Glutamate is the major excitatory neurotransmitter in the central nervous system and plays a critical role in maintaining normal neuronal function. However, excessive extracellular accumulation of glutamate under pathological conditions induces excitotoxicity, which is closely associated with oxidative stress, mitochondrial dysfunction, and subsequent neuronal cell death. S-allyl cysteine (SAC) is a compound derived from aged garlic, known for its antioxidant and potential cardioprotective properties. The present study investigated the neuroprotective effects of SAC against glutamate-induced cytotoxicity in mouse hippocampal HT22 cells. HT22 cells were exposed to glutamate to establish an in vitro oxidative neurotoxicity model. SAC was administered 2 h prior to glutamate exposure to evaluate its protective potential. Cell viability was assessed using the MTT assay, and glutamate-induced morphological changes were examined by phase-contrast microscopy. Glutamate treatment significantly reduced cell viability in a dose-dependent manner and induced characteristic neuronal damage, including cell shrinkage, dendritic loss, and decreased cell density. SAC treatment alone did not affect cell viability, indicating that SAC is non-cytotoxic within the tested concentration range. Notably, pretreatment with SAC significantly attenuated glutamate-induced cytotoxicity and improved glutamate-induced morphological alterations, thereby preserving neuronal structure and reducing cellular damage. In conclusion, SAC exerts significant protective effects against glutamate-induced oxidative neurotoxicity in HT22 cells. These findings suggest that SAC may serve as a promising neuroprotective agent for excitotoxicity-related neurological disorders.

This study was conducted to elucidate the effects of feeding betaine or monosodium glutamate on the growth and carcass performance of Hanwoo steers according to the fattening stage under high-temperature stress. Farms in an area where THI was 78 or higher for more than 100 days were selected, and 30 head in the early fattening stage (14-15 months of age), 30 head in the mid-fattening stage (16-18 months of age), and 30 head in the late fattening stage (24-25 months of age) were tested, and 10 head were assigned to each treatment group. The experimental group was divided into control, T1 with 96% of the amino acid compound additive and 4% betaine, and T2 with the amino acid complex additive and 4% monosodium glutamate. 50 g per head were fed every morning for a total of 5 months from May 1, 2022 to September 30. In this study, there was no effect of betaine and monosodium glutamate on the growth and rectal temperature of Hanwoo steers at each fattening stage, but monosodium glutamate had a positive effect on the increase in rib eye area and decrease in back fat thickness in steers in the late fattening stage (P<0.05). Therefore, the results of this study indicate that monosodium glutamate did not have a direct effect on the growth of fattening Hanwoo steers, but it is thought to have a positive effect on the rib eye area and back fat thickness through protein metabolism and muscle development.

Artificial photosynthesis, which mimics the natural process used by plants, offers a promising strategy for harnessing solar energy to produce valuable fuels. One intriguing approach is the photocatalyst-enzyme attached system, where a photocatalyst captures light energy and transfers it to an enzyme to drive specific chemical reactions. This study describes the synthesis of a novel photocatalyst (MWCNTCEBr) formed by coupling multiwall carbon nanotubes (MWCNTs) with a dye ethidium bromide (EBr) via a condensation reaction. The resulting photocatalyst exhibits excellent charge separation and migration abilities, leading to enhanced photocatalytic activity. Notably, MWCNTCEBr photocatalyst successfully converts α-Ketoglutarate to L-Glutamate (81.9%) and photo-regeneration of NADH (76.20%) under the influence of solar radiation. Therefore, the study demonstrates the development and the application of MWCNTCEBr photocatalyst for impressive NADH regeneration and bio-transformation.

