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Blockade of Rostral Ventrolateral Medulla (RVLM) Bombesin Receptor Type 1 Decreases Blood Pressure and Sympathetic Activity in Anesthetized Spontaneously Hypertensive Rats

Izabella S. Pinto, Aline A. Mourão, Elaine F. da Silva, Amanda S. Camargo, Stefanne M. Marques, Karina P. Gomes, James O. Fajemiroye, Angela A. da Silva Reis, Ana C. S. Rebelo, Marcos L. Ferreira-Neto, Daniel A. Rosa, André H. Freiria-Oliveira, Carlos H. Castro, Eduardo Colombari, Diego B. Colugnati, and Gustavo R. Pedrino

Bombesin (BBS) is an extract from a frog that is said to activate bombesin receptors as well as bombesin-like peptides. These are distributed in the central nervous system (CNS) as well as cardiac and respiratory systems. Administration of BBS is said to improve breathing as well as increase blood pressure, etc. Injection of BBS in normal rats is said to cause sympathoexcitation and administration of its antagonist decreased this response. The role of the rostral ventrolateral medulla (RVLM) in this response is not well understood even though it is said to regulate blood pressure and sympathetic tone. Therefore, this study was designed to understand whether an injection of BBS in the RVLM would affect cardiac responses and sympathoexcitation in normotensive and spontaneously hypertensive rats (SHR). Male Wistar normotensive as well as SHR were used to carry out this study. The results suggested that the injection of BBS into the RVLM led to sympathoexcitation with an increase in blood pressure in the normotensive as well as SHR. The use of an antagonist (blocking BBS type 1 receptor) decreased the mean arterial pressure and the resting sympathetic nerve activity in the SHR but not the normal tension rats. the results suggest that BBS can cause sympathoexcitation and maintain a higher level of mean arterial pressure in SHR by activating the RVLM.

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4889888/

Year: June 2016

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Hydrogen sulfide in the RVLM and PVN has no effect on cardiovascular regulation

Eloise Streeter, Mohammad Al-Magableh, Joanne Louise Hart, and Emilio Badoer

Hydrogen sulfide (H2S) is known to exert several effects on the body. It is said to have anti-oxidant, neurological, cardiovascular as well as anti-inflammatory effects. It has been known to have cardioprotective effect as well as act as a vasodilator. Injection of hydrogen sulfide in the brain has been known to increase blood pressure (BP). Sodium hydrogen sulfide (NaHS) is a hydrogen sulfide donor. Its injection into the rostral ventrolateral medulla (RVLM) which regulates the blood pressure is not properly understood. This study was designed to find the effects of H2S on the brain regions in normotensive and hypertensive conditions. The lumbar sympathetic nerve activity (LSNA), BP and heart rate were investigated after injecting of NaHS in the RVLM and the paraventricular nucleus (PVN). Male Wistar Kyoto were normotensive rats and spontaneously hypertensive (SHR) were used during this study. The results suggested that H2S did not have a significant effect on any of the parameters like LSNA, BP in both the types of rats and in both the RVLM and the PVN. The use of the H2S inhibitor also failed to have any effect. Thus, scientists have concluded that H2S does not have an important role in the PVN and RVLM for the short-term regulation of BP, HR, and LSNA.

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3171070/

Year: September 2011

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Role of Nitric Oxide Synthase Uncoupling at Rostral Ventrolateral Medulla in Redox-Sensitive Hypertension Associated With Metabolic Syndrome

Kay L.H. Wu, Yung-Mei Chao, Shiow-Jen Tsay, Chen Hsiu Chen, Samuel H.H. Chan, Ima Dovinova, and Julie Y.H. Chan

Metabolic syndrome comprises of an individual suffering from 3 or more metabolic disorders like obesity, hypertension, hypercholesterolemia, etc. This is highly prevalent worldwide and is related to hypertension and oxidative stress. The RVLM is the area contributing to sympathetic nerve activity owing to the presence of the sympathetic neurons. Reactive oxygen species (ROS) have several sources and are products of metabolism within the cells. In the RVLM, generation of ROS plays an important neural role in hypertension. Nitric oxide synthase (NOS) is said to increase ROS within the brain. In this study, the scientists tried to identify the source of the ROS and its interaction with nitric oxide synthase (NOS) in the RVLM in combination with hypertension. Male Sprague Dawley rats were used for this study and were divided into two groups. One was fed with normal diet and the other was fed with a high-fructose diet (HFD) to mimic obesity and metabolic syndrome. The results suggest that HFD causes an increase in the amount of ROS within the RVLM as compared to NOS. This, however, leads to the production of oxidative stress within the RVLM causing sympathoexcitation and hypertension in the presence of metabolic syndrome.

