5-IODO-A-85380 dihydrochloride - CAS 213764-92-2
Main Product
Product Name:
5-IODO-A-85380 dihydrochloride
Catalog Number:
5-IODO-A-85380 dihydrochloride; 3-[(2S)-2-Azetidinylmethoxy]-5-iodopyridine dihydrochloride
CAS Number:
Molecular Weight:
Molecular Formula:
Canonical SMILES:
Chemical Structure
CAS 213764-92-2 5-IODO-A-85380 dihydrochloride

Reference Reading

1.Presynaptic nicotinic α7 and non-α7 receptors stimulate endogenous GABA release from rat hippocampal synaptosomes through two mechanisms of action.
Zappettini S1, Grilli M, Lagomarsino F, Cavallero A, Fedele E, Marchi M. PLoS One. 2011 Feb 8;6(2):e16911. doi: 10.1371/journal.pone.0016911.
BACKGROUND: Although converging evidence has suggested that nicotinic acetylcholine receptors (nAChR) play a role in the modulation of GABA release in rat hippocampus, the specific involvement of different nAChR subtypes at presynaptic level is still a matter of debate. In the present work we investigated, using selective α7 and α4β2 nAChR agonists, the presence of different nAChR subtypes on hippocampal GABA nerve endings to assess to what extent and through which mechanisms they stimulate endogenous GABA release.
2.Beta Amyloid Differently Modulate Nicotinic and Muscarinic Receptor Subtypes which Stimulate in vitro and in vivo the Release of Glycine in the Rat Hippocampus.
Zappettini S1, Grilli M, Olivero G, Mura E, Preda S, Govoni S, Salamone A, Marchi M. Front Pharmacol. 2012 Jul 27;3:146. doi: 10.3389/fphar.2012.00146. eCollection 2012.
Using both in vitro (hippocampal synaptosomes in superfusion) and in vivo (microdialysis) approaches we investigated whether and to what extent β amyloid peptide 1-40 (Aβ 1-40) interferes with the cholinergic modulation of the release of glycine (GLY) in the rat hippocampus. The nicotine-evoked overflow of endogenous GLY in hippocampal synaptosomes in superfusion was significantly inhibited by Aβ 1-40 (10 nM) while increasing the concentration to 100 nM the inhibitory effect did not further increase. Both the Choline (Ch; α7 agonist; 1 mM) and the 5-Iodo-A-85380 dihydrochloride (5IA85380, α4β2 agonist; 10 nM)-evoked GLY overflow were inhibited by Aβ 1-40 at 100 nM but not at 10 nM concentrations. The KCl evoked [(3)H]GLY and [(3)H]Acetylcholine (ACh) overflow were strongly inhibited in presence of oxotremorine; however this inhibitory muscarinic effect was not affected by Aβ 1-40. The effects of Aβ 1-40 on the administration of nicotine, veratridine, 5IA85380, and PHA543613 hydrochloride (PHA543613; a selective agonist of α7 subtypes) on hippocampal endogenous GLY release in vivo were also studied.
3.Dual effect of beta-amyloid on α7 and α4β2 nicotinic receptors controlling the release of glutamate, aspartate and GABA in rat hippocampus.
Mura E1, Zappettini S, Preda S, Biundo F, Lanni C, Grilli M, Cavallero A, Olivero G, Salamone A, Govoni S, Marchi M. PLoS One. 2012;7(1):e29661. doi: 10.1371/journal.pone.0029661. Epub 2012 Jan 11.
BACKGROUND: We previously showed that beta-amyloid (Aβ), a peptide considered as relevant to Alzheimer's Disease, is able to act as a neuromodulator affecting neurotransmitter release in absence of evident sign of neurotoxicity in two different rat brain areas. In this paper we focused on the hippocampus, a brain area which is sensitive to Alzheimer's Disease pathology, evaluating the effect of Aβ (at different concentrations) on the neurotransmitter release stimulated by the activation of pre-synaptic cholinergic nicotinic receptors (nAChRs, α4β2 and α7 subtypes). Particularly, we focused on some neurotransmitters that are usually involved in learning and memory: glutamate, aspartate and GABA.
4.Pre-synaptic nicotinic receptors evoke endogenous glutamate and aspartate release from hippocampal synaptosomes by way of distinct coupling mechanisms.
Zappettini S1, Grilli M, Salamone A, Fedele E, Marchi M. Br J Pharmacol. 2010 Nov;161(5):1161-71. doi: 10.1111/j.1476-5381.2010.00958.x.
BACKGROUND AND PURPOSE: The present work aimed to investigate whether and through which mechanisms selective α7 and α4β2 nicotinic receptor (nAChR) agonists stimulate endogenous glutamate (GLU) and aspartate (ASP) release in rat hippocampus.