Baicalin, a flavonoid isolated from Scutellaria baicalensis, has anti-inflammatory, antioxidant, and neuroprotective effects. Glutamate is a major neurotransmitter that plays an important role in brain function, but excessive release of glutamate causes excitotoxicity and damages cells. We investigated the neuroprotective effects of baicalin in glutamate-exposed neurons. The mouse hippocampal neuronal cell line (HT22) was cultured in a general manner, glutamate and/or baicalin were treated on the cells. Baicalin was administered 1 hr before glutamate treatment. Cells were collected 24 hr after glutamate, and cell viability was measured using MTT assay. Reactive oxygen species (ROS) and lipid peroxidation (LPO) assays were performed to measure oxidative stress. Glutamate reduced cell viability in a dose- and time-dependent manner. MTT assay showed that baicalin treatment ameliorated the decrease in cell viability due to glutamate toxicity. The effect of baicalin is dose-dependent. Glutamate caused severe nerve damage, including condensation of the cell shape, loss of dendrites and axons. However, baicalin treatment attenuated these morphological changes, and the effect of baicalin was dose-dependent. ROS and LPO analyses showed that glutamate increases oxidative stress, and baicalin attenuates this change due to glutamate toxicity. The effect of baicalin on these results was dose-dependent. We confirmed that baicalin performs an antioxidant function against glutamate toxicity in neurons. In conclusion, these results suggest that baicalin exerts neuroprotective effects on damaged neurons through antioxidant activity.

Glutamate-mediated oxidative stress causes neuronal cell death by increasing intracellular Ca2+ uptake, reactive oxidative species (ROS) generation, mitogen-activated protein kinase (MAPK) activation, and translocation of apoptosis-inducing factor (AIF) to the nucleus. In the current study, we demonstrated that corydaline exerts potent neuroprotective effects against glutamate-induced neurotoxicity. Treatment with 5 mmol/L glutamate increased cellular Ca2+ influx, ROS generation, MAPK activation, and AIF translocation. In contrast, corydaline treatment decreased cellular Ca2+ influx and ROS generation. Western blot analysis revealed that glutamate-mediated MAPK activation was attenuated by corydaline treatment. We further demonstrated that corydaline treatment inhibited the glutamate-mediated translocation of AIF to the nucleus. We propose that corydaline is a promising lead structure for the development of safe and effective neuroprotectants.

Effects of glutamic acid (Glu) and monosodium glutamate (MSG) on oxidative stability of oil-in-water (O/W) emulsions with different emulsifier charges during riboflavin (RF) photosensitization were evaluated by analyzing headspace oxygen content and conjugated dienes. Cetyltrimethylammonium bromide (CTAB), Tween 20, and sodium dodecyl sulfate (SDS) were used as cationic, neutral, and anionic emulsifiers, respectively. Glu acted as an antioxidant in CTAB- and Tween-20-stabilized O/W emulsions during RF sensitization, whereas Glu acted as prooxidants in SDS-stabilized O/W emulsions in the dark. However, adding MSG did not have a constant impact on the degree of oxidation in O/W emulsions irrespective of the emulsifier charge. In RF-photosensitized O/W emulsions, the emulsifier charge had a greater influence on antioxidant properties of Glu than on those of MSG.

Ischemic stroke leads to severe brain damage and high mortality. Chlorogenic acid is a phenolic compound known to have neuroprotective properties. Bcl-2 family protein plays an important role in the regulation of apoptosis. We investigated whether chlorogenic acid exerts neuroprotective effects against ischemic injury by modulating Bcl-2 and Bax proteins. Middle cerebral artery occlusion (MCAO) was performed to induce cerebral ischemia and rats were injected intraperitoneally with phosphate buffered saline or chlorogenic acid (30 mg/kg) for 2 h after MCAO. Cortical tissues were collected 24 h after MCAO injury and reverse transcription-quantitative real time polymerase chain reaction and Western blot analyses were performed to investigate the expression of Bcl-2 and Bax. The regulation of Bcl-2 and Bax proteins by chlorogenic acid during glutamateinduced cell damage were examined. Cells were collected at 24 h after administration of glutamate (5 mM) and chlorogenic acid (10, 30, 50 μM). These results showed a decrease in Bcl-2 expression and an increase in Bax expression in MCAO animals, but chlorogenic acid treatment alleviated these changes by MCAO damage. Glutamate significantly reduced cell viability, and chlorogenic acid treatment alleviated this reduction in a dose-dependent manner. Glutamate induced a decrease in Bcl-2 expression and an increase in Bax expression, but chlorogenic acid treatment alleviated these changes. We found that chlorogenic acid alleviates changes in the expression of Bcl-2 and Bax proteins induced by brain injury. Therefore, our findings provide an evidence that chlorogenic acid has neuroprotective effects against MCAO damage by modulating Bcl-2 and Bax proteins.

