Documenta Ophthalmologica

, Volume 80, Issue 4, pp 273–300

Interrelationship between retinal ischaemic damage and turnover and metabolism of putative amino acid neurotransmitters, glutamate and GABA

  • Leonie N. Robin
  • Michael Kalloniatis
Article

DOI: 10.1007/BF00154376

Cite this article as:
Robin, L.N. & Kalloniatis, M. Doc Ophthalmol (1992) 80: 273. doi:10.1007/BF00154376

Abstract

Conditions causing a reduction of oxygen availability (anoxia), such as stroke or diabetes, result in drastic changes in ion movements, levels of neurotransmitters and metabolites and subsequent neural death. Currently, there is no clinically available treatment for anoxia induced neural cell death resulting in drastic and permanent central nervous system dysfunction. However, there have been some exciting developments in experimentally induced anoxic conditions where several classes of drugs appear to significantly reduce neural cell death. This report aims to provide the foundations for understanding both the basic mechanisms involved in retinal ischaemic damage and experimental treatments used to prevent such damage. We discuss the normal release, actions and uptake of the fast retinal neurotransmitters, glutamate and GABA, in the vertebrate retina. Immunocytochemistry is used to demonstrate that both glutamate and GABA are found in the macaque retina. Following this is a discussion on how ischaemia may enhance neurotransmitter release or disrupt its uptake, thus causing an increase in extracellular concentration of these neurotransmitters and subsequent neuronal damage. The mechanisms involved in glutamate neurotoxicity are reviewed, because excess glutamate is the likely cause of retinal ischaemic damage. Finally, the mechanisms behind four possible modes of treatment of neurotransmitter toxicity and their advantages and disadvantages are discussed. Hopefully, further research in this area will lead to the development of a rational therapy for retinal, as well as cerebral ischaemia.

Key words

Anoxia GABA glutamate immunocytochemistry ischaemia neurotransmitters retina 

Abbreviations

α-KG

α-ketoglutarate

AAT

aspartate amino transferase

AC

amacrine cell

ACL

amacrine cell layer

BC

bipolar cell

CNS

central nervous system

EAA

excitatory amino acids

G'ase

glutaminase

GABA

γ-amino butyric acid

GABA-T

GABA transaminase

GAD

glumatic acid decarboxylase

GC

ganglion cell

GCL

ganglion cell layer

GDH

glutamate dehydrogenase

gj

gap junction

GS

glutamine synthetase

HC

horizontal cell

ILM

inner limiting membrane

INL

inner nuclear layer

IPC

inter-plexiform cell

IPL

inner plexiform layer

IS

inner segment of photoreceptor

NFL

nerve fibre layer

NMDA

N-methyl-D-aspartate

OLM

outer limiting membrane

ONL

outer nuclear layer

OPL

outer plexiform layer

OS

outer segment of photoreceptor

Ox

acetateoxaloacetate

RL

receptor layer

SSAD

succinate semi-aldehyde decarboxylase

Succinate SA

succinate semi aldehyde

TCA cycle

tricarboxylic acid cycle

Copyright information

© Kluwer Academic Publishers 1992

Authors and Affiliations

  • Leonie N. Robin
    • 1
  • Michael Kalloniatis
    • 1
  1. 1.Department of OptometryUniversity of MelbourneParkvilleAustralia
  2. 2.Department of OptometryUniversity of MelbourneParkvilleAustralia

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