NR AJIS
AU Pereira,G.S.; Walz,R.; Bonan,C.D.; Battastini,A.M.; Izquierdo,I.; Martins,V.R.; Brentani,R.R.; Sarkis,J.J.
TI Changes in cortical and hippocampal ectonucleotidase activities in mice lacking cellular prion protein
QU Neuroscience Letters 2001 Mar 23; 301(1): 72-4
PT journal article
AB Animals lacking cellular prion protein (PrPc) expression are more susceptible to seizures. Adenosine is an endogenous anticonvulsant agent and it levels in the synaptic cleft are regulated by ectonucleotidases. We evaluated ectonucleotidase activities in synaptosomes from hippocampus and cerebral cortex of adult PrPc null mice and wild-type mice (genetic background 129/Sv X C57BL/6J). There was an increase (47%) in adenosine triphosphate (ATP) hydrolysis in hippocampal synaptosomes of PrPc knockout mice as compared with the wild-type animals. In cortical synaptosomes, ATP hydrolysis was similar in both PrPc mice and controls. However, there was a significant decrease in adenosine diphosphate (ADP) hydrolysis in both hippocampal (-39%) and cortical (-25%) synaptosomes in PrPc null animals compared to wild-type mice. Changes in brain ectonucleotidases activities related to modifications in the PrPc expression may contribute, at least in part, to the higher sensitivity to seizures of PrPc null mice.
MH Adenosine Diphosphate/*metabolism; Adenosine Triphosphate/*metabolism; Animal; Cerebral Cortex/*metabolism; Hippocampus/*metabolism; Hydrolysis; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Nucleotidases/*metabolism; *Prions/genetics; Support, Non-U.S. Gov't; Synaptosomes/metabolism
AD Departamento de Bioquimica, ICBS, UFRGS, Avenida Ramiro Barcellos 2600, 90035-003, RS, Porto Alegre, Brazil.
SP englisch
PO Irland