Activation of transient receptor potential vanilloid 1 (TRPV1), a calcium permeable channel expressed in primary sensory neurons, induces the release of glutamate from their central and peripheral afferents during normal acute and pathological pain. However, little information is available regarding the glutamate release mechanism associated with TRPV1 activation in primary sensory neurons. To address this issue, we investigated the expression of vesicular glutamate transporter (VGLUT) in TRPV1-immunopositive (+) neurons in the rat trigeminal ganglion (TG) under normal and complete Freund’s adjuvant (CFA)-induced inflammatory pain conditions using behavioral testing as well as double immunofluorescence staining with antisera against TRPV1 and VGLUT1 or VGLUT2. TRPV1 was primarily expressed in small and medium-sized TG neurons. TRPV1+ neurons constituted approximately 27% of all TG neurons. Among all TRPV1+ neurons, the proportion of TRPV1+ neurons coexpressing VGLUT1 (VGLUT1+/ TRPV1+ neurons) and VGLUT2 (VGLUT2+/TRPV1+ neurons) was 0.4% ± 0.2% and 22.4% ± 2.8%, respectively. The proportion of TRPV1+ and VGLUT2+ neurons was higher in the CFA group than in the control group (TRPV1+ neurons: 31.5% ± 2.5% vs. 26.5% ± 1.2%, VGLUT2+ neurons: 31.8% ± 1.1% vs. 24.6% ± 1.5%, p < 0.05), whereas the proportion of VGLUT1+, VGLUT1+/TRPV1+, and VGLUT2+/TRPV1+ neurons did not differ significantly between the CFA and control groups. These findings together suggest that VGLUT2, a major isoform of VGLUTs, is involved in TRPV1 activation-associated glutamate release during normal acute and inflammatory pain.

본 연구는 케일(Brassica oleracea L. var. acephala)의 노지 재배 시, 생육 초기에 노출될 수 있는 건조 스트레스 조건에서 Glutamate (Glu)의 스트레스 경감 및 생육 회복 효과를 구명하기 위해 실시하였다. 건조 조건(D)에 노출된 케일에 5㎛ Glu 용액을 경엽처리하였다(D+Glu). Glu 처리 전 및 처리 후 4, 8일 차(0, 4, 8DAT)의 생육과 엽록소 함량을 측정하고 식물 체내의 ABA와 Glu, Pro의 함량을 분석하여 정상 환경 및 D, D+Glu 처리구 간의 비교를 실시하였다. 엽록소 함량의 경우, 8DAT에서 D+Glu 처리구는 일정한 수준을 유지한 반면에, D처리구는 14% 감소하였다. 엽면적으로 대표되는 생장 또한 D+Glu 처리구가 D 처리구에 비해 높게 나타났다. 또한 4, 8일차의 ABA 함량이 D 처리구에서 D+Glu 처리구에 비해 44.13, 49.18% 높게 나타났으며, 체내 아미노산 대사 및 건조저항성 지표인 Glu, Pro 함량은 D 처리구에 비해 D+Glu 처리구에서 보다 높은 수준을 유지하였다. 이러한 결과를 통해, Glu 처리에 의해 건조 스트레스가 경감되고 생육이 회복될 수 있다고 판단된다.

