









































GSR Journal
 

Georgetown Scientific Research Journal

Volume 1 | Edition 2
July 31, 2021

Danya Adams
         ISSN 2767-6420   





GPR40 and Postsynaptic NMDA 
Receptors: A Pair Against

Epilepsy
Vidya Mullangi,* Nikita Shah,* Hyunwook Nam,* Alexa Asch,* 

Lauren Cox, Clarisa Mendoza
*Indicates equal contribution

Volume One 
Edition Two
Spring 2021

 
GEORGETOWN SCIENTIFIC
RESEARCH JOURNAL

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GPR40	and	Postsynaptic	NMDA	Receptors:	A	Pair	Against	
Epilepsy	
	
Vidya Mullangi*, Nikita Shah*, Hyunwook Nam*, Alexa Asch*, Lauren Cox, 
Clarisa Mendoza 
 
*Indicates equal contribution 
Department of Biology, Georgetown University, Washington D.C.  
E-mail: vm491@georgetown.edu, ns1217@georgetown.edu, hn210@georgetown.edu, 
aa2142@georgetown.edu, lec122@georgetown.edu, cem328@georgetown.edu 
https://doi.org/10.48091/gsr.v1i2.19    
   

Abstract 

Epilepsy is a chronic neurological condition characterized by abnormal brain activity, unusual behavior, 
and loss of awareness. One of the most common features is the spontaneous recurrence of unprovoked 
seizures that mainly affect the hippocampus and cortical regions of the brain. Although the exact cause of 
epilepsy is still unknown, a mix of genetic, neurological, and environmental factors play a role. A novel 
study by Yang et al. explores the metabotropic receptor GPR40 which is suspected to be involved in the 
regulation of epileptic seizures, specifically through its modulatory role on NMDA receptors in the central 
nervous system. Their findings suggest that GPR40 induces NMDA receptor endocytosis via direct 
interaction with NR2A and NR2B subunits of postsynaptic NMDA receptors. Through this mechanism, 
NMDA-mediated postsynaptic currents are altered, resulting in reduced seizure-like activity. This review 
article discusses these novel findings which not only shed light on the potential molecular mechanisms of 
epilepsy but also push the scientific community closer to developing a treatment for this disorder.  

Keywords: Epilepsy, GPR40, seizures, NMDA receptors, NR2A and NR2B subunits, excitatory 
postsynaptic currents, cortex, and hippocampus

1. Introduction 
 Epilepsy is a chronic neurological condition 
that affects an estimated one to three percent of the 
population; it is characterized by the spontaneous 
recurrence of unprovoked seizures, seizures that 
occur without apparent triggers.1 Epilepsy can also 
be characterized by abnormal brain activity, 
unusual behavior or sensations, and even a loss of 
awareness, though these are often common 
characteristics of other neurological disorders as 
well.2 Other general symptoms of epilepsy may 
include temporary confusion, uncontrollable 
motor function, loss of consciousness, and even 

psychological symptoms, such as anxiety, fear, or 
deja vu.2  
 The exact cause of epilepsy has not yet been 
determined. However, the neurological disorder 
has been connected to a variety of factors.2 The 
onset of epilepsy has been associated with several 
developmental disorders including autism and 
neurofibromatosis. It has also been associated with 
infectious diseases such as meningitis, acquired 
immunodeficiency syndrome, and viral 
encephalitis. Brain trauma caused by stroke or 
brain tumors can also lead to the onset of epilepsy; 
in fact, stroke is known to be a common cause of 
epilepsy in individuals over thirty-five years old.2 