Source: https://www.ahajournals.org/doi/full/10.1161/HYPERTENSIONAHA.114.03777

Year: May 2014

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Direct effects of Glucose, Insulin, GLP-1, and GIP on bulbospinal neurons in the rostral ventrolateral medulla in neonatal wistar rats

NAOKI OSHIMA, HIROSHI ONIMARU, HIDEHITO MATSUBARA, TAKAHIRO UCHIDA, ATSUSHI WATANABE, TOSHIHIKO IMAKIIRE, YASUHIRO NISHIDA AND HIROO KUMAGAI

In this study the author hypothesised that the bulbospinal neurons in the RVLM are affected by the levels of glucose, insulin, glucagon like peptide-1 [GLP-1] or glucose-dependent insulinotropic peptide [GIP] in diabetes mellitus patients and this may be the underlying cause for the development of hypertension.

For this purpose, whole cell patch clamp technique was used to examine the changes in the membrane potentials of bulbospinal RVLM neurons during superfusion with all these in neonatal wistar rats.

Brainstem-spinal cord preparation was used for the experiments. Low level of glucose infusion stimulated the bulbospinal neurons in the RVLM. While insulin infusion depolarised almost all the neurons and GLP-1 & GIP caused hyperpolarization in the RVLM neurons.

Histological examination was done to identify the specific receptors which was identified as GLUT-3 for glucose. Also for others specific receptors could be identified. All these results suggest that the low level glucose stimulates bulbospinal neurons in RVLM via specific receptors in the neurons

Also increase in insulin and decrease in GLP-1 & GIP may also cause hypertension by stimulating RVLM neurons by their specific receptors.

Mahesh

Year: 2017

Source: https://www.ncbi.nlm.nih.gov/pubmed/28062192

In renovascular hypertension, TNF-a type-1 receptors in the area postrema mediate increases in cardiac and renal sympathetic nerve activity and blood pressure

Willian S. Korim, Khalid Elsaafien, Jeremy R. Basser, Anthony Setiadi, Clive N. May, and Song T. Yao

The main aim of this study is to identify the role of TNF-a in area postrema that causes sympathoexcitation and increase in blood pressure. For this purpose, rats with renovascular hypertension were used.

In these rats TNF-a receptor 1 (TNFR1) expressing neurons in AP were constantly activated and injection of TNFR1 neutralising antibody into AP returned BP to normal levels.

In normotensive rats, nanoinjection of TNF-a increased BP and sympathetic nerve activity in heart and also in kidneys which was abolished by prior injection of TNFR1 neutralising antibody.

All these results suggest that the TNF-a and its receptor TNFR1 play an important role in causing blood pressure and increasing cardiac and renal sympathetic nerve activity.

Mahesh

Year: 2019

Source: https://www.ncbi.nlm.nih.gov/pubmed/30358805

Adipocyte deficiency of ACE2 increases systolic blood pressures of obese female C57BL/6 mice

Robin Shoemaker, Lisa R. Tannock, Wen Su, Ming Gong, Susan B. Gurley, Sean E. Thatcher, Frederique Yiannikouris, Charles M. Ensor and Lisa A. Cassis

The main hypothesis of this study is that the deficiency of adipocyte ACE2 contributes to obesity-hypertension of females. For this purpose, male and female mice with adipocyte ACE2 deficiency or littermate controls were fed a low (LF) or a high fat (HF) diet for 16 weeks and blood pressure was quantified by radiotelemetry.

HF diet mice were then given acute ANGII injection blood pressure was recorded. A proof-of-principle study in obese transwomen in which systemic angiotensin peptides and blood pressure were quantified prior to and after 12 weeks of gender-affirming 17β-estradiol hormone therapy.

Adipocyte ACE2 had no effect on the development of obesity but HF diet increased the systolic blood pressure in males and females. Obese females with adipocyte ACE2 deficiency had augumented SBP increase to acute AngII injection.

