Prenatal Cannabinoid Exposure Affects Memory through Alterations in Glutamatergic Receptor Expression
Disciplines
Animal Studies | Behavioral Neurobiology | Cognitive Neuroscience | Molecular and Cellular Neuroscience
Abstract (300 words maximum)
As the legalization of cannabis has increased, prenatal exposure to cannabis has also increased significantly and is expected to continue rising. Currently, no therapy is available for cognitive deficits associated with prenatal cannabinoid exposure (PCE). Cognition can be researched through learning and memory which occurs in the hippocampus of the brain through the neurotransmitter, glutamate. The two major glutamate receptors in the hippocampus, N-Methyl D-Aspartate Receptor (NMDAR) and Alpha-Amino-3-Hydroxy-5-Methyl-4-Isoxazole Propionic Acid Receptor (AMPAR) are required for learning and memory formation. This project hypothesizes that behavioral deficits observed in PCE offspring are due to the upregulation of AMPA and NMDA receptor subunits. To test our hypothesis, pregnant Sprague Dawley rats were orally gavaged with 5 mg/kg of pure D9-tetrahydrocannabinol (THC) from gestational day five to post-natal day nine and examined between PND 40-50. To evaluate the learning capacity and memory retention behavioral experiments were performed such as elevated plus maze (EPM), trace fear conditioning (TFC), and contextual fear conditioning (CFC). Immunoblotting of hippocampal proteins revealed that PCE significantly increased the expression of GluA2, a subunit of AMPA receptors. GluN2A, a subunit of NMDA receptors also showed increased expression due to PCE. In brief, our studies demonstrate, at least in part, the molecular mechanisms of hippocampal-dependent memory deficits associated with PCE.
Academic department under which the project should be listed
CSM - Molecular and Cellular Biology
Primary Investigator (PI) Name
Vishnu Suppiramaniam
Additional Faculty
Kawsar Chowdhury, Biology, kchowdhu@kennesaw.edu
Erica Holliday, Psychology, ehollid1@kennesaw.edu
Prenatal Cannabinoid Exposure Affects Memory through Alterations in Glutamatergic Receptor Expression
As the legalization of cannabis has increased, prenatal exposure to cannabis has also increased significantly and is expected to continue rising. Currently, no therapy is available for cognitive deficits associated with prenatal cannabinoid exposure (PCE). Cognition can be researched through learning and memory which occurs in the hippocampus of the brain through the neurotransmitter, glutamate. The two major glutamate receptors in the hippocampus, N-Methyl D-Aspartate Receptor (NMDAR) and Alpha-Amino-3-Hydroxy-5-Methyl-4-Isoxazole Propionic Acid Receptor (AMPAR) are required for learning and memory formation. This project hypothesizes that behavioral deficits observed in PCE offspring are due to the upregulation of AMPA and NMDA receptor subunits. To test our hypothesis, pregnant Sprague Dawley rats were orally gavaged with 5 mg/kg of pure D9-tetrahydrocannabinol (THC) from gestational day five to post-natal day nine and examined between PND 40-50. To evaluate the learning capacity and memory retention behavioral experiments were performed such as elevated plus maze (EPM), trace fear conditioning (TFC), and contextual fear conditioning (CFC). Immunoblotting of hippocampal proteins revealed that PCE significantly increased the expression of GluA2, a subunit of AMPA receptors. GluN2A, a subunit of NMDA receptors also showed increased expression due to PCE. In brief, our studies demonstrate, at least in part, the molecular mechanisms of hippocampal-dependent memory deficits associated with PCE.