It is known that elderly people suffering from heart disease can have memory problems. The hippocampus is the part of the brain that is essential for memory formation and is one of the areas that is most vulnerable to cerebral hypoperfusion. Long-term potentiation is widely accepted as the cellular basis for memory. Upregulation of glutamate receptors of the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-D-aspartate (NMDA) type in the synaptic membranes is important to make the synapses more efficient during long-term potentiation. While animal models of acute global or focal brain ischemia have been widely investigated, the brain effects caused by a dysfunctional heart have been insufficiently studied, in particular with respect to cellular and molecular mechanisms that link heart failure to cognitive impairment. To address the issue of a relation between heart failure and cognitive impairment, we have used a mouse model with specific, inducible expression of the mutUNG1enzyme in the heart. The mutUNG1 enzyme generates mitochondrial DNA damage in the form of apurinic/apyrimidinic sites which leads to mitochondrial impairment in cardiomyocytes and ultimately a dysfunctional heart. This gives the opportunity to study possible changes in the brain of a chronic heart failure mouse model. The aim of this thesis was to investigate whether a dysfunctional heart affects the expression of AMPA and NMDA receptors in the hippocampus, which would provide a possible explanation to the memory deficits experienced by patients suffering from heart disease. Quantitative polymerase chain reaction was used to quantify the gene expression of AMPA and NMDA receptors. Quantitative electron microscopy, by the use of postembedding immunogold labelling, was used to study the number of AMPA and NMDA receptors present in excitatory synapses of the hippocampus, as well as synaptic morphology in the form of postsynaptic density length. The results obtained by qPCR showed large variations in gene expression within both groups, but no significant difference was found between them. Quantitative electron microscopy showed no significant differences in number of receptors at the protein level and in the length of postsynaptic densities. These results show that acute heart failure as induced in this mouse model may not be sufficient to have an impact on the brain. Nonetheless, the use of a different chronic heart failure model in future studies could show a link between heart failure and cognitive decline.