In humans, plasma 17β-estradiol concentrations increased in obese transwomen administered 17β-estradiol and correlated positively with plasma Ang(1-7)/AngII balance, and negatively to SBP.

All these results suggest that the adipocyte ACE2 deficiency can increase the SBP in obese females.

Mahesh

Year: 2019

Source: https://bsd.biomedcentral.com/articles/10.1186/s13293-019-0260-8

Exposure to mild stress and brain derived neurotrophin factor (BDNF) immunoreactivity in the hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei: Comparison between aged and adult rats

Ewa Badowska-Szalewska, Beata Ludkiewicz, Rafał Krawczyk, and Janusz Morys

The hypothalamic supraoptic nucleus (SON) and paraventricular nucleus (PVN) are associated with stress and stress-related response. Their functions relate to the brain-derived-neurotrophin-factor (BDNF). BDNF stimulates the synthesis of neuropeptides in the hypothalamus. It plays an important role in the development and survival of neurons. BDNF is also involved in stress response by involving in the activity of the hypothalamic-pituitary-adrenal (HPA) axis via the SON and the PVN. A decrease in the activity of BDNF causes cell death, especially during aging. The interaction between stress, aging, and BDNF in the neurons of the hypothalamus has not been evaluated much. This study was designed to study the effects of emotional stressors on the amount of BDNF immunoreactive (BDNF-ir) neurons in the PVN and SON.

Adult (90-day old) and aged (720-day old) male Wistar Hannover rats were used for this study. They were divided into two groups of control and experiment each. The control groups were not stressed and were handled just for a few minutes by a handler. The experiment group was exposed to acute or chronic stressors like the forced swim test and the high light open field test. The acute stimulation was for the duration of 15 to 20 minutes once while the chronic test was conducted once a day for 21 days in 15 to 20 minutes sessions. The results showed that the forced swim test did not change the level of BDNF-ir while the high light open field test altered the levels of this protein in both the old and adult rats. Aging was not a factor that caused a change in the level of BDNF in the PVN or SON. So, the decrease in BDNF due to age must be through some other pathway.

Source: https://www.ncbi.nlm.nih.gov/pubmed/27565677

Year: August 2016

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Distribution of D1 and D2 receptor- immunoreactive neurons in the paraventricular nucleus of the hypothalamus in the rat

Xuerui Ran, Yanli Yang, Yamei Meng, Yong Li, Li Zhou, Zhiyong Wang, and Jinxia Zhu

The paraventricular nucleus (PVN) is one of the most important parts of the brain which is divided into two different parts; one containing the magnocellular subnuclei, and the other containing the parvicellular subnuclei. The former synthesizes vasopressin (VP) and oxytocin (OT) and mostly work via the posterior pituitary. The latter synthesizes thyrotropin-releasing hormone (TRH) and corticotropin-releasing hormone (CRH) which are released from the axons into capillaries of the hypothalamo-hypophyseal system. Hence, the PVN is very important in regulating the body homeostasis.

Dopamine is an important neurotransmitter which regulates behavior, locomotion, cognition, and even endocrine functions. In Parkinson’s disease, there is a loss in dopaminergic neurons along with metabolic abnormalities like digestive dysfunction, olfactory disorders, etc. Dopaminergic receptors are classified into D1-like receptors comprising of D1 and D5 receptors while D2-like receptors comprise of D2, D3, and D4 receptors. Dopamine receptors affect the blood pressure (BP) through VP and OT and therefore the present study was designed to identify the localization of D1-like and D2-like receptors in the PVN and their response to the VP and OT. Twenty adult Sprague Dawley rats were used for this experiment and they were anesthetized, their left ventricle was pumped with 4% formaldehyde to perfuse all the vessels in their bodies. The results showed that D1-like and D2-like receptors were present in each subnucleus of the PVN, but the D1-like receptors were more abundant. Both these receptors coexist with VP and OT providing important evidence for the dopamine receptor function in the PVN.