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Additionally, head trauma and traumatic brain 
injury can play a role in the development of 
epilepsy. Lastly, research has supported links 
between epilepsy and specific genes in the human 
genome. Some genes may contribute to making an 
individual more susceptible to environmental 
conditions that might trigger seizures, making 
genetic influence another factor in the 
development of epilepsy.2   
 The relationship between genetic influence, 
gene expression, and protein synthesis has shed 
light on a new protein, G-protein coupled receptor 
40 (GPR40), that is involved in the regulation of 
epileptic seizures, specifically through its role in 
regulating NMDA receptors in the central nervous 
system.3 The novel study conducted by Yang et al, 
“GPR40 modulates epileptic seizure and NMDA 
receptor function,” investigated the impact of 
GPR40 on epileptic brains, and more specifically, 
how expression of GPR40 affected NMDA 
receptor function and NMDA receptor-mediated 
synaptic transmission. This study determined the 
specific localization of GPR40 in the brain and 
central nervous system, how the upregulation of 
the receptor affects epileptic seizures, and how 
NMDA receptor mediated synaptic transmission 
function is affected, through regulation of specific 
subunits of the NMDA receptor on the 
postsynaptic neuron.3 

 Various antiepileptic drugs (AEDs) have been 
synthesized to combat seizure activity in epileptic 
individuals. A meta-analysis reviewing the efficacy 
of 11 antiepileptic drugs administered to over 900 
patients revealed that pregabalin, tiagabine, and 
vigabatrin yielded the most significant reductions 
in seizures (>50%).5 However, similar meta-studies 
have revealed alternative drugs as the most 
effective, taking factors such as adverse side effects 
and tolerability of the drugs into account. While 
many of these AEDs have adequate efficacy, 30% 
of patients using these drugs continue to 
experience some side effects of the treatment, 
including insomnia, depression, and dizziness.3 
These antiepileptic drugs target 
neurotransmission, specifically to maintain the 
balance of excitatory and inhibitory 

neurotransmission that is normally disrupted in 
epileptic brains.3 For the development of a more 
effective antiepileptic drug that can both treat and 
limit the side effects of epileptic seizures, many 
factors must be taken into account, including the 
neurological root of the disorder. The investigation 
conducted by Yang et al. aims to obtain a deeper 
understanding of the root cause of epileptic 
seizures and the onset of epilepsy.3 These studies 
may contribute to the future development of a 
more effective cure for this chronic neurological 
condition.  
 As aforementioned, epilepsy is characterized 
by excessive and abnormal neuronal activity. The 
precise mechanism is yet to be discovered as 
epilepsy is known to have multiple 
pathophysiological causes including genetic 
mutation, traumatic brain injury, and exposure to 
toxins. However, the imbalance of excitatory and 
inhibitory neurotransmitters is understood as the 
most common mechanism of various epileptic 
seizures.6 To elaborate, seizures are often the result 
of sudden synchronized neuronal signaling and 
changes in inhibitory and excitatory stimulation. 
Many neurotransmitters and hormones such as 
serotonin, norepinephrine, histamine, are involved 
in epilepsy.7 Gamma-aminobutyric acid (GABA) 
and nicotinic acetylcholine (ACh) receptors, in 
particular, have been implicated. Mutations in 
GABA receptors have been shown to cause ER 
stress and ion imbalance, contributing to 
epileptogenesis. Additionally, dysfunctional 
acetylcholine signaling has been shown to 
aggravate inflammation, a key feature of epilepsy.7 

 Although epilepsy can occur in any region of 
the brain, it is known to affect the frontal lobe and 
the temporal lobe most commonly, particularly the 
hippocampus.8 Therefore, studying the regulatory 
mechanisms of neurotransmitters in cortical and 
hippocampal regions of the brain is important in 
furthering our understanding of epilepsy. 
Interestingly, recent studies have found that 
GPR40 plays a role in modulating synaptic 
transmission, especially in the cortex and 
hippocampus.3 Therefore, the Yang et al. study 

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was set out to investigate the role of GPR40 in 
epileptic seizure.3 