A γ-aminobutyric acid (GABA) producing microorganism was isolated from Sun-Tae Jeotgal, a Korean traditional fermented seafood. Two thousand presumptive lactic acid bacteria (LAB) isolates were screened for GABA production by thin layer chromatography. One isolate, T118, produced GABA profusely, and identified as Lactobacillus brevis. Growth of Lb. brevis T118 was examined during 120 h cultivation in MRS broth under different conditions. Lb. brevis T118 grew well at 30-37℃, initial pH of 4-7, and up to 5% NaCl (w/v). A gene, gadB, encoding glutamate decarboxylase (GAD) was cloned by PCR. gadC encoding a glutamate/GABA antiporter was cloned and gadC located immediately upstream of gadB, indicating gadCB operon structure. The operon structure was confirmed by reverse transcription (RT)-PCR. gadB was overexpressed in Escherichia coli BL21 (DE3) and recombinant GAD was purified. The size of recombinant GAD was 54.4 kDa by SDS-PAGE, which matched well with the calculated size from the nucleotide sequence.

This study was designed to determine the effect of monosodium glutamate (MSG) on in vitro maturation (IVM) of oocytes and early development of parthenogenesis (PA) embryos in pigs. Each IVM and IVC medium was supplemented with various concentrations (0, 0.1, 0.5 and 5 mM) of MSG and non-essential amino acids (NEAA) depending on the experimental design. Immature pig oocytes were matured for 44 h and then oocytes reached metaphase II (MII) stage were electrically activated to induce parthenogenesis (PA). When immature oocytes were treated with MSG in the absence of NEAA during IVM, nuclear maturation (83.1-87.1%), intra-oocyte glutathione content, cumulus expansion, and cleavage (91.4-93.4%) of PA embryos were not influenced by MSG treatment at all concentrations. However, blastocyst formation of PA embryos was significantly increased by 5.0 mM MSG (45.3 ± 6.2%) compared to control (25.6 ± 3.4%). MSG treatment during IVM in the presence of NEAA did not show significant effect on nuclear maturation of oocytes and blastocyst formation after PA while 0.5 mM MSG (89.3 ± 1.9%) decreased (P < 0.05) cleavage of PA embryos compared to 0.1 mM MSG (94.6 ± 1.1%). When PA embryos were treated for 7 days with MSG during IVC, 5.0 mM MSG significantly decreased blastocyst formation (27.8 ± 4.9%) compared to no treatment (41.4 ± 1.9%) while no decrease in blastocyst formation was observed in 0.1 and 0.5 mM (37.4 ± 3.4% and 34.4 ± 2.6%, respectively). Our results demonstrated that 5 mM MSG in a NEAA-free chemically defined maturation medium showed positive effect on PA embryonic development while 5 mM MSG treatment during IVC was deleterious to PA embryonic development in pigs.

The present study investigated the role of spinal glutamate recycling in the development of orofacial inflammatory pain or trigeminal neuropathic pain. Experiments were carried out on male Sprague–Dawley rats weighing between 230 and 280 g. Under anesthesia, a polyethylene tube was implanted in the atlanto-occipital membrane for intracisternal administration. IL-1β-induced inflammation was employed as an orofacial acute inflammatory pain model. IL-1β (10 ng) was injected subcutaneously into one vibrissal pad. We used the trigeminal neuropathic pain animal model produced by chronic constriction injury of the infraorbital nerve. DL-threo-β -benzyloxyaspartate (TBOA) or methionine sulfoximine (MSO) was administered intracisternally to block the spinal glutamate transporter and the glutamine synthetase activity in astroglia. Intracisternal administration of TBOA produced mechanical allodynia in naïve rats, but it significantly attenuated mechanical allodynia in rats with interleukin (IL)-1 β-induced inflammatory pain or trigeminal neuropathic pain. In contrast, intracisternal injection of MSO produced antiallodynic effects in rats treated with IL-1β or with infraorbital nerve injury. Intracisternal administration of MSO did not produce mechanical allodynia in naive rats. These results suggest that blockade of glutamate recycling induced pro-nociception in naïve rats, but it paradoxically resulted in anti-nociception in rats experiencing inflammatory or neuropathic pain. Moreover, blockade of glutamate reuptake could represent a new therapeutic target for the treatment of chronic pain conditions.

