As the legalization of cannabis has increased, prenatal exposure to cannabinoids has also increased significantly and is expected to continue rising. Currently, no therapy is available for cognitive deficits associated with prenatal cannabinoid exposure (PCE). Our project hypothesizes that PCE causes altered expression and function of glutamatergic receptors, namely the NMDAR (N-Methyl D-Aspartate Receptor) and AMPAR (α-Amino-3-Hydroxy-5-methyl-4-isoxazole Propionic acid receptors) leading to cognitive and memory deficits. Pregnant Sprague Dawley rats were orally gavaged with either sesame oil or 5mg/kg of pure  D9-tetrahydrocannabinol (THC) from gestational day five to post-natal day nine and were examined between PND 40-50. Immunoblotting of hippocampal synaptosomal proteins revealed that PCE altered glutamate receptor levels. To further evaluate if these receptor-level changes translated into functional changes at the cellular level, we recorded whole-cell spontaneous currents from hippocampal pyramidal cells and field activity from hippocampal CA3-CA1 Schaffer collaterals of PCE offspring. Spontaneous postsynaptic currents driven by AMPA and NMDA receptors showed alterations in frequency and amplitude between PCE and control animals. Long-term potentiation, a cellular correlate of learning and memory, within the CA3-CA1 neuronal pathway was also altered in PCE offspring. Our study elucidates the molecular mechanisms of hippocampal-dependent memory deficits associated with PCE.