## 4 Discussion  
The excessive activation of AMPARs has been associated with numerous neurological diseases; as a result, has been the target of many drugs. However, only one pharmaceutical drug is currently on the market, and is known as perampanel. This drug is primarily used as an antiepileptic drug, yet has numerous serious side effects, such as depression, anxiety, paranoia, weight gain, and joint and back pain [21]. In response, the current study investigates two conventional essential oils; the Citronellol and Geraniol oils as possible AMPAR antagonist. In an attempt to reduce the side effect seen from perampanel, these oils have been documented to be antidepressants, anti-inflammatory, diuretics, etc. Hence the result of the study indicates that not only do they inhibit AMPARs but provide a natural antagonist of no side effects. In the same manner as the reduction in peak current, the desensitization and deactivation rates also decreased, insinuating the action of EOs target all biophysical properties of the AMPAR subunits in the same way. The level of inhibition between the EOS was distinct as the Citronellol oil inhibited AMPARs subunit by four folds while the Geraniol oil inhibition was by only three-fold. Moreover, the inhibition between AMPAR subunits was also biased in that specific subunits were more susceptible to inhibition than others hence, the AMPAR subunit that was significantly impacted the most was GluA1 followed by its heteromeric subunit GluA1/A2, then GluA2 and finally GluA2/3. Both oils portrayed the same bias to specific AMPAR subunits, suggesting the action of these oils is similar and target the same antagonist site. However, due to the discrepancy seen in inhibition, the Citronellol is a more favorable and stable antagonist for AMPARs than the Geraniol oil. Although both oils favor specific AMPAR subunits, they remained to significantly inhibit all tested subunits, which is critical significance because unlike Talampanel [22] that failed in clinical trials, due to its effectiveness on specific AMPAR subunits, these oils deploy their neuroprotective properties on all AMPARs. Finally, the inhibition of both  
Figure 3: Effect of oils and compounds on AMPAR Deactivation. (**A**). The graphical representation that summarizes the weighted time constants for deactivation (\(\tau_{\text{W}}\) deact) for the whole cell recordings of all AMPARs subunits, conducted at \(-60\) mV, pH 7.4, and 22 \({}^{\circ}\)C, upon 1 ms application of 10 mM glutamate alone (black), glutamate + Citronellol (white), and from glutamate + Geraniol (grey). (**B**). Pairs of representative whole-cell current traces from GluA1 channels (most significant) expressed in HEK-293 cells in the absence (left) and presence (right) of Citronellol oil. Data shown are mean \(\pm\) SEM; n = 4 (number of patch cells in the whole-cell configuration). A one-way ANOVA test was used to measure the significance: \({}^{*}p<0.05\); \({}^{**}p<0.01\); \({}^{***}p<0.001\); ns, not significant. essential oils was irrelevant to glutamate concentration, a suggestion they act as noncompetitive inhibitors. Due to excessive concentration of glutamate and as a result over activation of AMPARs, noncompetitive inhibitors are a significantly essential and desirable target in drug synthesis to treat the disease associated with AMPARs. The administration of multi-components or single essential oils or their constituents in conventional medicine, complementary alternative medicine, folk medicine, and aromatherapy has been known for a long time, and its relevance is steadily growing [16; 17; 18]. In the last few years, many scientific investigations were established to assess the effectiveness and the mechanisms of action of these compounds on the central nervous system [19; 23; 24]. The results of the current study demonstrate the tested EOs implement their calming effects by directly inhibiting AMPARs but also reducing the desensitization and deactivation rates.