Use este identificador para citar ou linkar para este item: https://repositorio.ufrn.br/jspui/handle/123456789/23258
Título: Medial septal dysfunction by ABeta-induced KCNQ channel-block in glutamatergic neurons
Autor(es): Richardson N. Leão
Luis V. Colom
Lotta Borgius
Ole Kiehn
André Fisahn
Palavras-chave: Amyloid Beta peptide;Medial septum;Theta oscillations;Glutamatergic neurons;Cholinergic neurons;GABAergic neurons;M-current;A-current
Data do documento: Jul-2011
Resumo: Amyloid (A ) peptides play a central role in the pathophysiology of Alzheimer’s disease (AD). The cellular mechanisms underlying A toxicity, however, are poorly understood. Here we show that A 25-35 and A 1-40 acutely and differentially affect the characteristics of 3 classes of medial septum (MS) neurons in mice. In glutamatergic neurons A increases firing frequency and blocks the A- and the M-current (IA and IM, respectively). While the IA block is similar in other MS neuron classes, the block of IM is specific to glutamatergic neurons. IM block and a simulated A block mimic the A -induced increase in spontaneous firing in glutamatergic neurons. Calcium imaging shows that under control conditions glutamatergic neurons rarely fire while nonglutamatergic neurons fire coherently at theta frequencies. A increases the firing rate of glutamatergic neurons while nonglutamatergic neurons lose theta firing coherence. Our results demonstrate that A -induced dysfunction of glutamatergic neurons via IM decrease diminishes MS rhythmicity, which may negatively affect hippocampal rhythmogenesis and underlie the memory loss observed in Alzheimer’s disease.
URI: http://hdl.handle.net/123456789/23258
ISSN: 0197-4580
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