15 postnatal days of the AChE–/– retina, three major calretinin sublaminae of the inner plexiform layer (IPL) are disturbed. Thereby, processes of amacrine and ganglion cells diffusely criss‐cross throughout the IPL. In contrast, parvalbumin cells present a nonlaminar IPL pattern in the wild‐type, but in the AChE–/– mouse their processes become structured within two ‘novel’ sublaminae. During this early period, photoreceptors become arranged regularly and at a normal rate in the AChE–/– retina. However, during the following 75 days, first their outer segments, and then the entire photoreceptor layer completely degenerate by apoptosis. Eventually, cells of the inner retina also undergo apoptosis. As butyrylcholinesterase (BChE) is present at a normal level in the AChE–/– mouse, the observed effects must be solely due to the missing AChE. These are the first in vivo findings to show a decisive role for AChE in the formation of the inner retinal network, which, when absent, ultimately results in photoreceptor degeneration.

Autoren

Afrim H Bytyqi
Oksana Lockridge
Ellen Duysen
Yuxia Wang
Uwe Wolfrum
Paul G Layer

DOI

10.1111/j.1460-9568.2004.03753.x

eISSN

1460-9568

ISSN

0953-816X

Ausgabe der Veröffentlichung

11

Zeitschrift

European Journal of Neuroscience

Sprache

en

Online publication date

2004

Paginierung

2953 - 2962

Datum der Veröffentlichung

2004

Status

Published

Herausgeber

Wiley

Herausgeber URL

http://dx.doi.org/10.1111/j.1460-9568.2004.03753.x

Datum der Datenerfassung

2023

Titel

Impaired formation of the inner retina in an AChE knockout mouse results in degeneration of all photoreceptors

Ausgabe der Zeitschrift

20

Data source: Crossref

Abstract

Blinding diseases can be assigned predominantly to genetic defects of the photoreceptor/pigmented epithelium complex. As an alternative, we show here for an acetylcholinesterase (AChE) knockout mouse that photoreceptor degeneration follows an impaired development of the inner retina. During the first 15 postnatal days of the AChE-/- retina, three major calretinin sublaminae of the inner plexiform layer (IPL) are disturbed. Thereby, processes of amacrine and ganglion cells diffusely criss-cross throughout the IPL. In contrast, parvalbumin cells present a nonlaminar IPL pattern in the wild-type, but in the AChE-/- mouse their processes become structured within two 'novel' sublaminae. During this early period, photoreceptors become arranged regularly and at a normal rate in the AChE-/- retina. However, during the following 75 days, first their outer segments, and then the entire photoreceptor layer completely degenerate by apoptosis. Eventually, cells of the inner retina also undergo apoptosis. As butyrylcholinesterase (BChE) is present at a normal level in the AChE-/- mouse, the observed effects must be solely due to the missing AChE. These are the first in vivo findings to show a decisive role for AChE in the formation of the inner retinal network, which, when absent, ultimately results in photoreceptor degeneration.

Addresses

Darmstadt University of Technology, Developmental Biology & Neurogenetics, D-64287 Darmstadt, Germany.

Autoren

Afrim H Bytyqi
Oksana Lockridge
Ellen Duysen
Yuxia Wang
Uwe Wolfrum
Paul G Layer

DOI

10.1111/j.1460-9568.2004.03753.x

eISSN

1460-9568

Externe Identifier

PubMed Identifier: 15579149

Open access

false

ISSN

0953-816X

Ausgabe der Veröffentlichung

11

Zeitschrift

The European journal of neuroscience

Schlüsselwörter

Retina
Animals
Animals, Newborn
Mice, Knockout
Chickens
Mice
Retinal Degeneration
Tritium
Choline
Indoles
Acetylcholinesterase
Glutamate-Ammonia Ligase
Rhodopsin
Parvalbumins
Microscopy, Electron, Transmission
Immunohistochemistry
In Situ Nick-End Labeling
Radiometry
Age Factors
Apoptosis
Gene Expression Regulation, Developmental
Photoreceptor Cells
Calbindins
S100 Calcium Binding Protein G
Calbindin 2

Sprache

eng

Medium

Print

Paginierung

2953 - 2962

Datum der Veröffentlichung

2004

Status

Published

Datum der Datenerfassung

2004

Titel

Impaired formation of the inner retina in an AChE knockout mouse results in degeneration of all photoreceptors.

Sub types

Comparative Study
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Journal Article

Ausgabe der Zeitschrift

20

Data source: Europe PubMed Central

Abstract

Blinding diseases can be assigned predominantly to genetic defects of the photoreceptor/pigmented epithelium complex. As an alternative, we show here for an acetylcholinesterase (AChE) knockout mouse that photoreceptor degeneration follows an impaired development of the inner retina. During the first 15 postnatal days of the AChE-/- retina, three major calretinin sublaminae of the inner plexiform layer (IPL) are disturbed. Thereby, processes of amacrine and ganglion cells diffusely criss-cross throughout the IPL. In contrast, parvalbumin cells present a nonlaminar IPL pattern in the wild-type, but in the AChE-/- mouse their processes become structured within two 'novel' sublaminae. During this early period, photoreceptors become arranged regularly and at a normal rate in the AChE-/- retina. However, during the following 75 days, first their outer segments, and then the entire photoreceptor layer completely degenerate by apoptosis. Eventually, cells of the inner retina also undergo apoptosis. As butyrylcholinesterase (BChE) is present at a normal level in the AChE-/- mouse, the observed effects must be solely due to the missing AChE. These are the first in vivo findings to show a decisive role for AChE in the formation of the inner retinal network, which, when absent, ultimately results in photoreceptor degeneration.

Autoren

Afrim H Bytyqi
Oksana Lockridge
Ellen Duysen
Yuxia Wang
Uwe Wolfrum
Paul G Layer

Autoren-URL

https://www.ncbi.nlm.nih.gov/pubmed/15579149

DOI

10.1111/j.1460-9568.2004.03753.x

ISSN

0953-816X

Ausgabe der Veröffentlichung

11

Zeitschrift

Eur J Neurosci

Schlüsselwörter

Acetylcholinesterase
Age Factors
Animals
Animals, Newborn
Apoptosis
Calbindin 2
Calbindins
Chickens
Choline
Gene Expression Regulation, Developmental
Glutamate-Ammonia Ligase
Immunohistochemistry
In Situ Nick-End Labeling
Indoles
Mice
Mice, Knockout
Microscopy, Electron, Transmission
Parvalbumins
Photoreceptor Cells
Radiometry
Retina
Retinal Degeneration
Rhodopsin
S100 Calcium Binding Protein G
Tritium

Sprache

eng

Country

France

Paginierung

2953 - 2962

PII

EJN3753

Datum der Veröffentlichung

2004

Status

Published

Datum, an dem der Datensatz öffentlich gemacht wurde

2005

Titel

Impaired formation of the inner retina in an AChE knockout mouse results in degeneration of all photoreceptors.

Sub types

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.

Ausgabe der Zeitschrift

20

Data source: PubMed

Impaired formation of the inner retina in an AChE knockout mouse results in degeneration of all photoreceptors

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