δείτε την πρωτότυπη σελίδα τεκμηρίου στον ιστότοπο του αποθετηρίου του φορέα για περισσότερες πληροφορίες και για να δείτε όλα τα ψηφιακά αρχεία του τεκμηρίου*
Aberrant modulation of a delayed rectifier potassium channel by
glutamate in Alzheimer's disease
Poulopoulou, Cornelia
Markakis, Loannis
Davaki, Panagiota and
Tsaltas, Eleftheria
Rombos, Antonis
Hatzimanolis, Alexandros and
Vassilopoulos, Dimitrios
In Alzheimer’s disease (AD), potassium channel abnormalities have been
reported in both neural and peripheral tissues. Herein, using whole-cell
patch-clamp, we demonstrate an aberrant glutamate-dependent modulation
of K(V)1.3 channels in T lymphocytes of AD patients. Although intrinsic
K(V)1.3 properties in patients were similar to healthy individuals,
glutamate (1-1000 mu M) failed to yield the hyperpolarizing shift
normally observed in K(V)1.3 steady-state inactivation (-4.4 +/- 2.7 mV
in AD vs. -14.3 +/- 2.5 mV in controls, 10 mu M glutamate), resulting in
a 4-fold increase of resting channel activity. Specific agonist and
antagonist data indicate that this abnormality is due to dysfunction of
cognate group II mGluRs. Given that glutamate is present in plasma and
that both mGluRs and K(V)1.3 channels regulate T-lymphocyte
responsiveness, our finding may account for the presence of
immune-associated alterations in AD. Furthermore, if this aberration
reflects a corresponding one in neural tissue, it could provide a
potential target in AD pathogenesis. (c) 2009 Elsevier Inc. All rights
reserved.
(EN)
*Η εύρυθμη και αδιάλειπτη λειτουργία των διαδικτυακών διευθύνσεων των συλλογών (ψηφιακό αρχείο, καρτέλα τεκμηρίου στο αποθετήριο) είναι αποκλειστική ευθύνη των αντίστοιχων Φορέων περιεχομένου.
Aberrant modulation of a delayed rectifier potassium channel by glutamate in Alzheimers disease
Aberrant modulation of a delayed rectifier potassium channel by glutamate in Alzheimers disease
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