There will be a HazMat fee per item when shipping a dangerous goods. The HazMat fee will be charged to your UPS/DHL/FedEx collect account or added to the invoice unless the package is shipped via Ground service. Ship by air in Excepted Quantity (each bottle), which is up to 1g/1mL for class 6.1 packing group I or II, and up to 25g/25ml for all other HazMat items.
Type
HazMat fee for 500 gram (Estimated)
Excepted Quantity
USD 0.00
Limited Quantity
USD 15-60
Inaccessible (Haz class 6.1), Domestic
USD 80+
Inaccessible (Haz class 6.1), International
USD 150+
Accessible (Haz class 3, 4, 5 or 8), Domestic
USD 100+
Accessible (Haz class 3, 4, 5 or 8), International
Ibotenic acid has agonist activity at both the N-methyl-D-aspartate (NMDA) and trans-ACPD or metabolotropic quisqualate (Qm) receptor sites. Ibotenic acid (Ibo) is capable of acting at both NMDA and trans-ACPD receptors in the CNS, although only activation of NMDA receptors is involved in Ibo neurotoxicity. Ibotenic acid is toxic to cortical neurons exposes for 5 min with an EC50=77.3±8 μM (n=5) as measured by release of lactate dehydrogenase to the culture media[3]. Ibotenic acid was inhibitors of (S)-glutamic acid decarboxylase (GAD) in mouse brain homogenates, and was shown to undergo decarboxylation during incubation with brain homogenates. The formation of the decarboxylated product, muscimol, which primarily occurred in a synaptosomal fraction, was dependent on the presence of pyridoxal-5-phosphate (PALP) and was inhibited by (S)-glutamic acid, 3-mercaptopropionic acid (3MPA), aminooxyacetic acid (AOAA), and allyglycine, suggesting that ibotenic acid is a substrate for GAD. The overall decomposition rate for ibotenic acid (8.7 nmol min-1 mg-1 of protein), which apparently embraces other reactions in addition to decarboxylation to muscimol, was higher than the rate of decarboxylation of (S)-glutamic acid (3.2 nmol min-1 mg-1 of protein)[4]. Ibotenic acid induced similar neuronal migration impairments in control and alcohol-exposed pups (nodular heterotopia in the white matter and/or deep cortical layers, subpial ectopia, and micro- or polymicrogyria)[5].
Ibotenic acid/鹅膏氨酸 细胞实验
Cell Line
Concentration
Treated Time
Description
References
Primary cortical neurons
50 µM
3 and 6 hours
To evaluate the effect of ibotenate on neuronal autophagy, results showed increased LC3-II expression and enhanced SQSTM1 degradation, indicating enhanced autophagic flux.
Cell Death Dis. 2018 Aug 28;9(9):853
PC12 rat pheochromocytoma cells
1 mM
24 hours
To investigate the effect of ibotenic acid on the viability of PC12 cells under nutrient deprivation, results showed that ibotenic acid significantly reduced cell viability.
Cell Mol Life Sci. 2020 Sep;77(17):3383-3399
SH-SY5Y neuroblastoma cells
1 mM
24 hours
To investigate the effect of ibotenic acid on the viability of SH-SY5Y cells under nutrient deprivation, results showed that ibotenic acid significantly reduced cell viability.
Cell Mol Life Sci. 2020 Sep;77(17):3383-3399
Ibotenic acid/鹅膏氨酸 动物实验
Species
Animal Model
Administration
Dosage
Frequency
Description
References
CD-1 male mice
Surgery mouse model
Intracerebral injection into PVT region
300 nl 0.3% ibotenic acid
Single injection, behavioral tests performed after 5 days of recovery
After ibotenic acid-induced PVT neuronal injury, the consolation and anxious behaviors of familiar observers toward surgery mice were abolished
Theranostics. 2021 Feb 6;11(8):3813-3829
Rats
RMTg neuron lesion model
Intracerebral injection
1% in saline, 200 nL/side
Single injection
To evaluate the effect of RMTg neuron lesions on sleep-wake behavior. Results showed that lesions led to decreased NREM and REM sleep and increased wakefulness.
PLoS Biol. 2018 Apr 13;16(4):e2002909
Male Long-Evans rats
Rat gambling task (rGT) model
Bilateral injection into RAIC or CGIC regions
0.2 μl/side, 20 mg/ml
Single injection, 5 min diffusion time post-injection
To investigate the roles of RAIC and CGIC in rGT choice behavior. RAIC lesions resulted in a greater preference for options with higher reward frequency and lower punishment, while CGIC lesions had minimal effects on choice behavior.
Neuropsychopharmacology. 2015 Nov;40(12):2832-42
Rats
Lateral parabrachial nucleus (PBN) lesion model
Bilateral injection
20μg/μl
Single injection, observed for 24 hours
To evaluate the effect of PBN lesions on Ex4-induced hypophagia. Results showed that PBN-lesioned rats did not exhibit reduced food intake after Ex4 treatment, indicating that the PBN is necessary for Ex4 effects under the tested conditions.
Neuropsychopharmacology. 2015 Jul;40(8):2001-14
Sprague-Dawley rats
Aβ1-40 plus ibotenic acid-induced Alzheimer's disease model
Bilateral hippocampal injection
2 μL mixed Aβ1-40 and ibotenic acid solution
Single injection
Establish an Alzheimer's disease model for subsequent metabolomic analysis and drug evaluation
J Pharm Anal. 2022 Aug;12(4):627-636
Sprague-Dawley rat pups
Model of preterm excitotoxic brain injury
Intracerebral injection
10 µg
Single injection, evaluated at 24 h and 16 days
To investigate the role of ibotenate-induced autophagy in preterm brain injury, results showed enhanced autophagy associated with neuronal death, and the autophagy inhibitor 3-MA significantly reduced long-term brain injury.
Cell Death Dis. 2018 Aug 28;9(9):853
Sprague-Dawley rats
Parkinson’s disease rat model
Intracerebral injection
45 nM
Single injection
To investigate the effect of cortical lesions on striatal projection neurons and interneurons in a 6-hydroxydopamine-induced Parkinson’s disease model. Results showed that cortical lesions reversed the damage to striatal projection neurons induced by 6-hydroxydopamine and inhibited the hyperplastic reaction of interneurons.
Neural Regen Res. 2016 Dec;11(12):1969-1975
Sprague-Dawley rats
Parkinson's disease rat model
Intracerebral injection
45 nM
Single injection, observed for 4 weeks
To investigate the effect of ibotenic acid-induced decortication on dopamine depletion-induced striatal neuron lesions. Results showed that decortication alleviated the damage to dendritic spines and dendrites of striatal neurons caused by dopamine depletion.
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