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Acute hypoxic hypoxia transiently reduces GABA(A) binding site number in developing chick optic lobe
D J Rodríguez Gil1, M S Viapiano, S Fiszer de Plazas
1Instituto de Biología Celular y Neurociencias, Prof. E. De Robertis, Facultad de Medicina, Universidad de Buenos Aires, Paraguay 2155, 1121, Buenos Aires, Argentina.
Brain Research. Developmental Brain Research
|December 13, 2000
Summary
Prenatal hypoxic hypoxia significantly reduces GABA binding sites in chick embryos, impacting inhibitory neurotransmission. These effects are age-dependent and reversible upon return to normoxia.
Area of Science:
- Neuroscience
- Developmental Biology
- Biochemistry
Background:
- Prenatal-perinatal hypoxic-ischemic insults critically affect the Central Nervous System (CNS).
- These insults can lead to neural damage, seizures, apoptosis, and excitotoxicity due to neurotransmitter imbalance.
- Understanding the impact on neurotransmitter receptors is crucial for developing interventions.
Purpose of the Study:
- To establish a chick embryo model for normobaric acute hypoxic hypoxia.
- To evaluate changes in the GABA(A) receptor complex in the chick optic lobe following hypoxic injury.
- To assess the reversibility and age-dependency of these modifications.
Main Methods:
- Fertile White Leghorn chicken eggs were incubated and exposed to 8%O(2)/92%N(2) for 1 hour between embryonic days 12-18.
- Following hypoxia, embryos were either allowed recovery in normoxia or immediately processed for biochemical analysis.
- GABA binding assays and pharmacological characterization of the GABA(A) receptor complex were performed.
Main Results:
- Hypoxic treatment caused a significant, age-dependent reduction in GABA binding sites, most pronounced at ED12-16.
- At ED12, a decrease in B(max) but not K(d) for GABA binding was observed post-hypoxia.
- Positive allosteric modulation by a steroid and pentobarbital sodium was enhanced in hypoxic embryos.
- The reduction in [3H]GABA binding reversed after 48 hours of normoxic recovery.
Conclusions:
- Acute prenatal hypoxic hypoxia induces significant, reversible, and age-dependent alterations in CNS inhibitory neurotransmission in chick embryos.
- The GABA(A) receptor complex is a key target of hypoxic injury during development.
- The chick embryo model provides a valuable tool for studying developmental neuroprotection.