Long-term decrease in calbindin-D28K expression in the hippocampus of epileptic rats following pilocarpine-induced status epilepticus

Abstract

SummaryAcquired epilepsy (AE) is characterized by spontaneous recurrent seizures and long-term changes that occur in surviving neurons following an injury such as status epilepticus (SE). Long-lasting alterations in hippocampal Ca 2+ homeostasis have been observed in both in vivo and in vitro models of AE. One major regulator of Ca 2+ homeostasis is the neuronal calcium binding protein, calbindinD28k that serves to buffer and transport Ca 2+ ions. This study evaluated the expression of hippocampal calbindin levels in the rat pilocarpine model of AE. Calbindin protein expression was reduced over 50% in the hippocampus in epileptic animals. This decrease was observed in the pyramidal layer of CA1, stratum lucidum of CA3, hilus, and stratum granulosum and stratum moleculare of the dentate gyrus when corrected for cell loss. Furthermore, calbindin levels in individual neurons were also significantly reduced. In addition, the expression of calbindin mRNA was decreased in epileptic animals. Time course studies demonstrated that decreased calbindin expression was initially present 1 month following pilocarpine-induced SE and lasted for up to 2 years after the initial episode of SE. The results indicate that calbindin is essentially permanently decreased in the hippocampus in AE. This decrease in hippocampal calbindin may be a major contributing factor underlying some of the plasticity changes that occur in epileptogenesis and contribute to the alterations in Ca 2+ homeostasis associated with AE.

Correlation between calbindin expression in granule cells of the resected hippocampal dentate gyrus and verbal memory in temporal lobe epilepsy

“…Recently, we have shown that the degree of loss of CB in the granule cells is correlated with the age of onset and the duration of TLE [19]. This observation along with that of animal models of epilepsy suggest that decrease of CB mRNA and protein expression in the granule cells is a consequence of neuronal hyperactivity [66]. In fact, in animal models of TLE, the decreased CB expression can be detected only ipsilaterally but not contralaterally [67].…”

Protective Effects of Paeoniflorin Against Glutamate-Induced Neurotoxicity in PC12 Cells via Antioxidant Mechanisms and Ca2+ Antagonism

“…, protect the normal activation and function of the neuron and inhibit the apoptosis of neuron induced by the overload of intracellular Ca 2? (Meng et al 2007;Carter et al 2008). Pretreatment with paeoniflorin dose-dependently decreased intracellular Ca 2?…”

Distribución de calbindina y parvoalbúmina y efecto del virus de la rabia sobre su expresión en la médula espinal de ratones

“…Esto coincide con nuestros estudios previos en los que se demostró pérdida de CB en la corteza cerebral, el cuerpo estriado y el hipocampo (13,14,18). En diferentes afecciones del sistema nervioso central se ha encontrado disminución de la expresión de CB, por ejemplo, reducción del número de células de Purkinje positivas para CB en casos de degeneración espinocerebelar (27), así como disminución de la expresión de esta proteína en el hipocampo de ratas epilépticas (28). Son escasas las referencias relacionadas con pérdida de CB en la médula espinal.…”