2. Description of GPR40 Involvement in Regions 
of the Brain 
 While previous studies have shown that 
GPR40 is expressed in the cortex and 
hippocampus, the precise distribution and 
expression levels are poorly understood.9 The novel 
study by Yang et al., demonstrated the distribution 
and expression levels of GPR40 in both normal 
and epileptic rodent brains through 
immunofluorescence staining.3 This methodology 
revealed that GPR40 was highly expressed in the 
lacunosum moleculare layer and the pyramidal cell 
layer of the hippocampus, while it was not highly 
expressed in the dentate gyrus. The study further 
evaluated the cellular level localization of GPR40 
from a kainic acid (KA) induced temporal lobe 
epilepsy (TLE) model and normal control brain. 
GPR40 was colocalized with microtubule-
associated protein 2 (MAP2; a marker of 
dendrites) and postsynaptic density-95 (PSD95; a 
postsynaptic marker) but not with glial fibrillary 
acidic protein (GFAP; an astrocyte marker) in the 
hippocampus of both the epileptic brain and 
normal control brain.3 These results suggested that 
GPR40 is mostly expressed in postsynaptic 
excitatory neurons but not in astrocytes.3  
 Expression levels of GPR40 in the 
hippocampus of epileptic and nonepileptic tissues 
were compared to validate that GRP40 expression 
is meaningfully correlated with epilepsy.  
Immunofluorescence signals of GPR40 were 
significantly increased in the CA1 hippocampal 
region of the epileptic rodent brain model 
compared to those of the nonepileptic control 
mice. Consistent with this mouse model, high 
GPR40 expression was observed in the human 
neocortex of TLE patients. In the study, the team 
conducted a western blot experiment to further 
validate that GPR40 protein expression increased 
in epileptic rodent brain models compared to 
normal control brains. Congruent with the 
previous results, the epileptic brain models showed 
significantly higher GPR40 expression in the 

cortex and hippocampus compared to the control.3 
Elevated GPR40 levels in epileptic brains suggest 
a possible role of GPR40 in modulating epilepsy. 
 Therefore, the experiments suggest that 
GPR40 may be involved in epilepsy. However, 
further experiments must be conducted in order to 
discover the direct relationship between GPR40 
and epilepsy. If GPR40 directly downregulates or 
upregulates epileptic seizures, then it is crucial to 
further study its regulatory mechanisms and 
signaling pathway.  

3. NMDAR-Mediated GPR40 Signaling 
Modulates Epileptic Seizures 
 Also known as the Free Fatty Acid Receptor 1, 
GPR40 is bound and activated by long, 
unsaturated fatty acids called PUFAs. The existing 
literature has argued that PUFAs may have 
differential effects in the CNS.10, 11 In fact, one 
group in particular, omega-3 PUFAs, has been 
shown to have anticonvulsant effects. A study by 
the University of Toronto's Epilepsy Research 
Program found that various fatty acid chains, 
including ALA, EPA, and DHA, reduced the 
frequency of action potentials and excitatory 
signaling in vitro.10 However, they posited that the 
observed effects were modulated through voltage-
gated Na+ and Ca2+ channels, further supporting 
that seizure-like activity is dependent on a plethora 
of signaling pathways and factors. In contrast, 
other studies present confounding results, showing 
that low doses of certain PUFAs reduce seizure 
frequency whereas increased doses have no 
significant effects on seizure frequency.11 PUFAs 
may therefore act on many target locations, either 
reducing or increasing seizure-like activity. These 
conflicting results reveal the need for further 
research to fully understand the various, complex 
factors that modulate epileptic activity. 

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Figure 1: Activation of GPR40 via KA-induced and 
PTZ kindling models Yields Highest Survival Rates. 
a) Representation of KA-induced experimental 
timeline. After KA injection, mice were treated with 
DMSO, GW9508, or GW1100 (n=6 in each group). 
b) LFP recordings from each treatment group over 5 
minutes and zoomed in of 2 s. c) Corresponding 
frequency recordings of LFP. d-f) Comparing three 
groups in number, duration, and time spent in SLEs. 
g) Using the PTZ model, seizure activity was 
heightened in GW1100 and reduced in GW9508 
groups. h) Highest survival amongst GW9508 group 
and lowest survival amongst GW1100 group (Figure 
taken from Yang et al., 2018). 
 
