Premium
Chronic liver failure in rats impairs glutamatergic synaptic transmission and long‐term potentiation in hippocampus and learning ability
Author(s) -
Monfort Pilar,
Erceg Slaven,
Piedrafita Blanca,
Llansola Marta,
Felipo Vicente
Publication year - 2007
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2007.05444.x
Subject(s) - long term potentiation , ampa receptor , neuroscience , nmda receptor , glutamatergic , hippocampus , neurotransmission , long term depression , morris water navigation task , synaptic plasticity , excitatory postsynaptic potential , hippocampal formation , postsynaptic potential , glutamate receptor , biology , psychology , medicine , receptor , inhibitory postsynaptic potential
Cognitive function is impaired in patients with liver disease by unknown mechanisms. Long‐term potentiation (LTP) in the hippocampus is considered the basis of some forms of learning and memory. The aims of this work were to assess (i) whether chronic liver failure impairs hippocampal LTP; (ii) if this impairment may be due to alterations in glutamatergic neurotransmission, and (iii) if impairment of LTP is associated with reduced learning ability. It is shown that liver failure in Wistar rats induces the following alterations in the hippocampus; (i) alters the phosphorylation of NMDA and AMPA receptors; (ii) reduces the expression of NMDA and AMPA receptors in membranes, (iii) reduces the magnitude of excitatory postsynaptic potentials (EPSPs) induced by activation of NMDA or AMPA receptors, and (iv) impairs NMDA receptor‐dependent LTP. Liver failure also impairs learning of the Morris water maze task. Impairment of glutamatergic synaptic transmission and NMDA receptor‐mediated responses may be involved in the alterations of cognitive function in patients with liver disease.