Drinking during pregnancy leads to a range of mental and physical defects in the child which is known under an umbrella term called Fetal Alcohol Spectrum Disorder (FASD) After observing the FASD model in rats, moderate prenatal alcohol exposure demonstrated significant deficits in both learning and memory tasks, as well as reduced synaptic plasticity. Our previous studies have shown that these plasticity deficits are associated with reduced ILK activity and increased GluR2 AMPA receptors at the synapse. From this, we hypothesized that enhancing the ILK activity might restore the behavioural and plasticity deficits that were seen in the FASD model. 7,8-dihydroxyflavone (7,8-DHF) acts as a potent agonist for Brain Derived Neurotropic Factor (BDNF) receptor Tyrosine receptor kinase B (TrkB). Therefore, we hypothesize that intraperitoneal administration of 7,8-DHF in FASD rats, during the early postnatal days, may restore the alcohol associated memory deficits through increasing ILK activity and improve synaptic plasticity. Hence, we investigated the neuroprotective effects that 7,8-DHF in the FASD model. 7,8-DHF led to a significant improvement in the behavioural deficits associated with FASD by causing a significant increase in the ILK activity.