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Updated: Apr 12, 2026
Assay for Neural Induction in the Chick Embryo
Published on: February 13, 2009
Chick embryos have the same pattern of hypoxic lower-brain activation as fetal mammals
Jeremy P Landry1, Connor Hawkins1, Aaron Lee1
1Department of Psychology, McGill University, Montreal, Quebec, Canada, H3A 1B1.
Insights
Prenatal brain responses to hypoxia in chick embryos show conserved circuitry with mammals, with the nucleus of the solitary tract (NTS) playing a key role. This study investigates neuronal activation patterns during low oxygen conditions in developing brains.
Area of Science:
- Neuroscience
- Developmental Biology
- Physiology
Background:
- Neuronal activation patterns in response to hypoxia are crucial for understanding developmental responses to oxygen levels.
- Previous studies in mammalian fetuses identified specific brain regions responding to hypoxia.
Purpose of the Study:
- To investigate cFos expression, a marker of neuronal activation, in embryonic chick brains under varying oxygen conditions (normoxia, modest hypoxia, medium hypoxia).
- To compare hypoxic brain activation patterns in chick embryos with those observed in mammalian fetuses.
- To explore the role of O2-sensing A1/C1 neurons and heme oxygenase 2 (HMOX2) in prenatal hypoxic responses.
Main Methods:
- Embryonic day 18 chick embryos were exposed to normoxia (21% O2), modest hypoxia (15% O2), or medium hypoxia (10% O2) for 4 hours.
- cFos expression was analyzed in eight brainstem and hypothalamus regions.
- Specific attention was given to the A1/C1 region, examining HMOX2-positive and -negative catecholaminergic and non-catecholaminergic cells.
Main Results:
- Hypoxia induced significant cFos expression changes in multiple brain regions of chick embryos, largely mirroring patterns in mammalian fetuses.
- The medullary Raphe showed decreased hypoxic activation in chicks, unlike the no-change response in mammals, potentially due to greater anapyrexia in chicks.
- Activation in the A1/C1 region revealed changes in cFos expression across different cell types, with catecholaminergic cells showing larger population responses.
- Hypoxia-induced activation in lower brain regions correlated better with the nucleus of the solitary tract (NTS) than with HMOX2-containing A1/C1 neurons.
Conclusions:
- The functional circuitry for prenatal brain responses to hypoxia is highly conserved between birds and mammals.
- Neurons in the nucleus of the solitary tract (NTS) appear to be a more dominant driver of prenatal hypoxic cFos brain responses than O2-sensing A1/C1 neurons.
Abstract:
cFos expression (indicating a particular kind of neuronal activation) was examined in embryonic day (E) 18 chick embryos after exposure to 4 h of either normoxia (21% O2), modest hypoxia (15% O2), or medium hypoxia (10% O2). Eight regions of the brainstem and hypothalamus were surveyed, including seven previously shown to respond to hypoxia in late-gestation mammalian fetuses (Breen et al., 1997; Nitsos and Walker, 1999b). Hypoxia-related changes in chick embryo brain activation mirrored those found in fetal mammals with the exception of the medullary Raphe, which showed decreased hypoxic activation, compared with no change in mammals. This difference may be explained by the greater anapyrexic responses of chick embryos relative to mammalian fetuses. Activation in the A1/C1 region was examined in more detail to ascertain whether an O2-sensitive subpopulation of these cells containing heme oxygenase 2 (HMOX2) may drive hypoxic brain responses before the maturation of peripheral O2-sensing. HMOX2-positive and -negative catecholaminergic cells and interdigitating noncatecholaminergic HMOX2-positive cells all showed significant changes in cFos expression to hypoxia, with larger population responses seen in the catecholaminergic cells. Hypoxia-induced activation of lower-brain regions studied here was significantly better correlated with activation of the nucleus of the solitary tract (NTS) than with that of HMOX2-containing A1/C1 neurons. Together, these observations suggest that (1) the functional circuitry controlling prenatal brain responses to hypoxia is strongly conserved between birds and mammals, and (2) NTS neurons are a more dominant driving force for prenatal hypoxic cFos brain responses than O2-sensing A1/C1 neurons.
