Niemann-Pick type C1 (NPC1) disease is a neurodegenerative lysosomal storage 
disorder caused by mutations in the NPC1 gene which encodes a transmembrane 
protein of the acidic compartment. Albeit the NPC1(-/-) mouse is available 
serving as an appropriate animal model of the human disease, the precise 
function of this protein remains obscure. Here, we investigated the synaptic 
consequences of this disease and explored long-term potentiation (LTP) in slices 
taken from the hippocampal CA1 region, the dorsomedial striatum as well as the 
somatosensory neocortex in NPC1(-/-) mice using extracellular field potential 
recordings. We did not observe significant changes in synaptic excitability as 
well as LTP in the hippocampal CA1 region and the dorsomedial striatum of 
NPC1(-/-) mice when compared to wildtype littermates. However, neocortical 
excitability was significantly enhanced while LTP was abolished. These results 
suggest that at least in the somatosensory neocortex NPC1 protein is 
instrumental in synaptic function.