 Yang et al. discovered that GPR40 activation 
results in a layered cascade of signaling events. 
Overall, GPR40 affected NMDA receptor 
endocytosis by binding to NR2A and NR2B 
subunits found on neuronal membranes. To 
elaborate, the research team needed to confirm 
that GPR40 played a direct, causal role in 
modulating epileptic seizures. In order to 
accomplish this initial goal, they utilized an 
intrahippocampal KA-induced TLE model, 
meaning that KA was injected into mice’s 
hippocampi unilaterally to induce seizures (Figure 
1A). Previous studies have shown that KA, an 
excitatory amino acid, is a useful tool for seizure-
induction because it induces certain seizures that 

are commonly experienced by patients with 
temporal lobe epilepsy.12 Three days after the 
induction of epileptic activity, additional 
compounds were injected daily for one week. 
These treatments included a DMSO control, 
GW9508 agonist, or GW1100 antagonist of the 
target GPR40 receptor. After one-month, local 
field potentials, which were characterized as strong 
electrical signals between neurons, were measured 
(Figure 1B). These measurements reflected both 
the frequency and duration of any seizure-like 
events (SLE’s) experienced by the mice. The 
compiled data revealed that mice injected with the 
GW1100 antagonist experienced more seizure-
like events that lasted longer compared to the 
control (Figure 1D, F). In contrast, mice injected 
with the GW9508 agonist experienced fewer 
seizure-like events that lasted a significantly 
shorter time compared to the control (Figure 1D, 
F).3 

 To confirm their findings, the researchers 
repeated their experiment with a pentylenetetrazol 
(PTZ) kindling model. Like kainic acid, 
pentylenetetrazol, a GABA A receptor antagonist, 
was used to induce convulsive activity in the mice13; 
this model therefore represents the seizure-like 
symptoms experienced by many patients suffering 
with epilepsy. Like the previous model, the mice 
received intracerebroventricular injections of one 
of three treatments: the DMSO control, the 
GW9508 agonist, or the GW1100 antagonist. 
While all three mice groups showed increased 
seizure scores after PTZ treatment, the mice 
treated with GPR40 selective agonist exhibited 
significantly lower seizure scores compared to 
those treated with GPR40 antagonist. As PTZ 
injections continued to be administered, the mice 
treated with the agonist had the highest survival 
rate, while the mice treated with the antagonist 
had the lowest survival rate and were most prone 
to generalized tonic-clonic seizure (GTCS) related 
death (Figure 1G, H). These findings served as a 
key indication that activating or inhibiting GPR40 
receptors directly affects epileptic seizure activity; 
specifically, activating the receptor resulted in 
reduced epileptic activity and an increased chance 

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for survival, while inhibiting the receptor led to 
opposite observed effects.3 

 
Figure 2: Changes in Cell Surface NR2A and NR2B 
Subunit Expression in Hippocampal Tissue Samples 
in GPR40-treated Mice during Epilepsy. After KA 
injection or PTZ treatment, mice were treated with 
DMSO, GW9508, or GW1100 (n=5 in each group). 
a-b) KA model: cell surface and total N2RA and NR2B 
expression was quantified via western blot. c-d) PTZ 
model: cell surface and total NR2A and NR2B 
expression was quantified via western blot. Significant 
differences were observed in both treatment models 
between antagonist and agonist groups. One-way 
ANOVA and Tukey’s Test (Figure taken from Yang et 
al., 2018). 
 
