Beta-Amyloid peptide25-35 depresses excitatory synaptic transmission in the rat basolateral amygdala "in vitro".

Abstract:

:The effects of beta-amyloid peptide25-35 on resting membrane potential, spontaneous and evoked action potential and synaptic activity have been studied in basolateral amygdaloid complex on slices obtained from adult rats. Intracellular recordings reveal that perfusion with beta-amyloid peptide25-35 at concentrations of 400 nM and less did not generate any effect on resting membrane potential. However, concentrations in the range of 800-1200 nM produced an unpredictable effect, depolarization and/or hyperpolarization, which were blocked by tetrodotoxin or 6-cyano-7-nitroquinoxaline-2,3-dione+D-(-)-2-amino-5-phosphonopentanoic acid together with bicuculline. Excitatory and inhibitory evoked responses mediated by glutamic acid or gamma-aminobutyric acid decreased in amplitude after beta-amyloid peptide25-35 perfusion. Additionally, results obtained using the paired-pulse protocol offer support for a presynaptic mode of action. To determine which type of receptors and/or channels are involved in the presynaptic mechanism of action, a specific blocker of alpha-7 nicotinic receptors (methyllycaconitine citrate) or L-type calcium channel blockers (calcicludine or nifedipine) were used. beta-amyloid petide25-35 decreased excitatory postsynaptic potentials amplitude in control conditions and also in slices permanently perfused with methyllycaconitine citrate. However, this effect was blocked in slices perfused with calcicludine or nifedipine suggesting the involvement of the L-type calcium channels. On the whole, these experiments provide evidence that beta-amyloid peptide25-35 affects neurotransmission in basolateral amygdala and its action is mediated through L-type calcium channels.

journal_name

Neurobiol Aging

journal_title

Neurobiology of aging

authors

Ashenafi S,Fuente A,Criado JM,Riolobos AS,Heredia M,Yajeya J

doi

10.1016/j.neurobiolaging.2004.05.008

subject

Has Abstract

pub_date

2005-04-01 00:00:00

pages

419-28

issue

4

eissn

0197-4580

issn

1558-1497

pii

S0197-4580(04)00225-8

journal_volume

26

pub_type

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