Upregulation of anti-adhesive protein SPARC in mouse hippocampus after kainic acid administration

We have recently reported that the anti-adhesive glycoprotein SPARC (Secreted Protein Acidic and Rich in Cysteine) in basolateral amygdala nucleus contributes to the persistence of locomotor sensitization to morphine (Nat. Med. 6, 910-915, 2000). However, physiological function of SPARC in central n...

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Published in:Japanese Journal of Pharmacology 2001, Vol.85 (suppl.1), p.190-190
Main Authors: Mitsushi Ikemoto, Masatoshi Takita, Tomoyo Ochiishi, Koutarou Inoue, Shinya S Suzuki
Format: Article
Language:Japanese
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Summary:We have recently reported that the anti-adhesive glycoprotein SPARC (Secreted Protein Acidic and Rich in Cysteine) in basolateral amygdala nucleus contributes to the persistence of locomotor sensitization to morphine (Nat. Med. 6, 910-915, 2000). However, physiological function of SPARC in central nervous system (CNS) remains unknown. To investigate whether SPARC gene expression in CNS was regulated by neural activities, we examined the temporal changes of SPARC mRNA levels in mouse hippocampus after kainic acid (KA) administration (i.p., 25 mg/kg). Northern blotting analysis showed that SPARC mRNA levels in KA-evoked convulsive mouse hippocampus were reached to maximum (394 ± 52% of control, N = 6) after 7 days, and persisted about twice the control levels for 28 days. Histological examinations revealed that SPARC-like immunoreactivity was clearly up regulated in stratum radiatum of convulsive mouse hippocampus. The long-term effects of KA administration in this model include a progressive degeneration of the hippocampal CA1 areas. These results indicate that SPARC gene expression may be regulated in the neural activity-dependent manner and play an important role in synaptic plasticity.
ISSN:0021-5198