 The next aim was to determine how GPR40 
regulated seizure-like activity. They found that 
GPR40 regulated the functions of NR2A and 
NR2B as well as NMDAR-mediated synaptic 
responses. Interestingly, the different subunits of 
the NMDA receptor are referred to as a 
heterotetrameric assembly. Specifically, the role of 
the NR2 subunit in epilepsy was evaluated by 
determining the impact of GPR40 on NMDAR 
regulation (Figure 2). 
 In order to study the regulation and cell surface 
expression of NR2 subunits, the experimenters 
treated mice with KA and PTZ, then harnessed 
hippocampal slices from these mouse models. 
They quantified total expression and cell surface 
expression of both NR2A and NR2B subunits for 

the GW9508, GW1100, and DMSO groups and 
compared them against a standard control of b-
actin. It was found that when compared to the 
DMSO group, NR2A/B showed no significant 
change in total expression for both the GW9508 
and GW1100 models (Figure 2). However, the 
ratio of surface to total expression of both NR2A 
and NR2B was significantly reduced for the 
GW9508 agonist treatment group whereas the 
opposite results were observed for the GW1100 
antagonist treatment group. (Figure 2). These 
results suggest that GPR40 impacted the cell 
surface expression of both NMDA subunits in the 
hippocampal tissues. 

 
Figure 3. GPR40 Regulates NR2A and NR2B 
Endocytosis, thereby Affecting NMDA-mediated 
Postsynaptic Currents. CA1 Hippocampal neurons 
were isolated from brain tissue treated with endocytosis 
and exocytosis blockers. a-d) Measured NMDAR-
EPSCs after treatment with 0.1 M TeTx or 80 mM 
dynasore (n=5 in each group). Significant difference 
(*P < 0.05) observed between control and treatment 
groups when treated with TeTx. One-way ANOVA and 
Tukey’s Test. e-f) Confocal image and analysis 
showing differences in Alexa 594-transferrin uptake 
between 20 M GW9508 and DMSO treatment groups. 
g-h) Confocal image and analysis showing differences 
in Alexa 594-transferrin uptake between 20 M 
GW1100 and DMSO treatment groups (Figure taken 
from Yang et al., 2018). 
 

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 This finding was further analyzed, shedding 
light on the regulation of GPR40 on the surface 
level expression of NMDARs. This was done 
through the examination of NMDA-EPSCs 
(NMDA-excitatory postsynaptic currents) on 
specific CA1 hippocampal neurons that were 
obtained from brain tissue slices treated with 
endocytosis and exocytosis blockers. Interestingly, 
NMDA-EPSCs amplitudes were decreased in 
GW9508 but increased in GW1100 (Figure 3B). 
However, this effect was not seen in the presence 
of the endocytosis blocker dynasore, suggesting 
that GPR40 regulates MNDA transmission 
through endocytic mechanism (Figure 3B, D).  
 In order to quantify the effect of GRP40 on 
endocytosis, an Alexa-594-transferrin uptake assay 
of cultured neurons that had been previously 
treated with GW9508 and GW1100 was used. 
GW9508 showed an increase in comparison to 
DMSO whereas GW1100 showed a decrease in 
comparison to DMSO, which was seen via the 
levels of uptake/intensity of the fluorescently 
conjugated Alexa 594-transferrin (Figure 3F, H). 
Thus, this confirmed that GPR40 in fact has an 
important role in the regulation of NMDAR 
endocytosis. 
 The molecular mechanism regarding GPR40 
regulation of NMDAR-mediated excitatory 
synaptic transmission has yet to be uncovered, 
however, this study provided some preliminary 
support for GPR40 and NMDA receptor 
interaction. The surface expression of NMDARs 
was shown to have a critical role in NMDAR-
mediated postsynaptic responses, and their 
mislocalization would therefore explain the 
possible pathological impact on epilepsy.  
 An interesting implication from this paper is 
the role that interactions between proteins had on 
the surface cell expression of NMDARs. More 
specifically, the reciprocal co 
immunoprecipitation, a technique that serves to 
precipitate a protein antigen out of a solution via 
the use of a specific protein binding antibody, 
showed that GPR40 directly interacts with NR2A 
and NR2B. Additionally, the activation of GPR40 
led to decreased binding with NR2A/B, while the 

inhibition of GPR40 led to increased binding. 
This supports the idea that GPR40 is therefore 
involved in the regulation of both neuronal 
excitability and epileptic activity. The activation of 
GPR40 is thus thought to decrease epileptic 
seizures in animal models, as well as NMDAR-
mediated postsynaptic transmission, which 
allowed for a new antiepileptic target to be 
established.3 Overall, these results demonstrate 
that GPR40 activation decreases epileptic seizures 
through binding to NR2A/NR2B, inducing 
increased endocytosis of NMDA receptors, and 
therefore affecting NMDAR-mediated 
postsynaptic transmission and excitability. 

