Poster Title

Can Solidago Nemoralis Reduce Deficits Following Prenatal Ethanol Exposure in a Rodent Model

Grade Level at Time of Presentation

Senior

Major

Psychology

Minor

Neuroscience

Institution

University of Kentucky

KY House District #

28

KY Senate District #

28

Department

Psychology

Abstract

Alcohol ingestion during pregnancy can be detrimental to developing fetuses and can result in Fetal Alcohol Syndrome Disorder (FASD). FASD presents itself via behavioral, learning and cognition deficits and facial abnormalities. Existing studies suggest that drugs including Solidago nemoralis can reduce the effects of FASD by acting as an agonist on the alpha-7-nicotinic-acetylcholine-receptor. In the present study, ethanol was administered during a period of CNS development that overlaps the third trimester “brain growth spurt” of human pregnancy. ETOH (6g/kg/day) was given to Sprague-Dawley rat offspring on post-natal days (PND) 1-7. On PND 8, offspring were given either Solidago nemoralis or saline injections. To test for spatial learning and memory, a water maze paradigm was used in which the subject had to use external cues and an internal map to find a platform hidden under the water surface conducted on PND 40-45. The group that received ETOH paired with the Solidago nemoralis showed fewer deficits than the group that received only ETOH. The results in this study support the hypothesis that “third trimester” ETOH exposure impairs spatial learning and that a single administration of ETOH can result in deficits. It also showed that deficits associated with fetal alcohol exposure can be treated with Soliadgo nemoralis to help reduce effects of FASD and, in some cases, eliminate effects of FASD. The possible role of the alpha 7 in effects of prenatal ETOH exposure may also suggest that Solidago nemoralis has antioxidant properties. Further research is needed to understand the underlying mechanisms.

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Can Solidago Nemoralis Reduce Deficits Following Prenatal Ethanol Exposure in a Rodent Model

Alcohol ingestion during pregnancy can be detrimental to developing fetuses and can result in Fetal Alcohol Syndrome Disorder (FASD). FASD presents itself via behavioral, learning and cognition deficits and facial abnormalities. Existing studies suggest that drugs including Solidago nemoralis can reduce the effects of FASD by acting as an agonist on the alpha-7-nicotinic-acetylcholine-receptor. In the present study, ethanol was administered during a period of CNS development that overlaps the third trimester “brain growth spurt” of human pregnancy. ETOH (6g/kg/day) was given to Sprague-Dawley rat offspring on post-natal days (PND) 1-7. On PND 8, offspring were given either Solidago nemoralis or saline injections. To test for spatial learning and memory, a water maze paradigm was used in which the subject had to use external cues and an internal map to find a platform hidden under the water surface conducted on PND 40-45. The group that received ETOH paired with the Solidago nemoralis showed fewer deficits than the group that received only ETOH. The results in this study support the hypothesis that “third trimester” ETOH exposure impairs spatial learning and that a single administration of ETOH can result in deficits. It also showed that deficits associated with fetal alcohol exposure can be treated with Soliadgo nemoralis to help reduce effects of FASD and, in some cases, eliminate effects of FASD. The possible role of the alpha 7 in effects of prenatal ETOH exposure may also suggest that Solidago nemoralis has antioxidant properties. Further research is needed to understand the underlying mechanisms.