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Chemical Compound Review

Ibotenic acid     2-amino-2-(3-oxo-1,2-oxazol- 5-yl)ethanoic...

Synonyms: Ibotenate, CHEMBL284895, SureCN153359, AG-E-78364, SureCN4582627, ...
 
 
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Disease relevance of Ibotenic acid

  • To determine the role of the ventromedial hypoglycemia, we performed hypoglycemic clamp studies in conscious Sprague-Dawley rats with bilateral VMH lesions produced by local ibotenic acid injection 2 wk earlier [1].
  • When injected intracerebrally into newborn mice, the glutamatergic analog ibotenate induces white matter cysts mimicking human periventricular leukomalacia [2].
  • Ibotenic acid lesions of the hippocampus eliminated the majority of the label, which had been present over pyramidal cells, though labeling was increased over areas of reactive gliosis, suggesting that activated astrocytes can also synthesize CPE mRNA [3].
  • Bilateral ibotenic acid ablation of the lateral parabrachial nucleus was performed 4 weeks after induction of hypertension or sham operation [4].
  • In ibotenic acid-injected rats, hyperemia was preserved at the injection site, but the sudden decline of blood flow was abolished (maximal slope of flow decay: 5 +/- 3%/min compared with 53 +/- 8%/min at the control site; n = 5, p less than 0.001) and no significant hypoperfusion developed (103 +/- 20% of control at 60 minutes) [5].
 

Psychiatry related information on Ibotenic acid

 

High impact information on Ibotenic acid

 

Chemical compound and disease context of Ibotenic acid

 

Biological context of Ibotenic acid

  • Ibotenic acid lesions were made within the physiologically identified representation of the lower left visual field of area 17 [21].
  • Continuous recordings of penile erections, body temperature, and sleep-wake states were performed before and up to 3 weeks after ibotenic acid lesions of the preoptic forebrain in three groups of rats [22].
  • We examined the effects of bilateral ibotenic acid lesions of cat lateral suprasylvian (LS) cortex on motion perception [23].
  • Finally, BDNF exacerbated neuronal death produced by ibotenate at P0 through increased apoptosis and p75(NTR) receptors, while BDNF had no detectable effect on lesions induced at P10 [24].
  • Three days after surgery, CMRGlu and k3 (phosphorylation of FDG) were reduced similarly in the frontal cortex on the BPA-injected side and in the ibotenic acid-treated group, whereas K1 (transport rate of FDG from the plasma to brain) showed no marked changes [25].
 

Anatomical context of Ibotenic acid

  • This cholinergic component of Alzheimer disease can be modeled in the rat by ibotenic acid lesions of the cholinergic nucleus basalis magnocellularis [26].
  • Injection of ibotenic acid or colchicine into the caudate putamen decreased [3H]captopril-associated autoradiographic grains by 85% in the ipsilateral caudate putamen and by greater than 50% in the ipsilateral substantia nigra [27].
  • The dense labeling associated with hippocampal pyramidal cells was reduced significantly when the cells were eliminated by injection of the neurotoxin ibotenic acid but was not affected when electrolytic lesions were placed in the medial septum [28].
  • Loss of muscarinic receptors and of stimulated phospholipid labeling in ibotenate-treated hippocampus [29].
  • Electrolytic or ibotenic acid lesions of the central nucleus of the amygdala blocked fear-potentiated startle to both auditory and visual CSs, consistent with the idea that the central nucleus serves as a response independent, final common relay for fear conditioning [30].
 

Associations of Ibotenic acid with other chemical compounds

  • Further, IGlu is not mediated by a known metabotropic glutamate receptor since it was not activated by quisqualic acid, AP-4, ACPD, or ibotenate [31].
  • Striatal grafts derived from embryonic day 15 striatal primordia were implanted into the ibotenate-damaged host striatum of rats previously treated with 6-hydroxydopamine (6-OHDA) to destroy TH-containing dopaminergic nigrostriatal afferents [32].
  • The failure of ibotenic acid to affect LH-produced descending inhibition when microinjected into the dorsolateral pons, and the significant effect produced by lidocaine microinjected into the same area, implicates fibers of passage in the dorsolateral pons in descending inhibition of the TF reflex produced by focal electrical stimulation in the LH [33].
  • Compared with sham-operated control animals, which showed the same response as intact, nonlesioned rats, ibotenate lesions of the LDTg attenuated the stimulatory effects of intra-VTA neostigmine on DA efflux in the nucleus accumbens [34].
  • BDNF neuroprotection at P5 was maximal against lesions induced by NMDA or ibotenate but was moderate against lesions produced by an AMPA-kainate agonist [24].
 

Gene context of Ibotenic acid

  • In a similar manner, IL-9-overexpressing transgenic pups developed ibotenate-induced brain lesions, which were significantly larger than those induced in nontransgenic control pups [35].
  • In particular, the mutations K74Y and K317R induced dramatic triple-order-of-magnitude increases in the affinity of ibotenic acid at mGluR4, making the affinity equivalent to that of mGluR1 [36].
  • Cortical and white matter lesions induced by ibotenate at P5 were reduced by BDNF by up to 36 and 60%, respectively [24].
  • Systemically administered recombinant PRDX5 provided protection against ibotenate-induced excitotoxic stress [37].
  • In contrast, increased levels of the beta-chemokines MIP-1 alpha and -beta were seen early in the disease and were concentrated in regions of the brain rich in spongiosis, and the magnitude of responses was similar to that observed in the brains of mice injected with the glutamatergic neurotoxin ibotenic acid [38].
 

Analytical, diagnostic and therapeutic context of Ibotenic acid

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