## 1 Introduction  
Essential oils (EOs) are usually extracted from plants and are used for aromotherapy, which is an alternative medicine that demonstrates the healing effect to the aromatic compounds presented in the oil [1; 2]. Although its therapeutic potential remains controversial, the usage of essential oil has been increasingly popular in the general population [3]. Many EOs are currently being presented to showcase a wide range of benefits; two important EOs are the Citronellol and Geraniol oils. Citronellol oil is obtained from different species of lemongrass (_Cymbopogon_) and is mostly composed of Citronellol and Geraniol, which are found in over 70 other plants [4]. To the contrary, Geraniol oil is composed of different extracted molecules from the essential oils of various plants, including rose, geranium, and palmaroas species [4; 5; 6; 7]. The health benefits of Citronellol include antibacterial, antidepressant, antispecific, antispasmodic, anti-inflammatory, deodorant, diaphoretic, diuretic, febrileuge, fungicidal, insect repellent, stomachic, stimulant, tonic, and vermifuge effects. Although Geraniol is composed of a combination of plants, its health benefits are of similar to those observed by Citronellol oil [5; 6; 7]. Accumulating evidence suggests that both of these oils have a calming effect and reduce anxiety, stress, and depression, yet their neuroprotective properties remain obscure [3; 6]. Hence, the current study evaluates these EOs for neuroprotective qualities to the activity of the \(\alpha\)-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor, AMPARs. AMPARs are part of the ionotropic glutamate receptor family (iGluRs) that respond to glutamate. These receptors are responsible for the majority of the fastest excitatory neurotransmission and play a significant role in important brain activity, such as learning and memory formation [8; 9]. However, excessive AMPARs have been associated with neurotoxicity, which is linked to various neurodegenerative diseases. An increasing body of evidence suggests the progression and pathogenesis of several diseases are related to the mechanism of neuronal death caused by excitotoxicity [10]. Thus, glutamate-induced excitotoxicity has been implicated in many different neurological disorders, such as epilepsy, ischemia, amyotrophic lateral sclerosis (ALS), and Alzheimer's disease (AD) [11; 12]. In an attempt to treat various chronic neurodegenerative disorders, multiple studies researched the possibilities of potential AMPAR antagonists to reduce the excitotoxicity [8; 13]. In fact, due to drug resistance, a new target for anti-epileptic and anti-seizures is towards AMPAR inhibition, precisely drugs that act as non-competitive inhibitors [12; 13; 14; 15; 16]. However, many of the researched antagonists fail at the clinical trials due to low efficacy or severe side effects, such as respiratory depression, sedation, tolerance, dependence, and extrapyramidal symptoms [14]. Moreover, many of the possible drug candidates for AMPARs possess selectivity towards specific AMPAR subunits, which fails to be effective in many diseases, such as ALS [13]. Research is currently fixated on the neuroprotective properties of various essential oils and natural components to counteract undesired side effects [17; 18; 19; 20]. The current study investigates the possible mechanism for such an effect in AMPAR inhibition. Moreover, through a natural approach, we aim to investigate the potential possibility of these EOs on inhibiting the activity of AMPARs and provide a possible drug candidate for diseases associated with excessive AMPAR activation. Equally as important, the results of this study shed light on the protein-receptor interaction and allow a better understanding of AMPARs. The inhibition of AMPARs was calculated by using an electrophysiological approach to record the whole-cell current (patch clamp), with and without the administration of EOs into human embryonic kidney cells HEK293.