Monosodium glutamate (MSG)는 아미노산의 일종인 글루탐산에 나트륨이 결합된 것으로 구수한 맛, 감칠맛을 내는 인공조미료로 사용되고 있다. 이전 연구에 의하면 쥐에서MSG의 섭취가 난모세 포의 발달에 유해하다는 결과가 보고되었다. 본 연구에서는 돼지 난자의 체외성숙 및 체외 배양액 에 MSG 첨가가 난자의 성숙 및 배 발육에 미치는 영향을 검토하였다. 난자의 체외성숙배양액으 로는 10% 돼지 난포액이 첨가된 Medium-199 (positivecontrol) 또는 비필수아미노산이 제거된 Porcine zygote medium (PZM)-4를 기본배양액으로 하여 여기에 cysteine, pyruvate, epidermal growth factor, kanamycin, insulin 및 호르몬을 첨가하여 사용하였다. 실험설계에 따라 MSG를 각각 0, 0.1, 1, 10 mM 농도로 체외성숙 배양액에 첨가하였다. 체외성숙 난자는 전기자극을 통해 단위발생을 유도하였고 PZM-3배양액에서 7일간 체외 배양하였다. 체외배양에서의 MSG 효과를 알아보기 위하 여 돼지 난포액 첨가 Medium-199에서 체외성숙된 난자들 중 제1극체가 방출된 난자만을 선별하여 단위발생 유도 후 PZM-3 (positive control) 또는 비필수아미노산이 제거된 PZM-4에 0,0.1, 1, 10 mM의 MSG를 첨가하여 배 발육에 미치는 영향을 조사하였다. 체외성숙 단계에서 MSG 효과를 조 사한 결과 MSG 농도에 따른 체외성숙률(61.3-70.3%)에는 차이를 보이지 않았지만 10 mM의 MSG 처리군(83.5%)이 0.1 mM 처리군(93.7%)에 비해 유의적으로 낮은 분할률을 보였다. 또한 MSG 처리 군들이 (14.5-25.5%) 무처리군(30.0%)에 비해 낮은(P<0.05) 배반포 발달률을 보였다. 체외배양 단계 에서 MSG 효과를 조사한 결과 10mM MSG 처리군(90.8%)이 1 mM 처리군(96.5%)에 비해 유의적 으로 낮은 분할률을 보였으며, 10 mM 처리군(32.8%)이 0.1과 1 mM MSG 처리군에(55.1, 51.4%)에 비해 유의적으로(P<0.05) 낮은 배반포 발달률 보였으나 무처리 대조군(46.6%)과 유의적 차이는 없 었다. 이러한 결과를 보아 체외성숙 배양액 내 MSG 첨가는 난자의 핵 성숙률에는 영향을 주지 않지만 고농도의 MSG 처리는 단위발생 후 분할률을 억제하며 배반포 발육능을 억제하는 것으로 확인되었다.

The feasibility of reduction of sodium intake using sun-dried salt and monosodium glutamate (MSG) was studied. Preference test was performed to evaluate the sensory properties of bean-sprout soup and vegetable rice porridge soup. Sun-dried salt and MSG might be a partial substitute for refined salt. There was a significant difference in salt taste strength between sun-dried salt and refined salt. Sun-dried salts 0.45% with MSG 0.07% resulted in the highest taste preference compared to that of sun-dried salts 0.60% without MSG in bean-sprout soup, which resulted in 23.9% reduction of sodium intake. Sun-dried salts 0.38% with MSG 0.04% resulted in the highest taste preference compared to sun-dried salts 0.53% without MSG in vegetable rice porridge soup, which resulted in 25.4% reduction of sodium intake. There seemed to be a synergistic effect on reduced usage of sodium salt when MSG was used in vegetable rice porridge and bean-sprout soup with sun-dried salt.

