Importance of adrenergic receptors in prenatally induced cognitive impairment in the domestic chick

Marie Elizabeth Gibbs, Candice Lauren Rodricks, Dana Sabine Hutchinson, Roger James Summers, Suzanne Lee Miller

Research output: Contribution to journalArticleResearchpeer-review

2 Citations (Scopus)

Abstract

In the domestic chick, mild hypoxia (24h of 14 oxygen) at two stages of embryonic development results in post-hatch memory deficiencies tested using a discriminated bead avoidance task. The nature of the memory loss depends on the gestational age at which the hypoxia occurs. Hypoxia on embryonic day 10 (E10) of a 21 day incubation results in chicks with no short-term memory 10min after training, whereas hypoxia on day 14 (E14) results in chicks with good labile memory 30min after training but no consolidation of memory into permanent storage (120min). Hypoxia at E14 is associated with increased plasma levels of noradrenaline and therefore we suggest that altered catecholamine exposure within the brain contributes to cognitive problems by modifying the responsiveness of brain beta-adrenoceptors. In ovo administration of noradrenaline, or the beta(2)-adrenoceptor agonist formoterol, at E14 had the same effect on memory consolidation as hypoxia. Following hypoxia at E14, memory could be rescued after training by central injection of a beta(3)-adrenoceptor agonist, but not by a beta(2)-adrenoceptor agonist. The differences in the responsiveness of memory processing to beta(2)-adrenoceptor agonists suggests alterations to the receptors or downstream of the receptor activation. However, both types of beta-adrenoceptor agonists rescued memory in E10 treated chicks implying that at this age hypoxia does not affect the receptors. In summary, hypoxia or increased levels of stress hormones during incubation alters beta-adrenoceptor responsiveness; the outcome of the insult depends upon the cellular developmental processes at a given embryonic stage. [DOI:10.1016/j.ijdevneu.2008.10.005]
Original languageEnglish
Pages (from-to)27 - 35
Number of pages8
JournalInternational Journal of Developmental Neuroscience
Volume27
Publication statusPublished - 2009

Cite this

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title = "Importance of adrenergic receptors in prenatally induced cognitive impairment in the domestic chick",
abstract = "In the domestic chick, mild hypoxia (24h of 14 oxygen) at two stages of embryonic development results in post-hatch memory deficiencies tested using a discriminated bead avoidance task. The nature of the memory loss depends on the gestational age at which the hypoxia occurs. Hypoxia on embryonic day 10 (E10) of a 21 day incubation results in chicks with no short-term memory 10min after training, whereas hypoxia on day 14 (E14) results in chicks with good labile memory 30min after training but no consolidation of memory into permanent storage (120min). Hypoxia at E14 is associated with increased plasma levels of noradrenaline and therefore we suggest that altered catecholamine exposure within the brain contributes to cognitive problems by modifying the responsiveness of brain beta-adrenoceptors. In ovo administration of noradrenaline, or the beta(2)-adrenoceptor agonist formoterol, at E14 had the same effect on memory consolidation as hypoxia. Following hypoxia at E14, memory could be rescued after training by central injection of a beta(3)-adrenoceptor agonist, but not by a beta(2)-adrenoceptor agonist. The differences in the responsiveness of memory processing to beta(2)-adrenoceptor agonists suggests alterations to the receptors or downstream of the receptor activation. However, both types of beta-adrenoceptor agonists rescued memory in E10 treated chicks implying that at this age hypoxia does not affect the receptors. In summary, hypoxia or increased levels of stress hormones during incubation alters beta-adrenoceptor responsiveness; the outcome of the insult depends upon the cellular developmental processes at a given embryonic stage. [DOI:10.1016/j.ijdevneu.2008.10.005]",
author = "Gibbs, {Marie Elizabeth} and Rodricks, {Candice Lauren} and Hutchinson, {Dana Sabine} and Summers, {Roger James} and Miller, {Suzanne Lee}",
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journal = "International Journal of Developmental Neuroscience",
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Importance of adrenergic receptors in prenatally induced cognitive impairment in the domestic chick. / Gibbs, Marie Elizabeth; Rodricks, Candice Lauren; Hutchinson, Dana Sabine; Summers, Roger James; Miller, Suzanne Lee.

