Chronic inhibition of cortex microsomal Mg2+/Ca2+ ATPase‐mediated Ca2+ uptake in the rat pilocarpine model following epileptogenesis

• Published in: Journal of neurochemistry Vol. 79; no. 2; pp. 319 - 327
• Main Authors: Parsons, J. Travis, Churn, Severn B., DeLorenzo, Robert J.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Science Ltd 01.10.2001; Blackwell
• Subjects: Biological and medical sciences; calcium homeostasis; endoplasmic reticulum; epilepsy; Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy; Medical sciences; Nervous system (semeiology, syndromes); Neurology; SERCA; SREDs; status epilepticus; Antiglaucomatous agent; Animal model; Nervous system diseases; Calcium; Rat; Epilepsy; Rodentia; Pilocarpine; Inorganic element; Cerebral disorder; Parasympathomimetic; Vertebrata; Chronic; Mammalia; Central nervous system disease; Endoplasmic reticulum
• ISSN: 0022-3042; 1471-4159
• DOI: 10.1046/j.1471-4159.2001.00576.x

In the rat pilocarpine model, 1 h of status epilepticus caused significant inhibition of Mg2+/Ca2+ ATPase‐mediated Ca2+ uptake in cortex endoplasmic reticulum (microsomes) isolated immediately after the status episode. The rat pilocarpine model is also an established model of acquired epilepsy. Several weeks after the initial status epilepticus episode, the rats develop spontaneous recurrent seizures, or epilepsy. To determine whether inhibition of Ca2+ uptake persists after the establishment of epilepsy, Ca2+ uptake was studied in cortical microsomes isolated from rats displaying spontaneous recurrent seizures for 1 year. The initial rate and total Ca2+ uptake in microsomes from epileptic animals remained significantly inhibited 1 year after the expression of epilepsy compared to age‐matched controls. The inhibition of Ca2+ uptake was not due to individual seizures nor an artifact of increased Ca2+ release from epileptic microsomes. In addition, the decreased Ca2+ uptake was not due to either selective isolation of damaged epileptic microsomes from the homogenate or decreased Mg2+/Ca2+ ATPase protein in the epileptic microsomes. The data demonstrate that inhibition of microsomal Mg2+/Ca2+ ATPase‐mediated Ca2+ uptake in the pilocarpine model may underlie some of the long‐term plasticity changes associated with epileptogenesis.