Source: https://www.ncbi.nlm.nih.gov/pubmed/31018158

Year: April 2019

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Superoxide anions mediate the effects of angiotensin (1-7) analog, alamandine, on blood pressure and sympathetic activity in the paraventricular nucleus

Juexiao Gong, Yihui Shen, Peng Li, Kun Zhao, Xuguan Chen, Yong Li, Yanhui Sheng, Bin Zhou, and Xiangqing Kong

Sympathetic nerve activity (SNA) is said to increase in a variety of diseases and spontaneously hypertensive rats (SHRs) also demonstrate this activity. Hypertension is caused due to this and sympathetic denervation is said to negatively influence hypertension. The paraventricular nucleus in the hypothalamus is the main area controlling the sympathetic nerve activity and arterial pressure through the rostral ventrolateral medulla and the spinal cord and the renin-angiotensin system (RAS) regulates them with the help of the different Angiotensins (1-7 and II). a new peptide has been identified as a member of the RAS family which is vasoactive in nature called alamandine. This is similar in structure to the Angiotensins and this study was carried out to understand its function in the regulation of blood pressure and sympathetic nerve activity.

For this experiment, 13-14wk old male Wistar-Kyoto rats were used along with SHRs. The animals were anesthetized, and their right carotid artery was cannulated and connected to a pressure transducer to continuously record their blood pressures. The left renal sympathetic nerve was identified, and the renal sympathetic nerve activity was also recorded. The PVN was bilaterally microinjected with alamandine during the experiment which was confirmed by using a dye, Evans Blue. The results showed that alamandine increased the blood pressure and SNA in the PVN by increasing the superoxide anions. This is seen in both types of rats.

Source: https://www.ncbi.nlm.nih.gov/pubmed/31199949

Year: June 2019

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Senescence marker protein 30 inhibits angiotensin II-induced cardiac hypertrophy and diastolic dysfunction

Tomofumi Misaka, Satoshi Suzuki, Makiko Miyata, Atsushi Kobayashi, Akihito Ishigami, Tetsuro Shishido, Shu-ichi Saitoh, Isao Kubota, Yasuchika Takeishi

The author wants to test the hypothesis that up-regulation of SMP30 inhibits cardiac adverse remodeling in response to angiotensin II. For this purpose the author uses a transgenic mice developed with overexpression of cardiac SMP30 gene and also used a wild type control.

They were continuously infused with Angiotensin II @ 800ng/kg/min. after 14 days it was shown that the heart weight and the left ventricular weight was lower in transgenic mice eventhough the blood pressure eleveated similarly in both the groups.

Cardiac hypertrophy and diastolic dysfunction were prevented and the degree of cardiac fibrosis was less in transgenic mice when compared to wild type mice. Angiotensin II-induced generation of superoxide and subsequent cellular senescence were attenuated in transgenic mouse hearts compared with wild type mice.

All these results suggested that SMP30 has a cardio-protective role with anti-oxidative and anti-aging effects and could be a novel therapeutic target to prevent cardiac hypertrophy and remodeling due to hypertension.

Mahesh Kumar Sivasubramanian

Year: 2013

Source: https://www.sciencedirect.com/science/article/pii/S0006291X13013181

Hypertension Induces Somatic Cellular Senescence in Rats and Humans by Induction of Cell Cycle Inhibitor p16INK4a

Jens H. Westhoff, Karl F. Hilgers, Mario P. Steinbach, Andrea Hartner, Bernd Klanke, Kerstin Amann, Anette Melk

This study shows that the elevated blood pressure markedly induced p16INK4a expression in rat kidneys and hearts, as well as in human kidneys. In kidneys from deoxycorticosterone acetate-salt–treated (DOCA) rats, p16INK4a induction was found in tubular, glomerular, interstitial, and vascular cells and correlated with the typical histopathologic features of hypertensive target organ damage.

Also it was correlated with phospho-p38, a positive upstream regulator of p16INK4a expression. P16 expression was found in myocardium and cardiac arteries. Antihypertensive medications like hydrochlorothiazide, hydralazine, and reserpine attenuated all these changes in the kidneys of DOCA rats.

p16INK4a was also observed in kidneys from hypertensive transgenic rats and was prevented by the angiotensin II type 1 receptor blocker losartan. In human kidney biopsies showing hypertensive nephrosclerosis, increased p16INK4a expression was found compared with age-matched normotensive control subjects.

All these results suggests that hypertension induces cellular senescence via p16INK4a, possibly through p38, thereby contributing to hypertensive target organ damage.