4. Conclusion and Future Directions 
 Overall, more research is needed to understand 
the complex interaction between sleep and 
epilepsy. Sleep is a very important factor to 
consider in epilepsy patients and epileptic patients 
need to make sure they have a consistent sleep 
schedule.  
 In summary, Yang et al. found that increased 
GPR40 expression resulted in decreased binding 
to the NMDA receptor subunit NR2B which 
resulted in neuroprotective effects. One potential 
area of future research includes the downstream 
signaling interactions, as they can provide insight 
in the development of treatments.3 In a previous 
study by Frasca et al., NR2B was studied by 
pharmacologically blocking NMDA receptors 
with Ifenprodil.23 Their data suggests that the 
reduction of neurodegeneration during 
epileptogenesis was due to the block of 
excitotoxicity.23 The findings of Frasca et al.23 
apply to the research discussed by Yang et al.3, 
particularly in reference to the NR2B subunit. 
While the Yang study observed the binding of 
GPR40 to NR2B to be a method of NMDA 
receptor regulation, the Frasca study specifically 
examined the role of phosphorylation as a form of 
NR2B and NMDA receptor regulation. These 
two different approaches towards NMDA receptor 
regulation could influence future treatment 
development. The GPR40 and NMDA receptor 
interactions studied by Yang et al. showed an 

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increase in GPR40 expression. The 
phosphorylation of the NR2 subunit of NMDA 
receptors shown by Frasca et al. resulted in reduced 
cell death; perhaps an increase in GPR40 could 
induce the same effects.3, 14 More research is 
required to determine if GPR40 is indeed a 
therapeutic target and can mediate the effects of 
epilepsy. 
 Yang et al. established a connection between 
GPR40 and NMDA receptors, which is a first and 
necessary step in studying this pathway further. On 
a gross anatomy scale, expression of GPR40 is 
localized to the hippocampus and cortex. 
Additionally, they found that GPR40 expression 
increased in epileptic brains compared to non-
epileptic brains. These findings shed light on the 
effects of GPR40 on spine density and NMDA 
signaling amplitude.3  
  All of this further research can significantly 
contribute to the current understanding of 
epilepsy. This disease, characterized by the 
spontaneous recurrence of unprovoked seizures, 
significantly impacts the daily life of those afflicted 
with the condition.1 Furthermore, advancements 
in the understanding of epilepsy can potentially 
shed light on the causes of other symptoms of the 
condition at a molecular level, such as confusion, 
anxiety, and deja vu.1 Hopefully, the findings from 
Yang et al., along with future research on synaptic 
transmission in this field, can help push the 
scientific community one step closer to finding a 
treatment for this disorder.  

Acknowledgements 
 We would like to thank Dr. Katherine 
Maguire-Zeiss for leading our Synaptic 
Transmission course and this paper project in the 
fall of 2020 as well as the Georgetown Biology 
Department. 
 
References 
1. Shneker, B. F., & Fountain, N. B. (2003). 

Epilepsy. Dis Mon, 49(7), 426-78. 
http://doi.org/10.1016/s0011-5029(03)00065-8    

2. Epilepsy. (2020, May 05). Retrieved November 18, 
2020, from https://www.mayoclinic.org/diseases-

conditions/epilepsy/symptoms-causes/syc-
20350093 

3. Yang, Y., Tian, X., Xu, D., Zheng, F., Lu, X., 
Zhang, Y., Ma, Y., Li, Y., Xu, X., Zhu, B., & 
Wang, X. (2018). GPR40 modulates epileptic 
seizure and NMDA receptor function. Science 
advances, 4(10). 