본 연구에서는 소셜미디어 콘텐츠를 소프트웨어 시스템을 이용하거나 정성적으로 분석함으로써 L-글루타민산나트륨에 대한 소비자 인식도를 조사하고자 하였다. 첫 번째로, 1년 (2013.7~2014.6)의 기간 동안 네이버와 카페에서 작성된 글들을 수집하였으며, 수집한 문서들을 무료 텍스트 분석 소프트웨어인 TONK를 사용하여 분석하였다. 블로그와 카페에서 작성된 글들은 주로 L-글루타민산나트륨의 사용과 관련된 음식점 후기 및 MSG (L-글루타민산나트륨)-무첨가 제품에 대한 홍보 내용을 담은 글들로 파악되었으며, 기타 L-글루타민산나트륨의 안전성 또는 식품첨가물 제거법에 대한 내용으로 파악되었다. 두 번째로, 네이버 트렌드 검색 서비스를 이용하여 L-글루타민산나트륨에 대한 검색량 증가 구간에 발생한 언론보도 사건을 조사하였다. PC 검색량의 경우 총 5개 증가 구간 중 3개의 구간에서, 모바일 검색량의 총 9개 증가 구간 중 6개의 구간에서 시사 프로그램에서 L-글루타민산나트륨에 대해 보도한 것으로 나타났다. 나머지 구간에서는 일간지나 TV 뉴스로 기사를 보도한 구간들로 나타났다. 세 번째로 식품의약품안전처의 L-글루타민산나트륨의 안전성 발표를 보도한 연합뉴스의 댓글을 분석하였다. 공감수 100개 이상인 댓글의 내용을 분석한 결과, L-글루타민산나트륨의 안전성, 질 낮은 재료의 사용 지적, MSG (L-글루타민산나트륨) 과다사용에 대한 우려, 정부 불신을 표현하는 댓글들이 파악되었다. 시판 제품들의 표시사항을 분석한 결과, 일일섭취허용량을 설정할 필요가 없을 정도로 안전한 식품첨가물임에도 불구하고 L-글루타민산나트륨을 첨가하지 않은 제품들은 L-글루타민산나트륨 무첨가라는 표시를 강조하고 있는 것으로 조사되었다. 이는 국가기관, 교육청과 지방자치단체에서 MSG 미사용을 원칙으로 제도를 운용하고 있어 이러한 정책이 산업계와 소비자 인식에 영향을 미쳤을 가능성도 고려해볼 수 있다. 본 연구 결과 소비자들은 대체로 소셜 미디어를 이용하여 검색하거나 관련 제품을 구매하고자 할 때 L-글루타민산나트륨을 사용하지 않는 것이 좋다는 인식을 하게 될 가능성이 있는 것으로 파악되며, L-글루타민산나트륨의 과다 사용에 관심이 있는 것으로 나타났다. TV 시사 프로그램에서 방송하거나 일간지 또는 TV 뉴스에서 기사를 보도할 경우 네이버 검색량이 증가하였으며, 검색량 증가구간은 PC 환경에서보다는 모바일 환경에서 더욱 증가하는 것으로 나타났다. 따라서 L-글루타민산나트륨과 관련한 커뮤니케이션 수단으로 소비자들이 관심있어 하는 방송프로그램, 뉴스 프로그램 등 언론을 활용하고, PC보다는 모바일을 통하여 소비자에게 접근한다면 효과적으로 소비자에게 정보를 전달할 수 있을 것이다.

Calbindin-D28k is a calcium-binding protein that mediates intracellular calcium concentrations and exerts a neuroprotective effect against ischemic injury. Ferulic acid provides a neuroprotective effect against focal cerebral ischemia through its anti-oxidative and anti-inflammatory mechanisms. In this study, we investigated whether ferulic acid regulates calbindin-D28k expression during focal cerebral ischemia and glutamate treatment-induced neuronal cell death. Middle cerebral artery occlusion (MCAO) was performed to induce focal cerebral ischemia. Ferulic acid (100 mg/kg, i.v.) or vehicle was immediately administered after MCAO, and brain tissues were isolated 24 h after MCAO. RT-PCR and Western blot analyses showed a decrease in calbindin-D28k in MCAO-operated animals. We found that ferulic acid treatment prevented the MCAO-induced decrease in calbindin-D28k expression. Glutamate exposure elevated the intracellular calcium levels in cultured hippocampal cells, and ferulic acid prevented the glutamate exposure-induced increase in calcium levels. Moreover, ferulic acid also attenuated the glutamate toxicity-induced decrease in calbindin-D28k. Taken together, these in vivo and in vitro results demonstrate that ferulic acid regulates calbindin-D28k expression in neuronal cell injury. Therefore, these findings suggest that ferulic acid exerts a neuroprotective effect by modulating calbindin-D28k expression.