Mahesh Kumar Sivasubramanian

Year: 2008

Source: https://www.ncbi.nlm.nih.gov/pubmed/18504326

Pressure-Induced Cellular Senescence: A Mechanism Linking Venous Hypertension to Venous Ulcers

Andrew C. Stanley, Nathanial N. Fernandez, Karen M. Lounsbury, Kim Corrow, Turner Osler, Christopher Healey, Patrick Forgione, Steven R. Shackford, and Michael A. Ricci

The main hypothesis of this study is that neonatal fibroblasts (NNF) cultured under elevated pressure will demonstrate premature aging and that this effect will be augmented by an inflammatory mediator, transforming growth factor beta (TGF-b).

A unique pressure incubator was used to culture NNF at atmospheric pressure (ATM), ATM - 30 mmHg, ATM - 60 mmHg, and ATM -120 mmHg. Some pressure-exposed NNF were also cultured with TGF- b (1 ng/ml). Growth rate was assessed by flow cytometry and senescence was identified by SA-b-Gal Staining.

NNF cultured at ATM - 60 mmHg and ATM - 120 mmHg showed increased SA--Gal activity (P < 0.05), and reduced growth rates (P < 0.05) at 11 days. These effects were not seen at ATM - 30 mmHg. NNF grown with TGF- did not show augmented SA-b-Gal staining.

All these results suggests that pressure elevations result in altered cell function and accelerated aging that may contribute to the slowed healing seen in patients with venous insufficiency.

Mahesh Kumar Sivasubramanian

Year: 2005

Source: https://www.ncbi.nlm.nih.gov/pubmed/15734488

Astrocyte Senescence as a Component of Alzheimer’s disease

Rekha Bhat, Elizabeth P Crowe, Alessandro Bitto, Michelle Moh, Christos D. Katsetos, Fernando U. Garcia, Frederick Bradley Johnson, John Q. Trojanowski, Christian Sell, Claudio Torres

The main aim of this study is to determine whether the astrocyte senescence happens in AD and its significance. For this purpose the presence of senescence astrocytes was measured using p16INK4a and MMP1 in the brain tissue if aged and AD patients. It is shown that the p16INK4a was significantly increased in aged peoples when compared with the foetal samples.

Also it is shown that the frontal cortex of AD patients have significantly increased p16INK4a positive senescent astrocytes when compared with non AD age matched adults and foetal controls.

Also increased MMP1 correlated with the p16INK4a senescent astrocytes. The senescent astrocytes are also shown to produce increased cytokines like interleukin 6 (IL-6) regulated by p38MAPK. All these results suggests that the increased accumulation of p16INK4a senescent astrocytes may play a role in AD.

Mahesh Kumar Sivasubramanian

Year: 2012

Source: https://www.ncbi.nlm.nih.gov/pubmed/22984612

Spontaneously hypertensive rats exhibit higher sensitivity to ethanol induced hypotensive effects: Role of NMDA receptors and nitric oxide in rostral ventrolateral medulla

Hsun-Hsun Lin, Tz-Ting Cheng, Hsuan Lo, Yen-Chang Lin, Chih-Chia Lai

The main aim of this study is to examine the effects and mechanisms of acute administration of ethanol on BP in hypertensive and normotensive rats. Ethanol was given by intraperitoneal injection and BP was measured in conscious and urethane anaesthetized rats. Intraperitoneal (i.p.) injection of ethanol caused a significant decrease in BP in free-moving or in anesthetized SHRs but not in WKYs.

A higher dose of ethanol also caused the same effect in SHR and WKY rats but it was more significant in the SHRs. Bilateral microinjection of nitric oxide synthase (NOS) inhibitors or glutamatergic NMDA receptor antagonists into the RVLM 5 min after administration of ethanol significantly inhibited the ethanol-induced depressor effects in SHRs.

The NOx content in the RVLM areas 30 min after administration were significantly increased in SHRs, but not in WKYs. All these results showed that SHRs were more sensitive to ethanol-induced hypotensive effects than WKYs.

Mahesh Kumar Sivasubramanian

Year: 2018

Source: https://www.sciencedirect.com/science/article/pii/S074183291730993X

Cholesterol sulfate alters astrocyte metabolism and provides protection against oxidative stress

Jude Prah, Ali Winters, Kiran Chaudhari, Jessica Hersh, Ran Liu, Shao-Hua Yang

The main aim of this study is to examine the neuroprotective role of Cholesterol sulfate (CS) as well as its role in brain energy metabolism. For this purpose, primary astrocyte prepared from the cortex of postnatal day 0–2 C57BL/6 pups and a hippocampal HT-22 cell line were used.