4. Vasilenko, A. V., Onishchenko, L. S., Zhivolupov, 
S. A., Lobzin, S. V., Zabolotskii, N. N., & 
Bodrova, T. V. (2017). The Significance of Sleep 
Deprivation in the Development of Local Epilepsy 
from the Point of View of Neuroplasticity. 
Neuroscience and Behavioral Physiology, 47(9), 1102-
1108. http://doi.org/10.1007/s11055-017-0518-8  

5. Slater, J., Chung, S., Huynh, L., Duh, M. S., 
Gorin, B., McMicken, C., Ziemann, A., & 
Isojarvi, J. (2018). Efficacy of antiepileptic drugs in 
the adjunctive treatment of refractory partial-onset 
seizures: meta-analysis of pivotal trials. Epilepsy 
research, 143, 120-129. 

6. Fukata, Y., & Fukata, M. (2017). Epilepsy and 
synaptic proteins. Current opinion in 
neurobiology, 45, 1–8. 

7. Akyuz, E., Polat, A.K., Eroglu, E., Kullu, I., 
Angelopoulou, E., & Paudel, Y.N.  Revisiting the 
Role of Neurotransmitters in Epilepsy: An 
Updated Review. Life Sciences. 265. 
https://doi.org/10.1016/j.lfs.2020.118826 

8. Stretton, J., & Thompson, P. J. (2012). Frontal 
lobe function in temporal lobe epilepsy. Epilepsy 
research, 98(1), 1–13.  

9. Zamarbide, M., Etayo-Labiano, I., Ricobaraza, A., 
Martínez-Pinilla, E., Aymerich, M. S., Luis 
Lanciego, J., Pérez-Mediavilla, A., & Franco, R. 
(2014). GPR40 activation leads to CREB and 
ERK phosphorylation in primary cultures of 
neurons from the mouse CNS and in human 
neuroblastoma cells. Hippocampus, 24(7). 

10. Taha, A.Y., Burnham, W.M., & Auvin, S. (2010), 
Polyunsaturated fatty acids and epilepsy. Epilepsia, 
51, 1348-1358. https://doi.org/10.1111/j.1528-
1167.2010.02654.x   

11. DeGiorgio, C. M., Miller, P. R., Harper, R., 
Gornbein, J., Schrader, L., Soss, J., & Meymandi, 
S. (2015). Fish oil (n-3 fatty acids) in drug 
resistant epilepsy: a randomised placebo-controlled 
crossover study.  Journal of neurology, neurosurgery, 
and psychiatry, (86)1, 65-70. 
http://doi.org/10.1136/jnnp-2014-307749  

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12. Farivar, T., Nassiri, M., Johari, P., Najafipour, R., 
& Haijali, F. (2016). The Effects of Kainic Acid-
Induced Seizure on Gene Expression of Brain 
Neurotransmitter Receptors in Mice Using RT2 
PCR Array. Basic Clinical Neuroscience.  

13. Dhir, A. (2012). Pentylenetetrazol (PTZ) kindling 
model of epilepsy. Current Protocols in Neuroscience. 
https://doi.org/10.1002/0471142301.ns0937s58  

14. Frasca, A., Aalbers, M., Frigerio, F., Fiordaliso, F., 
Salio, M., Gobbi, M., ... & Di Luca, M. (2011). 
Misplaced NMDA receptors in epileptogenesis 
contribute to excitotoxicity. Neurobiology of disease, 
43(2), 507-515.   
  

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Danya Adams
  
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	Table of Contents
	Letter From the Editors
	An Investigation Into the Mathematics of DecryptionTechniques in RSA Encryption,With an Implementation in Python
	GPR40 and Postsynaptic NMDA Receptors: A Pair Against Epilepsy
	The Burn Behind the Bullet: Understanding Black Mothers’ Experiences After Losing a Child to Gun Violence in Washington,DC-Baltimore City Metropolitan Region
	Cancer Models to Defeat Therapy Resistance in Pancreatic Ductal Adenocarcinoma
	About the Authors
	Meet the Staff
	Acknowledgements



