Prenatal cocaine exposure alters alpha2 receptor expression in adolescent rats

Rosemarie M. Booze; David R. Wallace; Janelle M. Silvers; Barbara J. Strupp; Diane M. Snow; Charles F. Mactutus

doi:10.1186/1471-2202-7-33

Prenatal cocaine exposure alters alpha2 receptor expression in adolescent rats

Rosemarie M. Booze, David R. Wallace, Janelle M. Silvers, Barbara J. Strupp, Diane M. Snow, Charles F. Mactutus

Pharmacology and Physiology

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15 Scopus citations

Abstract

Background: Prenatal cocaine exposure produces attentional deficits which to persist through early childhood. Given the role of norepinephrine (NE) in attentional processes, we examined the forebrain NE systems from prenatal cocaine exposed rats. Cocaine was administered during pregnancy via the clinically relevant intravenous route of administration. Specifically, we measured α₂-adrenergic receptor (α₂-AR) density in adolescent (35-days-old) rats, using [³H]RX821002 (5 nM). Results: Sex-specific alterations of α₂-AR were found in the hippocampus and amygdala of the cocaine-exposed animals, as well as an upregulation of α₂-AR in parietal cortex. Conclusion: These data suggest that prenatal cocaine exposure results in a persistent alteration in forebrain NE systems as indicated by alterations in receptor density. These neurochemical changes may underlie behavioral abnormalities observed in offspring attentional processes following prenatal exposure to cocaine.

Original language	English
Article number	33
Journal	BMC Neuroscience
Volume	7
DOIs	https://doi.org/10.1186/1471-2202-7-33
State	Published - 18 Apr 2006

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title = "Prenatal cocaine exposure alters alpha2 receptor expression in adolescent rats",

abstract = "Background: Prenatal cocaine exposure produces attentional deficits which to persist through early childhood. Given the role of norepinephrine (NE) in attentional processes, we examined the forebrain NE systems from prenatal cocaine exposed rats. Cocaine was administered during pregnancy via the clinically relevant intravenous route of administration. Specifically, we measured α2-adrenergic receptor (α2-AR) density in adolescent (35-days-old) rats, using [3H]RX821002 (5 nM). Results: Sex-specific alterations of α2-AR were found in the hippocampus and amygdala of the cocaine-exposed animals, as well as an upregulation of α2-AR in parietal cortex. Conclusion: These data suggest that prenatal cocaine exposure results in a persistent alteration in forebrain NE systems as indicated by alterations in receptor density. These neurochemical changes may underlie behavioral abnormalities observed in offspring attentional processes following prenatal exposure to cocaine.",

author = "Booze, {Rosemarie M.} and Wallace, {David R.} and Silvers, {Janelle M.} and Strupp, {Barbara J.} and Snow, {Diane M.} and Mactutus, {Charles F.}",

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doi = "10.1186/1471-2202-7-33",

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T1 - Prenatal cocaine exposure alters alpha2 receptor expression in adolescent rats

AU - Booze, Rosemarie M.

AU - Wallace, David R.

AU - Silvers, Janelle M.

AU - Strupp, Barbara J.

AU - Snow, Diane M.

AU - Mactutus, Charles F.

PY - 2006/4/18

Y1 - 2006/4/18

N2 - Background: Prenatal cocaine exposure produces attentional deficits which to persist through early childhood. Given the role of norepinephrine (NE) in attentional processes, we examined the forebrain NE systems from prenatal cocaine exposed rats. Cocaine was administered during pregnancy via the clinically relevant intravenous route of administration. Specifically, we measured α2-adrenergic receptor (α2-AR) density in adolescent (35-days-old) rats, using [3H]RX821002 (5 nM). Results: Sex-specific alterations of α2-AR were found in the hippocampus and amygdala of the cocaine-exposed animals, as well as an upregulation of α2-AR in parietal cortex. Conclusion: These data suggest that prenatal cocaine exposure results in a persistent alteration in forebrain NE systems as indicated by alterations in receptor density. These neurochemical changes may underlie behavioral abnormalities observed in offspring attentional processes following prenatal exposure to cocaine.

AB - Background: Prenatal cocaine exposure produces attentional deficits which to persist through early childhood. Given the role of norepinephrine (NE) in attentional processes, we examined the forebrain NE systems from prenatal cocaine exposed rats. Cocaine was administered during pregnancy via the clinically relevant intravenous route of administration. Specifically, we measured α2-adrenergic receptor (α2-AR) density in adolescent (35-days-old) rats, using [3H]RX821002 (5 nM). Results: Sex-specific alterations of α2-AR were found in the hippocampus and amygdala of the cocaine-exposed animals, as well as an upregulation of α2-AR in parietal cortex. Conclusion: These data suggest that prenatal cocaine exposure results in a persistent alteration in forebrain NE systems as indicated by alterations in receptor density. These neurochemical changes may underlie behavioral abnormalities observed in offspring attentional processes following prenatal exposure to cocaine.

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Prenatal cocaine exposure alters alpha2 receptor expression in adolescent rats

Abstract

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