TY  - JOUR
A1  - Gonzalo-Ruiz, Alicia 
A1  - Delso, Maria 
A1  - Carrero, Isabel 
A1  - Gonzalo Vicente, Pilar 
A1  - Sanz-Anquela, José Miguel 
A1  - Rodríguez, Manuel 
A1  - Arévalo-Serrano, Juan 
T1  - A rat model of oligomeric forms of beta-amyloid (AÃ?) peptide: neuronal loss, synaptic alteration, astrogliosis, and calcium-binding proteins activation in vivo
JO  - Eur. J. Anat.
SN  - 1136-4890
Y1  - 2011
VL  - 15
SP  - 47
EP  - 72
UR  - http://www.eurjanat.com/web/paper.php?id=110005ag
KW  - Alzheimerâ??s disease
KW  - Retrosplenial cortex
KW  - Astrocytosis
KW  - S100B
KW  - Calpain-1
N2  - Oligomers of Beta-amyloid (AÃ?) peptide are presumed to cause synaptic and cognitive dysfunction in Alzheimerâ??s disease (AD). However, their contribution to other pathological features of AD remains unclear. To address the latter, we applied microinjections of AÃ?1-42 oligomers into the retrosplenial cortex of the rat. We observed that AÃ?1-42 induced a greater reduction in neuronal density as compared with that seen at control (AÃ?42-1) injections. Oligomers of AÃ?1-42 peptide caused synaptic alterations, as evidenced by the decrease in the presynaptic marker synaptophysin and the increase in chromogranin A. We also detected a marked interaction between GFAP-, and AÃ?immunoreactive material in a time-dependent manner. To address the possible mechanisms involved in astrocyte activation, we analyzed the interaction between the calcium-dependent protease, calpain-1, and the calcium-binding protein, S100B, and astrogliosis in response to AÃ? toxicity. Calpain-1 activation was studied by immunoblotting. Three immunopositive protein bands (80kDa, 76kDa, and 18kDa) were detected. Densitometry analyses revealed a significant increase in calpain-1 at 76kDa and at position 18kDa in AÃ?1-42-treated animals as compared with the corresponding bands in control animals. Confocal analysis showed codistribution of AÃ?-, and calpain 1-immunoreactivities in cortical cells, and in reactive astrocytes surrounding the injection of AÃ?, and both cortical and leptomeningeal blood vessels. A colocalization of GFAP and S100B proteins was observed in astrocytes that surrounded the AÃ? injection, and also in reactive astrocytes in close association with blood vessels. In conclusion, our results suggest that calpain-1 and S100B might play a critical role in astroglisois in response to AÃ? toxicity.
ER  -