Using whole cell current- and voltage-clamp recording we investigated the characteristics and pharmacology of group I metabotropic glutamate receptor (mGluR)-mediated responses in rat medial vestibular nucleus (MVN) neurons. In current clamp conditions, activation of mGluR I by application of the group I mGluR agonist (R,S)-3,5-dihydroxyphenylglycine (DHPG) induced a direct excitation of MVN neurons that is characterized by depolarization and increased spontaneous firing frequency. To identify which of mGluR subtypes are responsible for the various actions of DHPG in MVN, we used two subtype-selective antagonists. (S)-(+)- alpha-amino-a-methylbenzeneacetic acid (LY367385) is a potent competitive antagonist that is selective for mGluR1, whereas 2-methyl-6-(phenylethynyl)-pyridine (MPEP) is a potent noncompetitive antagonist that is selective for mGluR5. In voltage clamp conditions, DHPG application increased the frequency of spontaneous and miniature inhibitory postsynaptic currents (IPSCs) but had no effect on amplitude distributions. Antagonism of the DHPG-induced increase of miniature IPSCs required the blockade of both mGluR1 and mGluR5. DHPG application induced an inward current, which can be enhanced under depolarized conditions. DHPG-induced current was blocked by LY367385, but not by MPEP. Both LY367385 and MPEP antagonized the DHPG-induced suppression of the calcium activated potassium current (IAHP). These data suggest that mGluR1 and mGluR5 have similar roles in the regulation of the excitability of MVN neurons, and show a little distinct. Furthermore, mGluR I, via pre- and postsynaptic actions, have the potential to modulate the functions of the MVN.

Neurotoxicity and oxidative injury induced by glutamate cause neuronal degeneration related to various central nervous system diseases. Resveratrol, a polyphenolic compound, is known to have antioxidative and anti-inflammatory effects. The aim of this study was to investigate the question of whether resveratrol has a neuroprotective effect against glutamate-induced toxicity in cultured cortical neurons. Following exposure to glutamate for 15 min, cortical neurons originating from ICR mouse fetuses on embryonic days 15-16 were then treated with resveratrol for 24 h in the post-treatment paradigm. Glutamate induced a significant reduction in cell viability; however, resveratrol induced a significant increase in cell viability. Glutamate induced generation of ROS and apoptotic neuronal death; however, these were decreased by exposure to resveratrol. mRNA expression in antioxidant enzymes, cytoplasmic glutathione peroxidase, copper/zinc superoxide dismutase (SOD), and manganese SOD, and anti-apoptotic regulator Bcl-xL were decreased by exposure to glutamate, however, exposure to resveratrol resulted in a significant increase in their mRNA levels. In addition, mRNA expression of pro-inflammatory cytokines, interleukin-1β and tumor necosis factor-α, was increased by glutamate insult, but significantly reduced by resveratrol. These findings indicate that resveratrol is neuroprotective against glutamate-induced toxicity, suggesting a useful therapeutic application in treatment of neurodegenerative disorders.

The molecular mechanisms and genetics of abamectin resistance mediated by target site insensitivity in the two-spotted spider mite, Tetranychus urticae, were investigated by comparing two isogenic AbaS and AbaR strains. Cloning and sequencing of full-length cDNA fragments of GABA-gated chloride channel genes revealed no polymorphisms between the two strains. However, sequence comparison of the full-length cDNA fragment of a T. urticae glutamate-gated chloride channel gene (TuGluCl) identified a G323D point mutation as being tentatively related with abamectin resistance. In individual F2 progenies obtained by backcrossing, the G323D genotype was confirmed to correlate with abamectin resistance. Bioassays using progeny from reciprocal crossings revealed that the abamectin resistance trait due to TuGluCl insensitivity is incompletely recessive.