CS protected HT-22 cells against glutamate and rotenone-induced cell death. Treatment of CS decreased glutamate-induced increase of total ROS levels, mitochondrial membrane potential collapse, and rescued cells from apoptosis.

CS increased astrocyte ATP production and inhibited AMPK pathway. CS also significantly increases the mitochondrial oxygen consumption rate but has no effect on extracellular acidification rate although there was an increase in lactate production by the cells. Additionally, CS activates the Akt/Bcl2 pathway.

All these results shows that CS modulates brain energy metabolism and its neuroprotective effects might be due to the activation of Akt signaling or its ability to decrease reactive oxygen species production.

Mahesh Kumar Sivasubramanian

Year: 2019

Source: https://www.sciencedirect.com/science/article/pii/S0006899319304329?via%3Dihub

Impact of astrocyte and lymphocyte interactions on the blood-brain barrier in multiple sclerosis

X.-B. Yan, Y.-F. Zhao, Y.-M. Yang, N. Wang, B.-Z. He, and X.-T. Qiu

Multiple sclerosis (MS) is a demyelinating disease of the central nervous system (CNS). The blood-brain barrier (BBB) is a selective molecular transport barrier which separates the CNS from the rest of the circulatory system. This barrier controls the microenvironment within the CNS which gets disturbed in case of damage to the BBB. This damage to the BBB can happen during MS.

Forkhead box P3 (Foxp3) is a gene associated with transcription factors. Mutations within this gene can cause severe autoimmune disorders like MS. MS does not have specific genetic markers but, with the combination of other markers, Foxp3 can be a specific enough marker for MS. The interactions between the astrocytes and the lymphocytes (LCs) at the BBB are not yet fully understood. Primary cell cultures of rat brain microvascular endothelial cells (rBMECs) are used as an invitro model for the BBB and simulates an invitro microenvironment. Nowadays, new BBB models which are primary astrocytes co-cultured with rBMECs are better than the old BBB models as the exhibit better permeability and transendothelial electrical resistance (TEER).

In the present study, rBMECs, and astrocytes from the rat brain were co-cultured together to establish new in-vitro BBB models to investigate the effects of the LCs on the BBB. The TEER and permeability of these were also estimated. The levels of the inflammatory cytokines were also studied. The current study also generated a three-culture model consisting of rBMECs, LCs, and astrocytes to study the pathogenesis of MS. The triculture model exhibited higher levels of MMP-2 and reductions in the levels of IFN-γ and IL-17 which is a result of LCs-astrocytes interactions. This current model provides an MS model which can be studied in the future for therapeutic interactions with MS.

Source: https://www.sciencedirect.com/science/article/pii/S0035378717308020

Year: April 2019

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Aqueous extract of Launaea acanthodes induces glutamate uptake and GABA release in astrocyte cell culture via a ROS scavenging mediated process

Hamid Kasnavi Yazdi, Mohammad Fazilati, Raheleh Rahbarian, Gholamhossein Riazi, and Habibollah Nazem

Epileptic activity in the brain occurs due to many factors. Of all the neurotransmitters in the brain, glutamate and gamma-aminobutyric acid (GABA) is responsible for this activity. Although a lot of studies have been done on these neurotransmitters, to date their exact mechanisms are not known. Reactive astrocytes are those that are said to protect the brain from epilepsy. Increase in glutamate and decrease in the circulating levels of GABA can cause firing and excitatory activity of the brain. This can lead to several brain dysfunctions.

Launaea acanthodes (LA) is a medicinal plant whose extract as green tea is used for the treatment of mental disorders. It is said to have anti-convulsant, antioxidant activity. This study was designed to study the effect of LA on the release of GABA and glutamate from the astrocytes.

The astrocytes in the cell culture were treated with different concentrations of LA extract and the levels of GABA and glutamate were estimated from the cell culture with high-performance liquid chromatography (HPLC). The results showed that LA had a therapeutic effect on epileptic activity in the brain. It caused an increase in the reuptake of glutamate and enhanced the release of GABA at concentrations lesser than 3 mg/ml. This shows that LA can reduce the epileptic activity in the brain by reducing the excitatory activity of the brain and can be a potential therapeutic target which could help because of its anti-epileptic ability.

Source: https://www.ncbi.nlm.nih.gov/pubmed/28238867

Year: February 2017

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