Premium
Differential effect of ischemia, hypoxia, hyperglycaemia and hypoglycaemia on the rat retinal neurotransmittion
Author(s) -
VASILAKI A,
GRIVAS V,
SOURLAS V,
PAPAGEORGIOU E
Publication year - 2010
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2010.381.x
Subject(s) - endocrinology , hypoxia (environmental) , medicine , neurotransmission , retinal , excitotoxicity , ischemia , ex vivo , glutamatergic , chemistry , excitatory postsynaptic potential , in vivo , glutamate receptor , biology , inhibitory postsynaptic potential , oxygen , biochemistry , receptor , microbiology and biotechnology , organic chemistry
Purpose The time‐dependent effects of glucose and oxygen alterations on retinal neurotransmission, are not fully understood. The purpose of this study was to investigate ex vivo the influence of ischemia, hypoxia, hyper‐ and hypo‐glycaemia on the excitatory and inhibitory rat retinal neurotransmission during the first 70min after an initial insult. Methods For this purpose, 3H‐D‐Aspartate and 3H‐GABA release as well as choline acetyl‐transferase immunoreactivity (ChAT‐IR) were studied under ischemic (glucose to sucrose replacement and 95%N2/5%CO2 buffering), hypoxic (95%N2/5%CO2 buffering), hypoglycaemic (glucose to sucrose replacement) and hyperglycaemic (30mM glucose) conditions, using an ex vivo rat retinal superfusion system. Results Compared to normoxic conditions: i) ischemia led to an initial decrease of 3H‐D‐Aspartate release followed ~30min later by a delayed increase that was concurrent with an increase of 3H‐GABA release, ii) hypoxia led to a decrease of 3H‐D‐Aspartate release 8min after the initial insult, followed 20min later by a decrease of 3H‐GABA release, iii) hyperglycaemia led to a brief initial decrease of 3H‐D‐Aspartate release while, iv) hypoglycaemia led to a delayed increase of 3H‐GABA release followed by an increase of 3H‐D‐Aspartate release. ChAT‐IR in INL and GCL layers was minimally affected under hypoxic conditions; it was diminished under either hypoglycaemic or hyperglycaemic conditions, while it was abolished under ischemic conditions. Conclusion Hypoxia decreases retinal neurotransmission. Glutamatergic excitotoxicity is induced primarily under ischemia and to a lesser degree under hypoglycaemia. The GABA‐release compensatory mechanism is more prominent under ex vivo ischemia.