In: International Journal of Developmental Neuroscience, Vol. 27, 2009, p. 27 - 35.

Research output: Contribution to journalArticleResearchpeer-review

TY - JOUR

T1 - Importance of adrenergic receptors in prenatally induced cognitive impairment in the domestic chick

AU - Gibbs, Marie Elizabeth

AU - Rodricks, Candice Lauren

AU - Hutchinson, Dana Sabine

AU - Summers, Roger James

AU - Miller, Suzanne Lee

PY - 2009

Y1 - 2009

N2 - In the domestic chick, mild hypoxia (24h of 14 oxygen) at two stages of embryonic development results in post-hatch memory deficiencies tested using a discriminated bead avoidance task. The nature of the memory loss depends on the gestational age at which the hypoxia occurs. Hypoxia on embryonic day 10 (E10) of a 21 day incubation results in chicks with no short-term memory 10min after training, whereas hypoxia on day 14 (E14) results in chicks with good labile memory 30min after training but no consolidation of memory into permanent storage (120min). Hypoxia at E14 is associated with increased plasma levels of noradrenaline and therefore we suggest that altered catecholamine exposure within the brain contributes to cognitive problems by modifying the responsiveness of brain beta-adrenoceptors. In ovo administration of noradrenaline, or the beta(2)-adrenoceptor agonist formoterol, at E14 had the same effect on memory consolidation as hypoxia. Following hypoxia at E14, memory could be rescued after training by central injection of a beta(3)-adrenoceptor agonist, but not by a beta(2)-adrenoceptor agonist. The differences in the responsiveness of memory processing to beta(2)-adrenoceptor agonists suggests alterations to the receptors or downstream of the receptor activation. However, both types of beta-adrenoceptor agonists rescued memory in E10 treated chicks implying that at this age hypoxia does not affect the receptors. In summary, hypoxia or increased levels of stress hormones during incubation alters beta-adrenoceptor responsiveness; the outcome of the insult depends upon the cellular developmental processes at a given embryonic stage. [DOI:10.1016/j.ijdevneu.2008.10.005]

AB - In the domestic chick, mild hypoxia (24h of 14 oxygen) at two stages of embryonic development results in post-hatch memory deficiencies tested using a discriminated bead avoidance task. The nature of the memory loss depends on the gestational age at which the hypoxia occurs. Hypoxia on embryonic day 10 (E10) of a 21 day incubation results in chicks with no short-term memory 10min after training, whereas hypoxia on day 14 (E14) results in chicks with good labile memory 30min after training but no consolidation of memory into permanent storage (120min). Hypoxia at E14 is associated with increased plasma levels of noradrenaline and therefore we suggest that altered catecholamine exposure within the brain contributes to cognitive problems by modifying the responsiveness of brain beta-adrenoceptors. In ovo administration of noradrenaline, or the beta(2)-adrenoceptor agonist formoterol, at E14 had the same effect on memory consolidation as hypoxia. Following hypoxia at E14, memory could be rescued after training by central injection of a beta(3)-adrenoceptor agonist, but not by a beta(2)-adrenoceptor agonist. The differences in the responsiveness of memory processing to beta(2)-adrenoceptor agonists suggests alterations to the receptors or downstream of the receptor activation. However, both types of beta-adrenoceptor agonists rescued memory in E10 treated chicks implying that at this age hypoxia does not affect the receptors. In summary, hypoxia or increased levels of stress hormones during incubation alters beta-adrenoceptor responsiveness; the outcome of the insult depends upon the cellular developmental processes at a given embryonic stage. [DOI:10.1016/j.ijdevneu.2008.10.005]

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JO - International Journal of Developmental Neuroscience

JF - International Journal of Developmental Neuroscience

SN - 0736-5748

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