L-Allylglycine is an inhibitor for glutamate decarboxylase (GAD) that reduces the GABA biosynthesis in the brain [1]. L-Allylglycine leads to a decrease in SAM-DC activity as well as in the levels of spermidine and spermine, and affect the acetylation of putrescine and spermidine in mouse brain[2]. L-Allylglycine has been widely used to induce seizures in animals in order to study changes in brain function[3].
In vivo, L-Allylglycine treatment via an intravenous injection of 100mg/kg dose for 2 hours caused photosensitive epilepsy in the baboons, resulting in symptoms such as vomiting, persistent vertical nystagmus and intermittent extensor muscle spasms[4]. L-Allylglycine treatment (1.2mmol/kg; i.p.) induced convulsions within 90min in rats, characterized by violent running followed by tonic flexion and extension[5]. Injecting L-allylglycine (25μg) into the posterior hypothalamus of rats for 90min resulted in a decrease in local GABA levels and caused an increase in heart rate and blood pressure[6]. After injecting a single dose of 5μg/0.2μl of L-Allylglycine into the ventral regions of the periaqueductal gray (vPAG) of rats for 45 minutes, the rats exhibited intense hyperactivity, including jumping and standing on the hind legs[7].
References:
[1] Beart P M, Bilal K. Allylglycine: intranigral effects and reappraisal of actions on the GABA system[J]. Biochemical Pharmacology, 1979, 28(4): 449-454.
[2] Ortiz J G, Giacobini E, Schmidt-Glenewinkel T. Allylglycine affects acetylation of putrescine and spermidine in mouse brain[J]. Neuropharmacology, 1983, 22(10): 1237-1239.
[3] Chapman A G, Westerberg E, Premachandra M, et al. Changes in regional neurotransmitter amino acid levels in rat brain during seizures induced by l‐allylglycine, bicuculline, and kainic acid[J]. Journal of neurochemistry, 1984, 43(1): 62-70.
[4] Meldrum B S, Menini C, Naquet R, et al. Proconvulsant, convulsant and other actions of the D-and L-stereoisomers of allylglycine in the photosensitive baboon, Papio papio[J]. Electroencephalography and Clinical Neurophysiology, 1979, 47(4): 383-395.
[5] Horton R W, Chapman A G, Meldrum B S. Regional changes in cerebral GABA concentration and convulsions produced by D and by L‐allylglycine[J]. Journal of neurochemistry, 1978, 30(6): 1501-1504.
[6] Abshire V M, Hankins K D, Roehr K E, et al. Injection of L-allylglycine into the posterior hypothalamus in rats causes decreases in local GABA which correlate with increases in heart rate[J]. Neuropharmacology, 1988, 27(11): 1171-1177.
[7] Cunha J M, Zanoveli J M, Ledvinka-Filho E, et al. L-allylglycine dissociates the neural substrates of fear in the periaqueductal gray of rats[J]. Brain research bulletin, 2010, 81(4-5): 416-423.
L-Allylglycine是一种谷氨酸脱羧酶（GAD）抑制剂，可减少大脑中GABA的生物合成[1]。L-Allylglycine导致小鼠脑中SAM-DC活性以及亚精胺和精胺水平的下降，并影响腐胺和亚精胺的乙酰化[2]。L-Allylglycine已被广泛用于在动物中诱导癫痫发作，以研究脑功能变化[3]。
在体内，静脉注射100mg/kg剂量的L-Allylglycine 2小时，导致狒狒出现光敏性癫痫，引起呕吐、持续性垂直眼震和间歇性伸肌痉挛等症状[4]。L-Allylglycine（1.2mmol/kg；i.p.）在90分钟内诱导大鼠出现惊厥，表现为剧烈跑动后伴随强直性屈曲和伸展[5]。向大鼠下丘脑后部注射L-Allylglycine（25μg）90分钟，导致局部GABA水平下降，并引起心率和血压升高[6]。单次向大鼠导水管周围灰质腹侧区（vPAG）注射5μg/0.2μl的L-Allylglycine（45分钟），大鼠表现出强烈的过度活跃，包括跳跃和用后腿站立[7]。