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Xenopus laevis oocytes exposed to amyloid-β aggregate generated oscillatory electric activity (blips) that was recorded by two-microelectrode voltage-clamp. The cells exhibited a series of "spontaneous" blips ranging in amplitude from 3.8 ± 0.9 nA at the beginning of the recordings to 6.8 ± 1.7 nA after 15 min of exposure to 1 μM aggregate. These blips were similar in amplitude to those induced by the channel-forming antimicrobial agents amphotericin B (7.8 ± 1.2 nA) and gramicidin (6.3 ± 1.1 nA). The amyloid aggregate-induced currents were abolished when extracellular Ca(2+) was removed from the bathing solution, suggesting a central role for this cation in generating the spontaneous electric activity. The amyloid aggregate also affected the Ca(2+)-dependent Cl(-) currents of oocytes, as shown by increased amplitude of the transient-outward chloride current (T(out)) and the serum-activated, oscillatory Cl(-) currents. Electron microcopy revealed that amyloid aggregate induced the dissociation of the follicular cells that surround the oocyte, thus leading to a failure in the electro-chemical communication between these cells. This was also evidenced by the suppression of the oscillatory Ca(2+)-dependent ATP-currents, which require proper coupling between oocytes and the follicular cell layer. These observations, made using the X. laevis oocytes as a versatile experimental model, may help to understand the effects of amyloid aggregate on cellular communication.
Arellano,
Ion channels and membrane receptors in follicle-enclosed Xenopus oocytes.
1996, Pubmed,
Xenbase
Arellano,
Ion channels and membrane receptors in follicle-enclosed Xenopus oocytes.
1996,
Pubmed
,
Xenbase Arellano,
Cl- currents activated via purinergic receptors in Xenopus follicles.
1998,
Pubmed
,
Xenbase Arispe,
Architecture of the Alzheimer's A beta P ion channel pore.
2004,
Pubmed Arispe,
The ability of amyloid beta-protein [A beta P (1-40)] to form Ca2+ channels provides a mechanism for neuronal death in Alzheimer's disease.
1994,
Pubmed Avila,
Canonical Wnt3a modulates intracellular calcium and enhances excitatory neurotransmission in hippocampal neurons.
2010,
Pubmed Bourin,
Nicotinic receptors and Alzheimer's disease.
2003,
Pubmed Daniels,
The role of the MAP-kinase superfamily in beta-amyloid toxicity.
2001,
Pubmed Haass,
Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer's amyloid beta-peptide.
2007,
Pubmed Hsieh,
AMPAR removal underlies Abeta-induced synaptic depression and dendritic spine loss.
2006,
Pubmed Jang,
Models of beta-amyloid ion channels in the membrane suggest that channel formation in the bilayer is a dynamic process.
2007,
Pubmed Kawahara,
Alzheimer's beta-amyloid, human islet amylin, and prion protein fragment evoke intracellular free calcium elevations by a common mechanism in a hypothalamic GnRH neuronal cell line.
2000,
Pubmed Maccioni,
The protein kinase Cdk5. Structural aspects, roles in neurogenesis and involvement in Alzheimer's pathology.
2001,
Pubmed Mattson,
Dysregulation of cellular calcium homeostasis in Alzheimer's disease: bad genes and bad habits.
2001,
Pubmed Mezler,
A β-amyloid oligomer directly modulates P/Q-type calcium currents in Xenopus oocytes.
2012,
Pubmed
,
Xenbase Miledi,
A calcium-dependent transient outward current in Xenopus laevis oocytes.
1982,
Pubmed
,
Xenbase Miledi,
Effects of defolliculation on membrane current responses of Xenopus oocytes.
1989,
Pubmed
,
Xenbase Pandya,
Allosteric modulator Desformylflustrabromine relieves the inhibition of α2β2 and α4β2 nicotinic acetylcholine receptors by β-amyloid(1-42) peptide.
2011,
Pubmed
,
Xenbase Parodi,
Beta-amyloid causes depletion of synaptic vesicles leading to neurotransmission failure.
2010,
Pubmed Quist,
Amyloid ion channels: a common structural link for protein-misfolding disease.
2005,
Pubmed Reiser,
Changes in the properties of synaptic channels opened by acetylcholine in denervated frog muscle.
1989,
Pubmed Roberson,
100 years and counting: prospects for defeating Alzheimer's disease.
2006,
Pubmed Saldaña,
Native ion current coupled to purinergic activation via basal and mechanically induced ATP release in Xenopus follicles.
2009,
Pubmed
,
Xenbase Schroeder,
Expression cloning of TMEM16A as a calcium-activated chloride channel subunit.
2008,
Pubmed
,
Xenbase Scudieri,
The anoctamin family: TMEM16A and TMEM16B as calcium-activated chloride channels.
2012,
Pubmed Selkoe,
Alzheimer's disease is a synaptic failure.
2002,
Pubmed Sepulveda,
Synaptotoxicity of Alzheimer beta amyloid can be explained by its membrane perforating property.
2010,
Pubmed Shankar,
Natural oligomers of the Alzheimer amyloid-beta protein induce reversible synapse loss by modulating an NMDA-type glutamate receptor-dependent signaling pathway.
2007,
Pubmed Texidó,
Amyloid β peptide oligomers directly activate NMDA receptors.
2011,
Pubmed
,
Xenbase Tigyi,
A factor that activates oscillatory chloride currents in Xenopus oocytes copurifies with a subfraction of serum albumin.
1991,
Pubmed
,
Xenbase
