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The effect of hypoxia at different embryonic ages on impairment of memory ability in chicks
Candice L Rodricks1, Marie E Gibbs, Graham Jenkin
1Department of Physiology, Monash University, Clayton, 3800 Victoria, Australia.
Insights
Prenatal hypoxia can impair cognitive function. This study found that the timing and severity of oxygen deprivation during embryonic development critically influence memory deficits and stress responses in chicks, with specific sensitive periods around embryonic days 10 and 14.
Area of Science:
- Neuroscience
- Developmental Biology
- Environmental Health
Background:
- Prenatal hypoxia is a known cause of cognitive impairment.
- Understanding the impact of hypoxia timing and severity is crucial for predicting developmental outcomes.
Purpose of the Study:
- To investigate the effects of hypoxia duration, severity, and timing on cognitive function in chick embryos.
- To determine critical developmental windows sensitive to hypoxic insults.
Main Methods:
- Embryonic chicks were exposed to varying durations and severities of hypoxia and anoxia at different developmental stages (E9-E16).
- Memory function was assessed in post-hatch chicks.
- Corticosterone levels were measured as a stress indicator.
Main Results:
- Hypoxia at embryonic day 10 (E10) for 24 hours caused significant intermediate and long-term memory impairment.
- At E14, shorter hypoxia (24h) or anoxia (5min) impaired long-term memory.
- Elevated corticosterone levels indicated a significant stress response to hypoxia and anoxia at various developmental stages.
- Memory deficits were linked to specific sensitive periods around E10 and E14, regardless of insult duration (acute vs. chronic).
Conclusions:
- Developmental timing of prenatal hypoxia is a key determinant of cognitive deficits.
- Specific embryonic stages (around E10 and E14) are critical periods for adverse cognitive effects following hypoxia.
- The severity of the hypoxic insult influences the extent of memory impairment.
Abstract:
Hypoxia during the prenatal period is a principal antecedent to cognitive impairment after birth. In this study we have investigated the duration, severity and timing of acute hypoxia during chick embryonic development to elucidate the relative importance of these factors. Our results show that 24h of hypoxia (exposure to 14% oxygen) at embryonic day 10 (E10) results in significant impairment of intermediate and long-term memory in the post-hatch chick, which is the same as we observed with 4 days of hypoxia. At E14, 24h of hypoxia, 5min of anoxia, but not 1h of hypoxia, resulted only in impaired long-term memory; the same as 4 days of hypoxia from E14. Corticosterone levels, measured post-hatch as an indicator of a stress response, were significantly elevated in response to E10 hypoxia, and E14 hypoxia (both 1 and 24h) and anoxia. In a separate experiment we exposed embryos to 24h of hypoxia from E6 to E16, and found that memory deficits resulted from hypoxia at E9 and E10, and E13-E15, while corticosterone concentrations at hatch were significantly raised following E10-E16 hypoxia. These results demonstrate that the developmental age when the insult occurs determines the nature of the cognitive deficit and, if the severity of the insult is sufficient, then the outcome, or deficits in memory ability, are consistent whether the insult is acute or chronic. Importantly, there are two critical stages in development, which in the chick are around E10 and E14, when acute hypoxia results in significant adverse cognitive effects after hatch. These time-points correspond to two different stages in growth and development.
